持续气道正压通气对急性心源性肺水肿犬呼吸及循环功能的影响

目的研究持续气道正压(CPAP)通气对急性心源性肺水肿(ACPE)犬呼吸及循环功能的影响。方法分别监测10条犬健康状态及ACPE发生后自主呼吸、5cmH2O(1cmH2O=0.098kPa)、10cmH2O、15cmH2OCPAP时的胸腔负压(Pt)、中心静脉压(CVP)、心输出量(CO)、平均动脉压(BPm)、肺动脉楔压(PAWP)。结果与健康状态相比,ACPE犬呼吸增强、增快,Pt由-(4.90±0.09)cmH2O上升至-(10.90±0.75)cmH2O,CVP由(10.1±0.4)mmHg下降至(8.0±0.7)mmHg,CO由(1.52±0.13)L/min下降至(0.85±0.09)L/min,PAWP升高(P均<0.05)。CVP与Pt变化呈正相关(r=0.78,P<0.01)。5及10cmH2OCPAP时Pt值恢复至-(6.53±0.11)cmH2O和-(5.14±0.25)cmH2O,呼吸形式基本恢复正常,CVP升至(11.6±0.7)mmHg和(14.2±0.2)mmHg,CO增加至(1.45±0.11)L/min和(1.24±0.11)L/min,其中5cmH2OCPAP组PAWP下降(P均<0.05)。15cmH2OCPAP时,呼吸浅快,Pt为-(0.82±0.37)cmH2O,CO为(0.82±0.07)L/min,其他血流动力学指标皆恶化(P均<0.05)。结论犬ACPE发生时,呼吸运动显著增强,Pt升高,并导致CVP和CO的下降;适当CPAP通过改善呼吸功能,调节Pt改善ACPE犬的心功能。     

Hemodynamic effect of mannitol in a canine model of concomitant increased intracranial pressure and hemorrhagic shock

The use of mannitol in the management of head injury has been considered a threat to hemodynamic stability in hypotensive multiply injured patients. To evaluate this contention, we compared mannitol with normal saline administration in a canine model combining elevated intracranial pressure (ICP) and hemorrhagic shock. Mongrel dogs were bled to and maintained at a mean arterial pressure (MAP) of 60 mm Hg for 30 minutes. Following this, ICP was elevated to and sustained at 25 mm Hg for 45 minutes by inflating an epidural balloon. The dogs were then randomized to resuscitation with 2 g/kg of mannitol in saline (total volume, 20 mL/kg; n = 5) or 20 mL/kg of normal saline alone (n = 5). All dogs were successfully resuscitated, and MAP returned to baseline levels in both groups. ICP was significantly lower and urine output significantly higher in the mannitol group than in saline controls (P less than .01). Moreover, cerebral perfusion pressure, cardiac index, and left ventricular stroke work index were significantly improved in dogs given mannitol versus controls during the first hour of resuscitation (P less than .05). Mannitol ameliorates increases in ICP without compromising hemodynamic resuscitation in a canine model of concomitant increased ICP and shock.     

Hemodynamic effects of pneumatic external counterpressure in canine hemorrhagic shock

To assess the effects of external counterpressure in a hypovolemic canine model, mean right atrial pressure (RA), left ventricle end-diastolic pressure (LVEDP), mean aortic pressure (Ao), and cardiac output (CO) (indicator dilution technique or electromagnetic ascending aortic flow) were measured in eight closed-chest mongrel dogs following phlebotomy to an Ao of 50 to 60 mm Hg. Inferior vena cava (IVC) flow was measured electromagnetically with a cannulating probe in four animals. The antishock garment was inflated to pressures of 40, 60, 80, and 100 mm Hg. An extended shock "control" period preceded inflation to minimize the effect of reflex circulatory responses to acute blood loss. IVC flow (2 +/- 1 mL/min/kg) during and immediately following antishock garment inflation was not significantly different from control (3 +/- 1 mL/min/kg) regardless of inflation pressure. Ao, RA, and LVEDP measured 30 seconds and 15 minutes after garment inflation were increased, but CO was not significantly different from control values at each inflation pressure. Garment inflation significantly increased peripheral vascular resistance (PVR) at all inflation pressures, and there was a significant correlation (r = .53; P less than .001) between the change in Ao and PVR. These results indicate that the change in arterial pressure produced by external counterpressure is the result of an increase in PVR and not the result of an autotransfusion and subsequent increased left heart outflow in the canine shock model.     

