布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

烟碱对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of nicotine on myocardial iscbemia-reperfusion (IR) injury in rats. Methods Seventy-four male SD rats weighing 200-250 g were randomly divided into 5 groups: group Ⅰ sham operation (group S, n=10), group Ⅱ IR (n = 16), group Ⅲ nicotine 400 μg/kg (group N1,n = 16), group Ⅳ nicotine 40 μg/kg (group N2, n = 16) and group Ⅴ nicotine 400 μg/kg + a-bungarotoxin(group a-BGT, n = 16). Myocardial ischemia was induced by occlusion of left anterior descending branch (LAD) of coronary artery for 30 min followed by 60 min of reperfusiou. LAD was exposed, but not occluded in group S. Nicotine 400 and 40 μg/kg were injected iv via the right jugular vein in group N1 and N2 respectively, and a-bungarotoxin 1.0 μg/kg and nicotion 400 μg/kg were injected iv via the fight jugular vein in group a-BGT at 30 min before myocardial ischemia. Equal volume of normal saline was injected instead in group S and IR. Six animals in each group were killed at 60 min of reperfusion and the hearts removed to measure the left ventricular area (LVA), area at risk (MR) and infarct area (IA) in group IR, N1,N2 and α-BGT. AAP/LVA and IA/LVA were calculated. The blood samples from right carotid artery were obtained for determination of plasma concentrations of TNF-α and IL-1β and activities of CK-MB and LDH. The animals were then killed and the hearts removed to observe the myocardial ultrastrueture and determine the activity of MPO. Results Compared with group S, plasma concentrations of TNF-α and IL-1β and activities of CK-MB and LDH, and myocardial MPO activity were significantly increased in group IR, N1, N2 and a-BGT (P<0.05). Compared with group IB, IA/LVA,plasma concentrations of TNF-α and IL-1β and activities of CK-MB and LDH, and myocardial MPO activity were significantly decreased in group N1 (P < 0.05), but there was no significant difference in the indices mentioned above between group N2 and IB and between group α-BGT and IB (P > 0.05). Compared with group N1,IA/LVA, plasma concentrations of TNF-α and IL-1βand activities of CK-MB and LDH, and myocardial MPO activity were significantly increased in group N2 and α-BGT (P < 0.05). The injury to myocardial uhrastructure was attenuated in group N1 as compared with group IR, while aggravated in group N2 and α-BGT as compared with group N1. Conclusion Nicotine can ameliorate the myocardial IR in rats. The mechanism may be related to the activation of the cholinergic anti-inflanunatory pathway and inhibition of the inflammatory response.     

Vasopressor hormone response following mesenteric traction during major abdominal surgery

Background : We investigated the vasopressor hormone response following mesenteric traction (MT) with hypotension due to prostacyclin (PGI₂) release in patients undergoing abdominal surgery with a combined general and epidural anesthesia. Methods : In a prospective, randomized, placebo-controlled study we administered 400 mg ibuprofen (i.v.) in 42 patients scheduled for abdominal surgery. General anesthesia was combined with epidural anesthesia (T4-L1). Before as well as 5, 15, 30, 45, and 90 min after MT we recorded plasma osmolality, hemodynamics and measured 6-keto-PGFlα (stabile metabolite of PGI₂), TXB₂ (stabile metabolite of thromboxane A₂) active renin, and arginine vasopressin (AVP) plasma concentrations by radioimmunoassay. Catecholamine levels were assessed by high-pressure liquid chromatography (HPLC) with electrochemical detection. Results : Following MT, arterial hypotension occurred along with a substantial PGI₂ release. This was completely abolished by ibuprofen administration. Although plasma levels of 6-keto-PGF_1α (1133 (708) vs. 60 (3) ng/L, median (median absolute deviation), P=0.0001, placebo vs. ibuprofen) remained significantly elevated, blood pressure was restored within 30 min after MT in the placebo group. At the same point in time plasma concentrations of TXB² (164 (87) vs. 58 (1) ng/L, P=0.0001), epinephrine (46 (33) vs. 14 (6) ng/L, P=0.001), AVP (41 ± (18) vs. 12 (7) ng/L, P=0.0004), and active renin (27 (12) vs. 12 (4) ng/L, P = 0.001) were significantly higher in placebo-treated patients. Conclusion : Under combined general and epidural anesthesia arterial hypotension following MT due to endogenous PGI₂ release is associated with enhanced release of AVP, active renin, epinephrine and thromboxane A₂, presumably contributing to hemodynamic stability within 30 min after MT.     

