Epidural Baclofen in the Rabbit: Antinociceptive Effect and Neurotoxicity / 대한마취과학회지

BACKGROUND: Intrathecal baclofen has an analgesic effect. However, the analgesic effect and neurotoxicity of epidural baclofen has not been reported. METHODS: Twenty rabbits, weighing 2.5-3.0 kg, were randomly assigned to three groups; five rabbits receiving 0.9% saline (S), five rabbits receiving 0.1 mg morphine (M), ten rabbits receiving 0.5% baclofen (B). An epidural catheter was inserted at the L(6-7) interspace, and 0.6 ml of saline, morphine or baclofen was injected. Motor and sensory deficits were measured. After two weeks, a spinal cord segment 3 cm on each side of the catheter tip was removed for histological examination. RESULTS: In the M and B groups, no rabbits showed any response of the hindlimbs to the pinch toe test. On light microscopy findings, no inflammation of the meninges or degenerative myelopathy was observed in the S or M groups. In the B group, one rabbit showed local myelopathy of the white matter, and degenerative myelopathy of white and grey matter in the area adjacent to the epidural catheter. However, these changes are focal and minimal, and thought to be ischemic changes due to vascular damage caused by catheterization. Electron microscopy findings showed no morphologic difference between the S and B groups. CONCLUSIONS: Epidural 0.5% baclofen produced antinociceptive effect with slight motor weakness. No definite neurotoxicity was observed after a single epidural injection of 0.5% baclofen in the rabbit.

Effects of Body Temperature Changes on Hypoxic Pulmonary Vasoconstriction in Isolated Lungs of Rabbits / 대한마취과학회지

BACKGROUND: We studied the effects of body temperature changes and repeated hypoxic stimulation on hypoxic pulmonary vasoconstriction (HPV). METHODS: We isolated lungs from 15 rabbits and perfused them at a constant flow of 30 ml/kg/min with a 3% albumin-physiologic salt solution containing autologous blood. After a 30-minute stabilization, the temperature of the perfusate was changed from 38oC to 32oC gradually. The lungs were ventilated for 15 minutes with a hyperoxic gas mixture consisting of 95% oxygen and 5% carbon dioxide and then for 5 minutes with a hypoxic gas mixture consisting of 3% oxygen and 5% carbon dioxide with the balance being nitrogen. We repeated the hypoxic stimulation 3 times at the same temperature. The mean pulmonary artery pressure changes and ventilation-related parameters were measured at each hypoxic stimulation. RESULTS: With the first hypoxic stimulation, the hypoxic pressure response at the end of the 5-minute hypoxic period decreased significantly at 32oC. With the second and the third hypoxic stimulations, the hypoxic pressure responses at the end of the 5-minute hypoxic period decreased significantly at both 34oC and 36oC. With repeated hypoxic stimulations, the hypoxic pressure responses potentiated significantly at all temperatures. The baseline mean pulmonary artery pressure increased significantly below 34oC. CONCLUSION: The HPV decreased with the reduction in body temperature and was potentiated by repeated intermittent hypoxia; also, the pulmonary vascular resistance increased with the reduction in the body temperature.

Effect of Hemodilution on Brain Damage after Focal Cerebral Ischemia in Rabbits / 대한마취과학회지

BACKGROUND: Hemodilution after focal cerebral ischemia increases cerebral blood flow to ischemic brain tissue and reduces neurologic injury. With rare exceptions, most studies have reduced hematocrit (Hct) to no less than 30%. We studied the effect of moderate hemodilution (hematocrit 27%) on cerebral infarct volume after focal cerebral ischemia in rabbits. METHODS: Twenty rabbits were divided into a control group (n = 10) and a hemodilution group (n = 10). In the control group, cerebral infarction was induced by embolization of the middle cerebral artery using an autologous blood clot without hemodilution. In the hemodilution group (n = 10), hemodilution of around hematocrit 27% was achieved by exchanging arterial blood with 10% hydroxyethyl starch 1 hour before embolization of the middle cerebral artery in the hemodilution group. Seven hours after embolization, coronal brain slices were made with 2 mm thickness at 1 cm from the frontal pole and stained with 2% 2,3,5-triphenyltetrazolium chloride. The infarct volume was quantitated by image analysis of photography of the infarcted area. RESULTS: The infarct volume of the cerebral hemisphere (25.9 +/- 8.9%), subcortex (16.3 +/- 3.1%) in the hemodilution group was significantly smaller than in the control group (34.9 +/- 8.9%, 19.3 +/- 5.1%) (P<0.05), but, in the cortex, the difference of infarct volume is not statistically significant between the control group (23.5 +/- 11.9%) and the hemodilution group (15.6 +/- 2.7%). CONCLUSIONS: These results indicate that moderate hemodilution (hematocrit 27%) reduces neurologic injury after focal cerebral ischemia.