Comparison of standard external CPR, open-chest CPR, and cardiopulmonary bypass in a canine myocardial infarct model

STUDY OBJECTIVES: After cardiac arrest, open-chest CPR (OCCPR) and cardiopulmonary bypass (CPB) have demonstrated higher resuscitation rates when compared individually with standard external CPR (SECPR). We compared all three techniques in a canine myocardial infarct ventricular fibrillation model. TYPE OF PARTICIPANTS: Twenty-six mongrel dogs were block-randomized to receive SECPR and advanced life support (nine), CPB (nine), or OCCPR (eight). DESIGN AND INTERVENTIONS: All dogs received left anterior descending coronary artery occlusion followed by four minutes of ventricular fibrillation without CPR and eight minutes of Thumper CPR. At 12 minutes, dogs received one of three resuscitation techniques. After resuscitation, all animals received four hours of intensive care. Animals that were resuscitated had histochemical determination of ischemic and necrotic myocardial areas. MEASUREMENTS: Intravascular pressures were measured and coronary perfusion pressure was calculated during baseline, cardiac arrest, resuscitation, and postresuscitation periods. Percent necrotic myocardium, percent ischemic myocardium, and necrotic-to-ischemic ratios were determined for resuscitated animals. Epinephrine dosage and number of countershocks were determined for each group. MAIN RESULTS: Nine of nine CPB and six of nine OCCPR, compared with two of eight SECPR animals, were resuscitated (P less than .01). Three of nine CPB and OCCPR and two of eight SECPR dogs survived to four hours (P = NS). Coronary perfusion pressure two minutes after institution of technique was significantly higher with CPB (75 +/- 37 mm Hg) and OCCPR (56 +/- 31 mm Hg) than in SECPR animals (16 +/- 16 mm Hg, P less than .04). Epinephrine required for resuscitation was significantly less with CPB (0.10 +/- 0.02 mg/kg) than for SECPR (0.28 +/- 0.11 mg/kg, P less than .002). The ratio of necrotic to ischemic myocardium at four hours was significantly lower with CPB (0.15 +/- 0.31) and OCCPR (0.39 +/- 0.25) than for SECPR (1.16 +/- 0.31, P less than .02). CONCLUSION: OCCPR and CPB produce higher coronary perfusion pressures and improved resuscitation rates from ventricular fibrillation when compared with SECPR in this canine myocardial infarct cardiac arrest model. CPB and OCCPR yielded similar resuscitation results, although less epinephrine was required with CPB.     

The effect of vasopressin on gastric perfusion in catecholamine-dependent patients in septic shock

OBJECTIVE: To study the effect of continuous infusion of vasopressin on the splanchnic circulation in patients with severe septic shock. DESIGN: Prospective clinical study. SETTING: ICU in a teaching hospital. PATIENTS: Eleven consecutive patients with documented septic shock who remained hypotensive despite norepinephrine infusion at a rate > or =0.2 microg/kg/min. INTERVENTIONS: Insertion of a gastric tonometry catheter, and continuous infusion of vasopressin 0.04 U/min during 4 h. Measurements and main results: Difference between gastric and arterial CO(2) partial pressure (P[g-a]CO(2) gap), mean arterial pressure, and cardiac index were recorded at baseline and after 15 min, 30 min, 60 min, 120 min, and 240 min. RESULTS: The median P(g-a)CO(2) gap increased from 5 mm Hg at baseline to 19 mm Hg after 4 h (p = 0.022). Mean arterial pressure increased from 61 +/- 13 mm Hg at baseline to 68 +/- 9 mm Hg after 4 h (p = 0.055). No significant changes in cardiac index were noted. CONCLUSIONS: In norepinephrine-dependent patients in septic shock, continuous infusion of low-dose vasopressin results in a significant increase of the P(g-a)CO(2) gap compatible with GI hypoperfusion.     

Global end-diastolic volume as an indicator of cardiac preload in patients with septic shock

