摘要:

The authors have refined a model of cirrhosis in the rat and used it to determine whether the administration of halothane anesthesia adversely affects preexisting liver disease. Male Wistar rats were placed on phenobarbital water and were assigned randomly to two groups. Group 1 rats were exposed by inhalation to carbon tetrachloride (CCL4at weekly intervals for 12 exposures while Group 2 rats received only air. All treatment including phenobarbital then was withdrawn for 4 weeks. Rats then were bled for SGOT and SGPT determinations and 24 h later were exposed to 1.8% halothane in oxygen for 3 h (HAL); the remaining rats from each group were exposed to 100% oxygen for 3 h (O2). Twenty-four hours later, rats were killed and blood was obtained for SGOT and SGPT by cardiac puncture. Light microscopic histologic examination was performed blind on liver sections for cirrhosis and scored for superimposed acute focal necrosis. The weekly sublethal CCl4exposure resulted in histologically demonstrable cirrhosis in all surviving Group 1 animals. The mean (±SD) SGOT (128±32IU/±1) and SGPT (86±24IU/1) values for the Group 1 rats were significantly greater (P< 0.01) than those for Group 2 rats (98±18 IU/1 and 57±12 IU/1, respectively). Cirrhotic animals showed neither deterioration in liver function nor acute liver cell necrosis after Hal compared with O2. However, Group 2 rats showed a modest but significant increase in SGOT (P < 0.05) after HAL, while this change was not noted after O2. Thus, 1.8% halothane anesthesia in oxygen did not result in superimposition of acute liver cell injury in already cirrhotic rats.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The blood flow in the sciatic nerve of the rabbit was estimated from the wash out of intraneurally injected133Xe. To avoid diffusion of the tracer into the surrounding muscular tissue, the nerve was covered by a gas-tight plastic film. Using this technique, the basal blood flow in the sciatic nerve was estimated to 35 ml · min−1· 100 g−1. It was found that intraarterial norepinephrine and electrical stimulation of the lumbar sympathetic chain strongly reduced the wash out of133Xe, which only can be explained by a pronounced reduction of the blood flow in the nerve itself. The blood flow again increased within 4 min of stopping the infusion of norepinephrine or the sympathetic stimulation. The prolonged effect and higher neurotoxicity of local anesthetics containing adrenaline may be explained by an alpha receptor-mediated vasoconstriction of the microvessels of peripheral nerves.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Thirty-two fit patients scheduled for explorative arthrotomy of the knee were allocated randomly to either halothane/oxygen anesthesia or spinal anesthesia with bupivacaine 0.25 mg · kg−1. The day before and 1, 10, and 21 days after surgery, the aminopyrine breath test (ABT) was performed. The day before and 5, 10, and 21 days after surgery, the antipyrine clearance (APcl) was measured by the single sample saliva technique. The ABT as well as the APclwere increased significantly postoperatively (P< 0.01). The day after surgery the ABT was increased by 13±21% in the spinal anesthesia group only, whereas a late increase by 14±31% was found in the halothane group. Five days after surgery, the APclwas increased by 36±45% in the spinal anesthesia group and by 21±28% in the halothane group. Both tests returned to base line values within 3 weeks postoperatively. In five volunteers following the same sampling scheme but receiving bupivacaine 0.25 mg · kg−1im without surgery, no change in the ABT or the APclwas observed. The authors conclude that surgery may cause microsomal enzyme induction regardless of the anesthetic agent or technique used. The mechanism of this induction remains to be elucidated.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The study was undertaken to determine whether droperidol had an effect to induce catecholamine efflux from the adrenal medulla as a mechanism for the possible pressor effect of droperidol in patients with pheochromocytoma and, if so, to ascertain the site of action of this compound. The efflux of catecholamines from perfused dog adrenals was increased from control level, 0.15 μg/min, to 0.66 μg/min by the administration of droperidol 6.6 μm. This effect of droperidol was not dependent on extracellular Ca++, in contrast to acetylcholine. The concomitant secretion of catecholamines and dopamine-β-hydroxylase was observed in response to acetylcholine and caffeine. However, droperidol-, histamine-, and reserpine-induced catecholamine efflux was not accompanied by dopamine-ß-hydroxylase release. In additional studies, chromaffin granules were isolated with a Millipore·filter technique from the bovine adrenal medulla and were incubated for 10 min in an isotonic medium to examine the direct effects of droperidol. Droperidol did not enhance the efflux of catecholamines from the granules in contrast to histamine. The upake of14C-norepinephrine into the granules was inhibited by droperidol in a manner comparable to reserpine. The results suggest that droperidol induces catecholamine efflux from adrenal medullary cells and the efflux probably is caused by a nonexocytotic mechanism. A contributing mechanism was an inhibition of catecholamine uptake into chromaffin granules, resulting in an increased diffusion of catecholamines out of the cell.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The authors investigated the effect of prostaglandin F2αinfused into the pulmonary artery of an acutely atelectatic lung in dogs. Seven dogs were anesthetized with piritramid and pentobarbital and intubated with a Kottmeier canine endobronchial tube. Cardiac output, pulmonary arterial, capillary wedge, and systemic arterial pressure were measured via indwelling catheters. Ventilating both lungs with 66% O2, Pao2was 327±15 mmHg (mean±SD) and venous admixture (Q±sp/Q1) was 11±3%. One-lung atelectasis reduced Pao2to 91±12 mmHg and increased Q±sp/Qtto 40±4%. Prostaglandin F2αin doses of 0.4, 0.6, 1.2, and 1.8 μg ± kg−1· min−1was infused into the pulmonary artery of the atelectatic lung through a second pulmonary artery catheter. Up to a dose of 1.2 μg · kg−1· min−1there was a dose-dependent reduction in Q·sp/Qtto a minimum of 25±4% and an increase in Pao2to 168±25 mmHg, which could be explained by enhanced pulmonary vasoconstriction in the atelectatic lung with increased blood flow diversion toward the ventilated lung. Infusion of 1.8 μg · kg−1· min−1decreased Pao2to 156±32 mmHg and increased Q±sp/Qtto 32±9%. Increased systemic effects of prostaglandin F2αwere observed and presumably were related to saturation of prostaglandin-dehydrogenase leading to vasoconstriction in both lungs and thus reduced blood flow diversion toward the ventilated lung.