The Effect of Magnesium Pretreatment on Serum Potassium Concentration and Hemodynamic State in Rabbits during Continuous Regular Insulin(RI) Infusion / 대한마취과학회지

Background: Insulin is known to act as second effector that provides potassium transfer from extracellular fluid to intracellular fluid, thus causing hypokalemia and arrythmia. We evaluated the effect of magnesium sulfate treatment on hemodynamics and serum potassium concentration, induced by continuous infusion of regular insulin solution in rabbits. Method: Twenty-four rabbits were divided into four groups for the experiment. Group I was given intravenouse injection of 5 ml of normal saline and continuous dripping of 7.5 U of RI. Group II was pretreated with 30 mg/kg of magnesium sulfate, followed by continuous dripping of 7.5 U of RI. Group III was given 5 ml of normal saline and 15 U of RI. And Group IV was administered 15 U of RI after 30 mg/kg of magnesium sulfate pretreatment. Venouse blood sampling was done before pretreatment, and after 5, 30, 60 and 120 minutes respectively. Heart rate and arterial blood pressure were taken at the same intervals. Result: 1) There was no significant change in serum potassium concentration in groups injected with 7.5 units of RI respectively (groups I and II), regardless of magnesium pretreatment. But in groups injected with 15 units of RI, the group that was not pretreated with magnesium (Groups III) showed a decrease in serum potassium concentration from 3.39+/-0.57 Eq/L to 2.29+/-0.71 mEq/L, while the concentration in the pretreated group (Group IV) decreased more significantly from 3.35+/-0.50 mEq/L to 1.81+/-0.41 mEq/L. 2) Pulse rate did not change significantly in groups that received continuous infusion of 7.5 units of RI (groups I and II) regardless of magnesium pretreatment, but increased significantly in groups injected with 15 units of RI (groups III and IV), pretreated or not. The pretreated group (group IV) had a more significant rise in pulse rate compared with the group that was not pretreated (group III). 3) In all of the groups, those pretreated with magnesium (groups II and IV) and those not pretreated (groups I and III), there was no significant change in systolic and diastolic blood pressures. Nor was arrhythmia detected. Conclusion: The above results indicate that while magnesium sulfate pretreatment at 30 mg/kg with insulin infusion affects serum potassium concentration, has an antiarrhythmic effect, and may induce tachycardia, it does not have any significant effect on blood pressure.

Does Heparin Reduce Neurologic Injury in Rabbits That Occurs From Air Emboli? / 대한마취과학회지

BACKGROUND: Neurological injury after cerebral air embolism may be due to thromboinflammatory responses at sites of air-injured endothelium. Because heparin inhibits multiple thromboinflammatory processes. we hypothesized that heparin would decrease neurological impairment after cerebral air embolism. METHODS: Anesthetized rabbits received either heparin (n=14) or saline (n=13), 5 minutes before air injection (150 microliter/kg). Heparin was given as a 200 IU/kg bolus and followed by a constant infusion of 75 IU/kg/h for 2 hours. Equal volumes of salines were given to saline group. Two hours later, anesthesia was discontinued. Rabbits were neurologically evaluated 24 hours after air embolism. RESULTS: Heparin group had significantly less neurological impairment at 24 hours (34 14) than saline controls (52 8) (p=0.0013). CONCLUSIONS: When given prophylactically, heparin decreases neurological impairment caused by severe cerebral arterial air embolism.