STUDY OBJECTIVE: To assess the value of the global end-diastolic volume (GEDV) evaluated by transpulmonary thermodilution as an indicator of cardiac preload. DESIGN: Prospective clinical study. SETTING: Medical ICU of a university hospital (20 beds). PATIENTS: Thirty-six patients with septic shock. INTERVENTIONS: Volume loading and dobutamine infusion. MEASUREMENTS AND RESULTS: Hemodynamic parameters were evaluated in triplicate by the transpulmonary thermodilution technique: (1) before and after 66 fluid challenges in 27 patients, and (2) before and after 28 increases in dobutamine infusion rate in 9 patients. Volume loading induced a significant (p < 0.001) increase in central venous pressure (CVP) from 10 +/- 4 to 13 +/- 4 mm Hg, in GEDV index from 711 +/- 164 to 769 +/- 144 mL/m(2), in stroke volume index (SVI) from 36 +/- 12 to 42 +/- 12 mL/m(2), and in cardiac index (CI) from 3.4 +/- 1.1 to 3.9 +/- 1.2 L/min/m(2) (mean +/- SD). Changes in GEDV index were correlated (r = 0.72, p < 0.001) with changes in SVI, while changes in CVP were not. The increase in SVI was > 15% in 32 of 66 instances (positive response). The preinfusion GEDV index was lower (637 +/- 134 mL/m(2) vs 781 +/- 161 mL/m(2), p < 0.001) in the cases of positive response, and was negatively correlated with the percentage increase in GEDV index (r = - 0.65, p < 0.001) and in SVI (r = - 0.5, p < 0.001). Dobutamine infusion induced an increase in SVI (32 +/- 11 mL/m(2) vs 35 +/- 12 mL/m(2), p < 0.05) and in CI (2.8 +/- 0.6 L/min/m(2) vs 3.2 +/- 0.6 L/min/m(2), p < 0.001) but no significant change in CVP (13 +/- 3 mm Hg vs 13 +/- 3 mm Hg) and in GEDV index (823 +/- 221 mL/m(2) vs 817 +/- 202 mL/m(2)). CONCLUSION: In patients with septic shock, our findings demonstrate that, in contrast to CVP, the transpulmonary thermodilution GEDV index behaves as an indicator of cardiac preload.     

分侧肺通气时不同呼气末正压和潮气量对单侧肺损伤犬循环的影响

目的 观察不同步分侧肺通气和同步分侧肺通气对单侧急性肺损伤(ALI)犬循环的影响.方法 取健康杂种犬12只,建立盐酸所致单侧肺损伤动物模型,行容积控制通气,将犬按随机数字表法分为不同步分侧肺通气组(NS组)和同步分侧肺通气组(S组).参数:患侧潮气量3.5 ml/kg保持不变,呼气末正压(PEEP)选择15、20、25 cm H2O(1 cm H2O=0.098 kPa);患侧PEEP 10 cm H2O不变,潮气量用随机数字表法选择5、7.5、10 ml/kg.健侧通气参数始终不变,检测不同通气条件下两组犬血流动力学和氧动力学指标.结果 (1)患侧潮气量3.5 ml/kg不变,PEEP为15、20 cm H2O时,两组血流动力学和氧动力学参数差异无统计学意义.当患侧PEEP为25 cm H2O时,NS组心率、体循环平均压(mABP)、心输出量、氧合指数和混合静脉血氧饱和度(SvO2)分别为(98±8)次/min、(84±6)mm Hg(1 mm Hg=0.133 kPa)、(1.10±0.13)L/min、(199±14)mm Hg和(55±6)%,明显低于S组[分别为(124±9)次/min、(103±7)mm Hg、(1.52±0.28)L/min、(221±15)mm Hg和(62±4)%,t值分别为-7.852、-16.561、-15.043、-13.314和-5.653,均P＜0.01].(2)患侧PEEP 10 cm H2O不变,潮气量分别为5、7.5 ml/kg时,两组的血流动力学和氧动力学参数比较差异无统计学意义.当患侧潮气量为10 ml/kg时,NS组HR、mABP、心输出量、氧合指数和SvO2均低于S组(均P＜0.01).结论 在本实验动物模型中,患侧与健侧所用PEEP水平相差≤20 cm H2O或患侧潮气量≤7.5 ml/kg时,同步和非同步分侧肺通气均能保持循环稳定.若需要更高水平PEEP时,建议选用同步分侧肺通气.     

Hemodynamic response to digitalization in patients with hypertensive cardiovascular disease

Summary Twenty-eight patients with hypertensive cardiovascular disease (HCD) and incipient myocardial dysfunction underwent hemodynamic studies at rest and during exercise before and 30 minutes after administration of 0.6 mg betamethyl-digoxin intravenously. Measurements were made during right heart catheterization with a balloon-tipped catheter. The hemodynamic changes after administration of digitalis did not demonstrate a consistent and uniform improvement of cardiac performance in all patients with HCD and myocardial dysfunction. When separating 11 patients with previous myocardial infarctions or documented coronary artery disease (CAD) (=Group I) from the remaining 17 subjects without clinical and/or angiographic signs of CAD (=Group II), there were significant differences in the hemodynamic response to digitalis:In Group I, pulmonary artery wedge pressure (PAWP) after digitalis decreased only slightly and insignificantly from 8.7 to 7.4 mm Hg at rest and from 27.6 to 26.4 mm Hg during steady state exercise. Cardiac output (CO) remained essentially unchanged with a tendency to decrease after digitalis: 5.9 vs. 5.8 L/min at rest and 11.5 vs. 11.1 L/min during exercise.At rest, even patients of Group II showed only minor decrease of PAWP from 8.8 to 7.2 mm Hg; during exercise these patients demonstrated marked improvement of cardiac performance with a significant decrease of PAWP after digitalis from 27.8 to 22.3 mm Hg (p<0.01). With one exception, there was a more or less pronounced reduction of PAWP after the drug was given. No significant change of CO after digitalis was measured in this group: 6.2 vs. 5.9 L/min at rest and 13.4 vs. 13.5 L/min during exercise.The different hemodynamic patterns of responders and non-responders to the glycoside will be discussed.