A comparison of the inhibitory effects of four volatile anaesthetics on the metabolism of chlorzoxazone, a substrate for CYP2E1, in rabbits

Background: Halothane inhibits in vitro and in vivo activity of cytochrome P-450 (CYP) 2E1. There are several fluorinated volatile anaesthetics besides halothane, and most of them are defluorinated by CYP2E1. It is unclear whether other fluorinated anaesthetics inhibit the in vivo activity of CYP2E1.
Methods: We compared the inhibitory effects of therapeutic concentrations of four inhalational anaesthetics, halothane, enflurane, isoflurane, and sevoflurane, on chlorzoxazone metabolism in rabbits receiving artificial ventilation.
Results: All four inhalational anaesthetics decreased arterial blood pressure and increased plasma chlorzoxazone concentration. However, no significant differences in the plasma chlorzoxazone concentration were found between the four anaesthetics. The estimated chlorzoxazone clearance increased after beginning inhalation with all four agents, but no significant difference in clearance was noted between agents.
Conclusions: At therapeutic concentrations, the in vivo inhibitory effect on chlorzoxazone metabolism was similar for all four inhalational anaesthetics examined, even though their chemical characteristics and extent of hepatic metabolism differ considerably.     

A Teaspoon Pump for Pumping Blood with High Hydraulic Efficiency and Low Hemolysis Potential

Abstract: Virtually all blood pumps contain some kind of rubbing, sliding, closely moving machinery surfaces that are exposed to the blood being pumped. These valves, internal bearings, magnetic bearing position sensors, and shaft seals cause most of the problems with blood pumps. The original teaspoon pump design prevented the rubbing, sliding machinery surfaces from contacting the blood. However, the hydraulic efficiency was low because the blood was able to "slip around" the rotating impeller so that the blood itself never rotated fast enough to develop adequate pressure. An improved teaspoon blood pump has been designed and tested and has shown acceptable hydraulic performance and low hemolysis potential. The new pump uses a nonrotating "swinging" hose as the pump impeller. The fluid enters the pump through the center of the swinging hose; therefore, there can be no fluid slip between the revolving blood and the revolving impeller. The new pump uses an impeller that is comparable to a flexible garden hose. If the free end of the hose were swung around in a circle like half of a jump rope, the fluid inside the hose would rotate and develop pressure even though the hose impeller itself did not "rotate"; therefore, no rotating shaft seal or internal bearings are required.     

Microspheres Based Detoxification System: A New Method in Convective Blood Purification

Abstract: A variety of protein-bound or hydrophobic substances, accumulating as a result of pathologic conditions such as exogenous or endogenous intoxications, are removed poorly by conventional detoxification methods because of low accessibility (hemodialysis), insufficient adsorption capabilities (hemosorption), low efficiency (peritoneal dialysis), or economic limitations (high-volume plasmapheresis). Combining advantages of existing methods with microspheric technology, a module-based system was designed. Major operating parameters of the latter can be modified to allow for adjustment to individual clinical situations. An extracorporeal blood circuit including a plasmafilter is combined with a secondary high-velocity plasma circuit driven by a centrifugal pump. Different microspheric adsorbers can be combined in one circuit or applied in sequence. Thus, a prolonged treatment can be tailored using specially designed selective adsorber materials. Comparing this system with existing methods (high-flux hemodialysis, molecular adsorbent recycling system), results from our in vitro studies and animal experiments demonstrate the superior efficiency of substance removal.     

