Multicenter Randomized Comparison of Xenon and Isoflurane on Left Ventricular Function in Patients Undergoing Elective Surgery

Background: Volatile anesthetics are commonly used for general anesthesia. However, these can induce profound cardiovascular alterations. Xenon is a noble gas with potent anesthetic and analgesic properties. However, it is uncertain whether xenon alters myocardial function. The aim of this study was therefore to investigate left ventricular function during anesthesia with xenon compared with isoflurane.

Methods: The authors performed a randomized multicenter trial to compare xenon with isoflurane with respect to cardiovascular stability and adverse effects in patients without cardiac diseases scheduled for elective surgery. Two hundred fifty-nine patients were enrolled in this trial, of which 252 completed the study according to the protocol. Patients were anesthetized with xenon or isoflurane, respectively. Before administration of the study drugs and at four time points, the effects of both anesthetics on left ventricular function were investigated using transesophageal echocardiography.

Results: Global hemodynamic parameters were significantly altered using isoflurane (P < 0.05 vs. baseline), whereas xenon only decreased heart rate (P < 0.05 vs. baseline). In contrast to xenon, left ventricular end-systolic wall stress decreased significantly in the isoflurane group (P < 0.05 vs. baseline). Velocity of circumferential fiber shortening was decreased significantly in the xenon group but showed a more pronounced reduction during isoflurane administration (P < 0.05 vs. baseline). The contractile index (difference between expected and actually measured velocity of circumferential fiber shortening) as an independent parameter for left ventricular function was significantly decreased after isoflurane (P < 0.0001) but unchanged using xenon.     

Mucin profiles and potential for malignancy of human colorectal adenomatous polyps

The mucin histochemical and histologic features of 166 colorectal adenomatous polyps from 124 patients were studied. A majority of the polyps (62%) had a tubular growth pattern whereas 38% showed villous growth. Severe dysplasia was more frequently found in the latter group. A significant correlation (r = 0.27, P less than 0.001) was found between the severity of dysplasia and the size of the polyps. Moreover, the ratio between goblet and columnar cells was also found to decrease (P less than 0.0001) with the severity of dysplasia. Independent of the mucin stain used (periodic acid-Schiff, alcian blue, and high-iron diamine stains), mucin reactive cells were found to be negatively correlated (-0.17 less than r less than -0.44, P less than 0.01) with severity of dysplasia, especially in the tubular adenomas. These findings suggest that evaluation of mucin stain, related to dysplasia, may contribute to the assessment of premalignant and early malignant changes in adenomas of the colon.     

Cytomegalovirus infection induces vascular injury in the rat.

The role of cytomegalovirus (CMV) in the early development of atherosclerosis was studied in a rat model. Arterial samples derived from virus-infected normo- and hypercholesterolaemic animals were investigated by light microscopy at 1, 4, 8 and 16 weeks post infection. Early atherogenic lesions comparable to those seen in non-infected hypercholesterolaemic rats were found in CMV-infected normocholesterolaemic and hypercholesterolaemic animals, starting at 1 week post infection. The changes consisted of minimal endothelial cell damage, as shown by the en face technique, and a more than 10-fold increase in the number of leukocytes adhering to the aortic intima. The increased adhesion of leukocytes was observed in infected normocholesterolaemic rats but only in the non-infected rats which were hypercholesterolaemic. The infection of hypercholesterolaemic rats did not enhance this effect although it resulted in increased migration of the leukocytes into the subendothelial space. CMV infection of normocholesterolaemic rats induced lipid accumulation in the endothelium. In these animals approximately 1% of the endothelial cells contained lipid at 1 week post infection. In the non-infected hypercholesterol-fed animals 10% of the cells contained lipid. CMV infection in these rats induced an extra increase of the lipid-containing endothelial area. The changes in the CMV infected animals largely corresponded with the intimal injury observed in the hypercholesterolaemic rats. These results support the hypothesis that CMV may be one of the factors involved in atherogenesis.     

Respiratory Depression by Tramadol in the Cat: Involvement of Opioid Receptors

Background: Tramadol hydrochloride (tramadol) is a synthetic opioid analgesic with a relatively weak affinity at opioid receptors. At analgesic doses, tramadol seems to cause little or no respiratory depression in humans, although there are some conflicting data. The aim of this study was to examine whether tramadol causes dose-dependent inhibitory effects on the ventilatory carbon dioxide response curve and whether these are reversible or can be prevented by naloxone.

Methods: Experiments were performed in cats under [alpha]-chloralose-urethane anesthesia. The effects of tramadol and naloxone were studied by applying square-wave changes in end-tidal pressure of carbon dioxide (Petco2; 7.5-11 mmHg) and by analyzing the dynamic ventilatory responses using a two-compartment model with a fast peripheral and a slow central component, characterized by a time constant, carbon dioxide sensitivity, time delay, and a single offset (apneic threshold).

Results: In five animals 1, 2, and 4 mg/kg tramadol (intravenous) increased the apneic threshold (control: 28.3 +/- 4.8 mmHg [mean +/- SD]; after 4 mg/kg: 36.7 +/- 7.1 mmHg;P < 0.05) and decreased the total carbon dioxide sensitivity (control: 109.3 +/- 41.3 ml [middle dot] min-1 [middle dot] mmHg-1) by 31, 59, and 68%, respectively, caused by proportional equal reductions in sensitivities of the peripheral and central chemoreflex loops. Naloxone (0.1 mg/kg, intravenous) completely reversed these effects. In five other cats, 4 mg/kg tramadol caused an approximately 70% ventilatory depression at a fixed Pet co2 of 45 mmHg that was already achieved after 15 min. A third group of five animals received the same dose of tramadol after pretreatment with naloxone. At a fixed Petco2 of 45 mmHg, naloxone prevented more than 50% of the expected ventilatory depression in these animals.     

Recurrence of nephrocalcinosis after renal transplantation in an adult patient with primary hyperoxaluria type I

The medical history of a 42-year-old patient with primary hyperoxaluria type I is presented. Primary hyperoxaluria was suspected after renal transplantation, when oxalate deposits were found in a biopsy of the kidney graft. Diagnosis of type I hyperoxaluria was confirmed by the finding that significantly increased amounts of glycolic acid and oxalic acid were excreted. Treatment of the patient with 500 mg pyridoxine daily resulted in a decrease of the excretion of oxalate to normal values.     

Stress distribution around dental implants: influence of superstructure, length of implants, and height of mandible.

The stress distribution around dental implants was investigated by use of a two-dimensional model of the mandible with two implants. A vertical load of 100 N was imposed on abutments or the bar connection. The stress was calculated for a number of superstructures under different loading conditions with the help of the finite element method. The length of the implants and the height of the mandible were also varied. A model with solitary abutments showed a more uniform distribution of the stress when compared with a model with connected abutments. The largest compressive stress was also less in the model without the bar. Using shorter implants did not have a large influence on the stress around the implants. When the height of the mandible was reduced, a substantially larger stress was found in the bone around the implants because of a larger overall deformation of the lower jaw.