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Die hämodynamische Wirkung von Digitalis bei Patienten mit arterieller Hypertonie

Zusammenfassung Bei 28 Patienten mit arterieller Hypertonie und beginnender linksventrikulärer Funktionseinschränkung wurde die Hämodynamik in Ruhe und während Ergometerbelastung vor und 30 Minuten nach intravenöser Gabe von 0,6 mg Beta-Methyl-Digoxin untersucht. Mit Hilfe eines Swan-Ganz-Thermistor-Katheters wurden die Füllungsdrücke beider Ventrikel sowie das Herzzeitvolumen bestimmt. Die Änderung dieser Größen nach Digitalis zeigte keine einheitlich günstige Wirkung auf die Hämodynamik der untersuchten Patienten. Bei getrennter Betrachtung von 11 Hypertonikern mit koronarer Herzerkrankung (Gruppe I) und den übrigen 17 Patienten ohne klinische und/oder angiographische Zeichen einer koronaren Herzerkrankung (Gruppe II) ließ sich ein unterschiedliches hämodynamisches Verhalten nach Digitalis nachweisen:Bei Patienten derGruppe I nahm der durchschnittliche Pulmonalkapillar-druck (PAWP) in Ruhe und während Belastung nur gering und nicht signifikant von 8,7 mm Hg auf 7,4 mm Hg, bzw. von 27,6 mm Hg auf 26,4 mm Hg ab. Das Herzzeitvolumen (HZV) blieb weitgehend unbeeinflußt: Die durchschnittlichen Ruhewerte betrugen 5,9 L/min im Kontrollversuch und 5,8 L/min nach Digitalisierung. Die entsprechenden Belastungswerte unterschieden sich mit durchschnittlich 11,5 L/min gegenüber 11,1 L/min ebenfalls nicht signifikant.Bei Patienten derGruppe II konnte der Ruhewert des PAWP ebenfalls nur unwesentlich von durchschnittlich 8,8 mm Hg auf 7,2 mm Hg gesenkt werden. Dagegen kam es während Belastung zu einer deutlichen Besserung der linksventrikulären Funktion mit Reduktion des PAWP nach Beta-Methyl-Digoxin von 27,8 mm Hg auf 22,3 mm Hg (p<0,01). Mit einer Ausnahme zeigte der PAWP bei dieser Patientengruppe eine Normalisierungstendenz. Das HZV wurde auch bei Patienten der Gruppe II durch Digitalis nicht signifikant beeinflußt: Die Durchschnittswerte waren vor Digitalis 6,2 L/min (Ruhe) und 13,4 L/min (Belastung), nach Digitalis 5,9 L/min (Ruhe) und 13,5 L/min (Belastung).Die möglichen Ursachen der unterschiedlichen Digitaliswirkung bei Patienten mit Hypertonie werden diskutiert.

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With 4 figures     

The effect of allopurinol and catalase on cardiovascular hemodynamics during hemorrhagic shock