Tissue perfusion in relation to cardiac output during continuous positive-pressure ventilation and administration of propranolol or verapamil

Background : Our objective was to determine whether administration of propranolol or verapamil modifies the hemodynamic adaptation to continuous positive-pressure ventilation (CPPV), in particular the regional distribution of cardiac output (CO).
Methods : General hemodynamics and regional blood flows assessed by microsphere technique (15 (μm) were recorded in 16 anesthetized pigs during spontaneous breathing (SB) and CPPV with 8 cm H₂O end-expiratory pressure (CPPV8) before and after intravenous administration of propranolol (0.3 mg · kg⁻¹ followed by 0.15 mg · kg⁻¹ · h⁻¹, n=8) or verapamil (0.1 mg · kg⁻¹ followed by 0.3 mg · kg⁻¹ · h⁻¹, n=8).
Results : CPPV8 depressed CO by 25% without shifts in its relative distribution with the exception of a noteworthy increase in adrenal perfusion. Propranolol increased arterial blood pressure, and due to a fall in heart rate, CO dropped by 25%. The kidneys and, to a lesser extent, the splanchic region and central nervous system received increased fractions of the remaining CO at the expense of skeletal muscle flow. Similar patterns were seen during SB and CPPV8 such that the combination of propranolol and CPPV8 depressed CO by 50%. The circulatory effects of verapamil were less evident but myocardial perfusion tended to increase.
Conclusions : The combination of propranolol or verapamil with CPPV does not result in any specific hemodynamic interaction in anesthetized pigs, except that the combined effect of propranolol and CPPV may severely reduce CO.     

Volatile anaesthetics reduce adhesion of blood platelets under low-flow conditions in the coronary system of isolated guinea pig hearts

Background : Inhibitory effects of volatile anaesthetics on platelet aggregation have been demonstrated in several studies. However, the influence of volatile anaesthetics on intracoronary platelet adhesion has not been elucidated so far.
Methods : Isolated hearts of guinea pigs were perfused with buffer in the absence or presence of volatile anaesthetics (0.5 and 1 MAC) at constant coronary flow rates of 5 ml/min for 25 min, then 1 ml/min for 30 min and again 5 ml/min for 10 min. Before, during and after low-flow perfusion, a bolus of human platelets was applied into the coronary system. To simulate thrombogenic conditions, 0.3 U/ml human thrombin was infused during low-flow perfusion and reperfusion. The number of platelets sequestered to the endothelium was calculated from the difference between coronary in- and output of platelets. The myocardial production of lactate and consumption of pyruvate and coronary perfusion pressure were also determined.
Results : At a flow rate of 5 ml/min only about 3% of the applied platelets did not emerge from the coronary system, in any group. In contrast, 13.1±1.2% (mean±SEM) of infused platelets became adherent in low-flow perfusion in the control group without anaesthetic. The adherence was reduced with each 1 MAC isoflurane (to 6.2±1.2%), sevoflurane (to 4.4±0.9%) or halothane (to 3.2±1.5%) (each P <0.05 vs. control). Volatile anaesthetic, 0.5 MAC, did not inhibit platelet adhesion to a statistically significant extent in any case. Perfusion pressure and metabolic parameters were not statistically different between the control and the hearts exposed to anaesthetics.
Conclusion : Volatile anaesthetics in a concentration of 1 MAC can reduce the adhesion of platelets in the coronary system under reduced flow conditions. This action does not arise from vasodilation or inhibition of ischaemic stress.     

Bariatric Surgery in Some "Central and East-European (former Eastern bloc)"Countries - Current Status and Prediction for the Next Millennium

Background: Obesity is increasing globallly, including in the formerly "Eastern Bloc" countries. Methods: A survey was made of obesity and bariatric surgery. Results: In the 8 East and Central European countries studied, with total population 300 million, roughly 43% of the population was overweight (BMI 25-30), 23% obese (BMI > 30), with about 15 million people morbidly obese (BMI > 40). From 0-10 morbidly obese individuals/100,000/year undergo bariatric surgery. Conclusion: Most countries were found to provide inadequate treatment for obesity.The majority of the morbidly obese are not treated effectively. However, health-care awareness of obesity and bariatric surgeons are slowly increasing.     

Is the recovery profile of mivacurium independent of the rate of decay of its plasma concentration in patients with normal plasma cholinesterase activity?