The primary objective of this study was to determine the effect that the xanthine oxidase inhibitor allopurinol (ALLO) and the hydrogen peroxide scavenger catalase (CAT) have on the cardiovascular compensatory ability of the dog to respond to severe hemorrhagic hypotension. Twenty-four mongrel dogs were anesthetized with sodium pentabarbitol and surgically prepared to monitor 1) average arterial blood pressure (AAP), 2) central venous pressure (CVP), 3) heart rate (HR), 4) cardiac index (CI = CO/kg), and hindlimb skeletal muscle blood flow (MBF). Total body vascular conductance (TBC) and skeletal muscle vascular conductance (MVC) were calculated by dividing the CI or MBF by the difference between the AAP and CVP. Eight animals were placed into each of the following three groups, bled over a 1-hr period of time to an AAP of 50 mm Hg and monitored for an additional 2 hr. Group I controls received an intravenous volume of lactated Ringer's equivalent to that volume given to groups II and III. Group II was pretreated 24 hr prior to hemorrhage with 100 mg/kg ALLO orally and received a bolus injection of 25 mg/kg 15 min prior to hemorrhage plus an intravenous infusion of 5 mg/kg/hr over the 3-hr study. Group III was given the same ALLO treatment as group II plus an additional 5-mg/kg/hr intravenous infusion of CAT throughout the duration of the 3-hr study. The results show that the intense compensatory increase in total body vascular tone which occurs during severe hypovolemia is significantly reduced at the 60-, 120-, and 180-min periods in the ALLO/CAT group; however, when ALLO alone was used this effect lasted only through the 120-min period. A similar, but statistically less convincing, picture was seen in the skeletal muscle vascular bed. Thus, the ALLO/CAT group seemed to inhibit some free radical mechanisms better than the ALLO group during and immediately following hemorrhage. Allopurinol alone lost its effectiveness before the 3 hr, which suggests that a free radical mechanism may play an early role in the pathophysiologic shock sequence. As shock continues, however, other factors seem to override the free radical mechanism. One possible explanation for this early tissue protective action of allopurinol and catalase is the inhibition of the oxygen free-radical-induced microvascular swelling and plugging.     

Hypoxanthine in lethal canine endotoxin shock.

Endotoxin shock was induced in Labrador retriever dogs by intravenous infusion of a lethal dose of Escherichia coli endotoxin (2 mg/kg body weight) over a three-hour period in order to study plasma hypoxanthine concentrations. The animals succumbed within 14 hours after start of the infusion. Terminally when aortic blood pressure dropped below 30 mm Hg and bradycardia had developed, the animals were resuscitated by external cardiac massage, artificial ventilation, and volume therapy. During shock no significant alteration of plasma hypoxanthine concentrations occurred. During the 12-minute period of resuscitation, however, hypoxanthine concentrations of both arterial and venous plasma increased rapidly compared to the initial values. The changes of the hypoxanthine concentration revealed an exponential pattern. The likely explanation for this phenomenon is is that during shock bypoxanthine was accumlated in the tissues due to tissue hypoxia and that the metabolite was washed out into the circulation during resuscitation.     

Changes in expired end-tidal carbon dioxide during cardiopulmonary resuscitation in dogs: a prognostic guide for resuscitation efforts

Expired end-tidal carbon dioxide (PCO2) measurements made during cardiopulmonary resuscitation have correlated with cardiac output and coronary perfusion pressure when wide ranges of blood flow are included. The utility of such measurements for predicting resuscitation outcome during the low flow state associated with closed chest cardiopulmonary resuscitation remains uncertain. Expired end-tidal PCO2 and coronary perfusion pressures were measured in 15 mongrel dogs undergoing 15 min of closed chest cardiopulmonary resuscitation after a 3 min period of untreated ventricular fibrillation. In six successfully resuscitated dogs, the mean expired end-tidal PCO2 was significantly higher than that in nine nonresuscitated dogs only after 14 min of cardiopulmonary resuscitation (6.2 +/- 1.2 versus 3.4 +/- 0.8 mm Hg; p less than 0.05). No differences in expired end-tidal PCO2 values were found at 2, 7 or 12 min of cardiopulmonary resuscitation. A significant decline in end-tidal PCO2 levels during the resuscitation effort was seen in the nonresuscitated group (from 6.3 +/- 0.8 to 3.4 +/- 0.8 mm Hg; p less than 0.05); the successfully resuscitated group had constant PCO2 levels throughout the 15 min of cardiac arrest (from 6.8 +/- 1.1 to 6.2 +/- 1.2 mm Hg). Changes in expired PCO2 levels during cardiopulmonary resuscitation may be a useful noninvasive predictor of successful resuscitation and survival from cardiac arrest.     

Extravascular lung water in patients with septic shock during a fluid regimen guided by cardiac index

BACKGROUND: To elucidate whether patients with a septic shock develop pulmonary edema in a treatment protocol in which volume loading is guided by its effect on the cardiac output, rather than by preset values of pulmonary artery wedge pressure (PAWP). METHODS: 15 consecutive patients with the diagnosis of septic shock were studied in a prospective observational study. Cardiac output, PAWP and extravascular lung water index (EVLWI) were determined at regular intervals during the first 24 h of treatment. Fluid challenges were given if MAP was <80 mm Hg and/or CI was <4.5 l/min/m(2), and PAWP was <16 mm Hg. Further fluid challenges were only given if the preceding fluid challenge resulted in an increase in CI of more than 10% and PAWP was still <16 mm Hg. RESULTS: EVLWI was slightly above normal (10.4+/-1.2 ml/kg) and did not change during the treatment protocol. One third of the patients had an initial PAWP>16 mmHg. In these patients, EVLWI was significantly higher than in patients with an initial PAWP <16 mm Hg (14.1+/-1.1 ml/kg versus 10.0+/-0.9 ml/kg, P=0.026). No significant correlation was found between PAWP and EVLWI. CONCLUSION: In this study, patients with septic shock did not develop pulmonary edema during the first 24 h of treatment, when their fluid regimen was guided by the effects on cardiac output.     

Importance of the duration of inadequate coronary perfusion pressure on resuscitation from cardiac arrest

The effect of the duration of inadequate coronary perfusion pressure on resuscitation from cardiac arrest was examined in 32 mongrel dogs with a mean weight of 22 +/- 5 kg. In all dogs, the heart was electrically fibrillated and closed chest compression with assisted ventilation was performed for 15 minutes. At this time, all dogs had an inadequate coronary perfusion pressure (mean 7 +/- 9 mm Hg) and were randomized to a control group (group 1) with continued closed chest compression or to one of the three groups with open chest cardiac massage. These three groups differed only in the duration of continued closed chest compression before initiation of open chest massage (15, 20 and 25 minutes, respectively, in groups 2, 3 and 4). The control group (group 1) had no significant increase in coronary perfusion pressure, and only one of the eight dogs could be resuscitated. The three groups with open chest cardiac massage had a significant increase in coronary perfusion pressure (from 5 +/- 9 to 51 +/- 26 mm Hg, p less than 0.05), but the rate of successful resuscitation depended on the duration of inadequate coronary perfusion pressure before cardiac open chest massage. In group 2, six of eight dogs were resuscitated (p less than 0.05 compared with the control group); in group 3, three of eight dogs were resuscitated and in group 4 none of the eight dogs was resuscitated. The resuscitation rate was significantly (p less than 0.05) greater in group 2 than in group 4. These findings indicate that techniques that improve coronary perfusion pressure during cardiopulmonary resuscitation must be applied before extensive myocardial cellular dysfunction occurs if the probability of successful resuscitation is to be improved.     

Hemodynamic effects of amrinone in a canine model of massive pulmonary embolism.

Amrinone, an inotrope with vasodilating properties, is of potential use in managing the right ventricular failure and pulmonary vasoconstriction induced by massive pulmonary embolism (PE). Therefore, to determine the hemodynamic effects of amrinone in a canine model of massive PE, autologous blood clot was infused into ten dogs (eight treated and two control animals) in an amount sufficient to decrease mean systemic arterial pressure (MAP) by at least 25 percent. This resulted in an increase in mean pulmonary artery pressure (MPAP) from 13.4 +/- 3.7 mm Hg to 44.4 +/- 4.8 mm Hg (p less than 0.01), a decrease in MAP from 122 +/- 9.5 mm Hg to 35.6 +/- 9.8 mm Hg (p less than 0.01), and a decrease in cardiac output from 2.73 +/- 0.834 L/min to 1.22 +/- 0.61 L/min (p less than 0.01). Amrinone was administered in an initial bolus of 0.75 mg/kg followed by an infusion of 7.5 micrograms/kg/min, which resulted in significant hemodynamic improvement in all subjects, with a fall in MPAP to 35.3 +/- 5.1 mm Hg (p less than 0.01), an increase in MAP to 98.1 +/- 31.1 mm Hg (p less than 0.01), and an increase in cardiac output to 2.01 +/- 0.7 L/min (not significant) at 5 min. Cardiac output continued to increase to 2.56 +/- 0.16 L/min (p less than 0.01) at 35 min. We conclude that amrinone alleviated pulmonary hypertension, systemic hypotension, and low cardiac output in a canine model of massive PE.     

Reversal of low dose angiotension hypertension by angiotensin receptor antagonists

During acute angiotension II (Ang II) infusion (200 ng/kg/min i.v.) into anesthetized rats, mean arterial pressure rose from 124 +/- 1 to 154 +/- 2 mm Hg. The peptidic Ang II antagonist saralasin lowered arterial pressure in a dose-dependent manner. The maximal decrease in pressure was similar to that observed after the Ang II infusion was discontinued. The nonpeptide Ang II antagonist, 4'-[( 2-butyl-4-chloro-5-(hydroxymethyl)-1H-imidazole-1-yl] methyl) [1,1'-biphenyl] -2-carboxylic acid (SC-48742), lowered acutely elevated arterial pressure to a level similar to that on discontinuation of the angiotensin infusion. Chronic (8 days) infusion of Ang II (20 ng/kg/min i.v.) increased mean arterial pressure from 116 +/- 3 to 164 +/- 7 mm Hg, which then decreased to 121 +/- 6 mm Hg on termination of the infusion. Saralasin (10 micrograms/kg/min, a maximally effective dose during acute angiotensin infusion) decreased mean arterial pressure from 168 +/- 7 to 141 +/- 3 mm Hg, a pressure significantly higher (p less than 0.05) than the pressure observed after the angiotensin infusion was discontinued. SC-48742 decreased mean arterial pressure from 167 +/- 7 to 127 +/- 3 mm Hg, a pressure not statistically different from the minimum pressure observed after the angiotensin infusion was terminated. The mechanism of blood pressure elevation during acute high dose or chronic low dose Ang II infusion is different, the latter having a significant neural component as measured by the response to trimethaphan. The peptidic antagonist saralasin was fully effective in lowering acute angiotensin hypertension but only partially effective during chronic hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of temperature on naloxone treatment in canine hemorrhagic shock