Background: The duration of action of muscle relaxants is poorly correlated to the rate of decay of their plasma concentration. The plasma concentration of mivacurium may rapidly decrease below its active concentration because of the extensive hydrolysis of mivacurium. By inflating a tourniquet on one upper limb for 3 min after the administration of atracurium, mivacurium or vecuronium, we studied the influence of the initial decline of their plasma concentration on their effect. Methods: In 50 patients anaesthetised with thiopental, isoflurane and fentanyl, the effect of bolus doses of 0.15 or 0.25 mg . kg^?1 mivacurium (MIV 15, MIV 25), 0.3 or 0.5 mg . kg^?1 atracurium (ATR 30, ATR 50) and 0.06 or 0.1 mg . kg^?1 vecuronium (VEC 06, VEC 10) were measured on both arms (evoked response of the adductor pollicis to train-of-four stimulation every 12 s), a tourniquet being applied on one arm just before and during 3 min after the muscle relaxant bolus. Results: Tourniquet inflation of 3 min almost abolished the neuromuscular effect of mivacurium. In the vecuronium groups and in the ATR 50 group, tourniquet inflation did not modify the maximum degree of depression of the twitch response. Also, the duration of action of vecuronium was unaffected by the tourniquet. In the ATR 30 group, times to return of the twitch response to 25% (duration 25%) and 75% (duration 75%) of control response were significantly shorter in the cuffed arm, 23 min vs 27 min, and 41 min vs 45 min, respectively. In the ATR 50 group, only duration 25% was significantly shorter in the cuffed arm (41 min vs 45 min). Conclusion: The results suggest that the rate of decline of the plasma concentration of mivacurium is so rapid, that a very low and almost clinically ineffective concentration is present as soon as 3 min after its administration. The results also indicate that the recovery from a mivacurium-induced neuromuscular blockade is not influenced by the rate of decay of its plasma concentration in patients with genotypically normal plasma cholinesterase.     

Membranes in Artificial Organs

Abstract: Membrane processes play a pivotal and enabling role in modern replacement therapy for acute and chronic organ failure and in the management of immunologic diseases. In fact, virtually all contemporary extracorporeal blood purification methods employ membrane devices, and the next generation of artificial organs and tissue engineering therapies are almost certain to be similarly grounded in membrane technology. In this short essay, we comment on the similarities and differences among synthetic membranes and their natural counterparts and also provide a critical overview of the demographics and technology of hemodialysis, hemofiltration, apheresis, oxygenation, and emerging membrane technologies and applications.     

Synergistic interaction between the effects of propofol and midazolam with fentanyl on phrenic nerve activity in rabbits

Background: It has been shown that the depressive effects of both propofol and midazolam on consciousness are synergistic with opioids, but the nature of their interactions on other physiological systems, e. g. respiration, has not been fully investigated. The present study examined the effect of propofol and midazolam alone and in combination with fentanyl on phrenic nerve activity (PNA) and whether such interactions are additive or synergistic. Methods: PNA was recorded in 27 anaesthetised and artificially ventilated rabbits. In three groups, propofol, fentanyl and midazolam were administered intravenously in incremental doses to construct dose-response curves for the depressant effects of each one on PNA. In another two groups, the effect of pretreatment with either fentanyl 1 μg · kg^?1 i. v. or midazolam 0.05 mg · kg^?1 i. v. on the effects of propofol and fentanyl respectively on PNA were studied. Results: Propofol and fentanyl caused a dose-dependent depression of PNA with complete abolition at the highest total doses of 16 mg · kg^?1 i. v. and 32 μg · kg^?1 i. v., respectively. In contrast, midazolam in incremental doses to a total of 0.8 mg · kg^?1 reduced mean PNA by 63%, but approximately 12% of PNA remained at a total dose as high as 6.4 mg · kg^?1. The mean ED₅₀s, calculated from dose-response curves, were 5.4 mg · kg^?1, 3.9 μg · kg^?1 and 0.4 mg · kg^?1 for propofol, fentanyl and midazolam, respectively. Initial doses of either fentanyl 1 μg · kg^?1 i. v. or midazolam 0.05 mg · kg^?1 i. v. acted synergistically with subsequent doses of either propofol or fentanyl to abolish PNA at total doses of 8 mg · kg^?1 and 8 μg · kg^?1, respectively. Conclusion: Fentanyl has a synergistic interaction with both propofol and midazolam on PNA and hence potentially on respiration.