The effects of temperature on naloxone treatment in canine hemorrhagic shock were examined in 24 dogs hemorrhaged to a mean arterial blood pressure of 35 mm Hg (ambient temperature, 21 degrees C). After two hours of hypotension, the blood reservoir was clamped with no return of shed blood. Dogs were divided into three groups: Control (n = 8) received normal saline (0.5 cc/kg/hr); naloxone-cold (n = 8) and -warm (n = 8) received naloxone (2 mg/kg bolus and 2 mg/kg/hr constant infusion). Body temperature was maintained in four dogs with a warming blanket, and four dogs received no external warming. Rectal temperature fell to 34.2 +/- 0.9 degrees C in naloxone-cold animals; naloxone-warm animals were maintained at 38.6 +/- 0.1 degrees C by external warming. Control dogs rapidly deteriorated after reservoir clamping (survival, 18.6 +/- 5 min). Naloxone infusion significantly increased survival regardless of body temperature (cold, 125 +/- 21 min; warm, 199 +/- 13 min). Naloxone transiently increased mean arterial pressure and dP/dt in the colder dogs, while coronary perfusion, myocardial oxygen metabolism, and plasma beta-endorphin levels were unchanged. In the warmer dogs, naloxone significantly improved hemodynamic function and myocardial perfusion as indicated by the increased mean arterial pressure, cardiac output, stroke volume, dP/dt, and coronary blood flow. Furthermore, naloxone reduced plasma beta-endorphin levels and corrected the metabolic derangements of shock in this group. Our data indicate hypothermia significantly diminished the beneficial effects of naloxone treatment in canine hemorrhagic shock.     

不同动脉压水平对老年感染性休克患者血流动力学组织灌注和代谢的影响

目的 观察应用去甲肾上腺素联合多巴酚丁胺(NE+Dobu)在小同平均动脉压(MAP)水平对老年感染件休克患者血流动力学、组织灌注和代谢的影响. 方法 感染性休克患者18例,充分液体复苏后为基础状态,应用NE+Dobu并随机调节剂量,使MAP分别维持在65、75、85mm Hg 3种水平状态,持续4 h,观察不同MAP水平的血流动力学、氧合指标、血乳酸、肾功能和胃黏膜二氧化碳分压变化. 结果 当MAP达75 mm Hg和85 mm Hg时,心脏指数(4.7±0.6和5.1±0.7)、体循环阻力指数(1162±278和1276±319)、氧输送[(697±53)ml·min-1·m-2和(711±68)ml·min-1·m-2]、氧摄取率[(0.28±0.02)%和(0.27±0.02)%],均较MAP为65 mm Hg时[4.0±0.6、1011±225、(634±70)ml·min-1·m-2、(0.25±0.02)%]明显增加(P<0.05);尿量分别为(98±43)ml/h和(91±54)ml/h,较65 mm Hg时(74±49)ml/h有明显增加,但仅MAP75 mmHg时,差异有统计学意义(P<0.05). 结论 老年感染性休克患者充分液体复苏后,应用NE+Dobu提高MAP达75 mm Hg时,可改善全身血流动力学和肾功能,对于老年感染性休克患者可能需要适当提高MAP.     

Decreasing hydrostatic pressure does not uniformly decrease high-pressure pulmonary edema

Pulmonary artery wedge pressure (PAWP) of 30 mm Hg with left atrial balloon inflation for 1 1/2 hours produced pulmonary edema in eight dogs. PAWP was then decreased to 10 mm Hg for two hours, and shunt, lung water (extravascular thermal volume, or ETV, by thermal dye), and perfusion distribution (radiomicrosphere technique) were measured and compared with four other dogs (group 1) whose PAWP was maintained at 10 mm Hg. The eight dogs with PAWP of 30 mm Hg for 1 1/2 hours were retrospectively subdivided into two groups of four based on ETV (group 2, double baseline ETV; group 3, triple baseline ETV). Baseline ETV and shunt were similar for all groups and remained unchanged for group 1. At 1 1/2 hours, 2 hours (1/2 hour after decreasing PAWP), 2 1/2 hours, and 3 1/2 hours, respectively, ETV were: 13.9 +/- 1.9, 12.8 +/- 2.0, 9.3 +/- 1.5, and 8.5 +/- 1.0 ml/kg in group 2; and 21.9 +/- 2.1, 22.7 +/- 2.2, 22.5 +/- 2.0, and 22.2 +/- 2.0 ml/kg in group 3. A more variable rate of edema formation was detected in eight additional dogs, but failure to resolve higher levels of edema after decreasing PAWP was also demonstrated in this group. Edema was greatest in lower lobes and decreased lobar perfusion. Shunt was higher in group 3 than in group 2 at 1 1/2 hours and decreased in group 2 but not in group 3 at 3 1/2 hours. Changes in colloid osmotic pressure may account for the differences in edema formation and resolution, but our data suggest that, independent of the rate of edema formation, a decrease in vascular exchange surface area at higher levels of edema may inhibit edema resolution when PAWP is decreased.     

Effects of dobutamine on gastric mucosal perfusion and hepatic metabolism in patients with septic shock

We prospectively evaluated the effects of dobutamine on gastric mucosal perfusion and hepatocytic clearance in patients with septic shock. After resuscitation with volume expansion and norepinephrine (12 patients) as needed, 14 hemodynamically stable patients (median age: 60 yr, median SAPS II score: 47) were given an infusion of 7.5 microg/kg/min dobutamine for 1 h. Gastric mucosal perfusion and hepatocytic clearance were assessed with tonometry and indocyanine green (ICG) elimination, respectively. All measurements were made before dobutamine infusion, after 1 h of dobutamine infusion, and 1 h after the infusion ended. Cardiac output (thermodilution technique) increased with dobutamine from a baseline median level of 4.0 L/min/m(2) (range: 1.7 to 7.4 L/min/m(2)) to 5.0 L/min/m(2) (range: 3.5 to 8.9 L/min/m(2)) (p = 0.004) and returned to baseline levels after dobutamine infusion ended. The gastric-arterial PCO(2) difference decreased from a baseline median level of 13 mm Hg (range: 5 to 54 mm Hg) to 7 mm Hg (range: 5 to 48 mm Hg) (p = 0.005). ICG elimination was low in all patients at baseline (median plasma disappearance rate: 12.2%; range: 7.6 to 16.2%) and did not change significantly during or after dobutamine infusion. In summary, dobutamine increases gastric mucosal perfusion but does not alter hepatocytic clearance in patients with septic shock. The absence of a beneficial effect of dobutamine on hepatocytic clearance may be related to profound alterations in hepatocellular metabolism during septic shock.     

End tidal carbon dioxide as an haemodynamic determinant of cardiopulmonary resuscitation in the rat

End tidal PCO2 (PETCO2) has been found to be a good prognostic indicator of successful resuscitation from cardiac arrest. To explore the value of this measurement further, we carried out a series of experiments during cardiac arrest and closed chest resuscitation in 14 mechanically ventilated Sprague-Dawley rats. Ventricular fibrillation (VF) was induced by a 10 mA current delivered to the right ventricular endocardium. After 4 min of VF, precordial compression was begun with a mechanical thumper and defibrillation was attempted 2 min later. PETCO2 decreased abruptly during cardiac arrest to 0.3 mm Hg (0.04 kPa). With precordial compression, it increased to 11 mm Hg (1.5 kPa). Within 3 min of successful defibrillation, there was an overshoot in the PETCO2 to 44 mm Hg (5.8 kPa) with return to baseline levels approximating those of the pre-arrest control measurements over the 60 min that followed restoration of spontaneous circulation. The PETCO2 measurement during precordial compression predicted the success of defibrillation with return of spontaneous circulation. When PETCO2 exceeded 9 mm Hg (1.2 kpA), 7 of 8 animals were successfully resuscitated. When PETCO2 was less than 9 mm Hg during precordial compression, none of six animals were successfully resuscitated. The PETCO2 correlated with the mean aortic (r = 0.71) and coronary perfusion pressure (r = 0.80) generated during precordial compression. In corroboration of previously reported observations on pigs, dogs, and human patients, PETCO2 served as a non-invasive monitor of the effectiveness of precordial compression for maintaining coronary perfusion and therefore cardiac viability during CPR. The PETCO2 was also useful in that it promptly signalled restoration of spontaneous circulation.