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Enflurane is a direct myocardial depressant and may act as a myocardial protective agent during ischemia. The authors studied the effects of enflurane on myocardial high-energy phosphates and tolerance to ischemia in the normothermic, isolated rat heart. After isolation and perfusion with Krebs-Henseleit buffer, the hearts were perfused with either buffer (control) or buffer gassed with 2% enflurane for 10 minutes. Thereafter, hearts were made globally ischemic and elapsed times to initiation of ischemic contracture (IC) were determined. ATP and creatine phosphate (CP) were measured at the conclusion of control and enflurane administration and at IC. Ten hearts per group were reperfused with buffer following IC for 20 min; peak pressure and ATP and CP were determined. Administration of 2% enflurane significantly decreased peak pressure by 20% but did not alter baseline high-energy phosphate levels nor did it prolong time to IC. However, enflurane-treated hearts exhibited significantly greater (P< 0.01) recovery of function as defined by per cent return of peak pressure (67%±3%) when compared with those hearts not treated with enflurane preischemically (44%±5%). Also, enflurane-treated hearts had significantly higher (P< 0.01) ATP levels at the conclusion of reperfusion than hearts not perfused with enflurane (12.2±.8 μmol/g dry weightvs. 9.0·0.8 μmol/g dry weight). These findings suggest that enflurane administered prior to an ischemic interval enhances postischemic myocardial recovery.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Clonidine, an α2, adrenergic agonist, has analgesic properties and recently has been used to suppress opiate withdrawal. These two properties theoretically make it a suitable analgesic substitute in patients tolerant to opioids. The objectives of this study were to see if intrathecal clonidine is analgesic and whether it can modify morphine withdrawal at the spinal level. Rats chronically implanted with catheters in the lumbar subarachnoid space were utilized. In analgesia experiments, intrathecal clonidine produced analgesia with the peak effect in the paw-lick test occurring at 200 nM, and in the tail-flick test analgesia was apparent at 100 nM and peaked at 400 nM (in 10 μL Ringer's lactate). In dependency experiments, animals dependent on morphine (300 mg · kg−1) received intrathecal clonidine 25, 50, 200 nM in 10 μ1 Ringer's lactate 72 h after morphine. Following this, a naloxone challenge, 3 mg · kg−1was administered and withdrawal assessed.Clonidine-treated animals showed significant weight loss and decrease in temperature, and those treated with high doses showed marked hypothermia and hind-limb flaccidity. Intrathecal clonidine prevented the hyperalgesia associated with opiate withdrawal but did not affect the occurrence of the majority of behavioral signs (e.g., piloerection, irritability) associated with morphine withdrawal. Intrathecal clonidine prevented the naloxone-induced increase in blood pressure during withdrawal and in animals not treated with morphine-produced hypotension. Thus, intrathecal clonidine is analgesic, and part of the antiwithdrawal action of clonidine may be exerted at the spinal level.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

To examine the effect of sympathectomy induced by epidural blockade on the cardiovascular effects of ketamine anesthesia, the authors compared the changes in arterial blood pressure (AP) and heart rate (HR) following intravenous administration of ketamine in patients who had cervical epidural anesthesia (n = 18), lumbar epidural anesthesia (n = 16), or light general anesthesia alone (n = 16). Ketamine, 2 mg/kg, iv, produced statistically significant increases in both AP and HR in all patients studied. However, the per cent increases in systolic AP in the cervical group were statistically less than those in the lumbar epidural group and control groups (P< 0.05), which did not significantly differ from each other. The changes in HR following ketamine in the cervical group were significantly less than those in the other two groups (at 3–10 min following ketamine) (P< 0.05). These results indicate that the cardiovascular stimulatory effects of ketamine are suppressed partially by a high level of epidural anesthesia but not by a low level of epidural blockade. Since patients with cervical epidural anesthesia had an analgesic level extending between C4and Th3, the above attenuative effects of epidural blockade may be considered to be attributable to cardiac sympathectomy induced by a high level of epidural anesthesia.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Halothane-induced lipid peroxidation was studied in microsomes from phenobarbital-pretreated male rats at defined steady state oxygen partial pressures (Po·2). At Po·2less than 10 mmHg on addition of halothane to NADPH-reduced microsomes, significant increases in malondialdehyde (MDA) formation, oxygen uptake, and conjugated dienes were measured. At the maximum, near a Po2of 1 mmHg, halothane induced the formation of about 0.75 nmol MDA · mg microsomal protein−1· min−1; it also stimulated microsomal oxygen uptake twofold to threefold, and caused an almost threefold increase in conjugated diene absorption. Moreover, at this Po2, microsomal glucose-6-phosphatase lost about 70% of its activity. At Po2greater than 10 mmHg, no significant effects of halothane on MDA formation, oxygen uptake, conjugated diene absorption, and glucose-6-phosphatase activity were observed; likewise under anaerobic conditions there was only a slight increase in conjugated dienes. The findings demonstrate that halothane induces microsomal lipid peroxidation at low Po2and in the presence of particular cytochrome P-450 isoenzymes, and that the halothane-induced lipid peroxidation leads to severe microsomal lesions, as indicated by the loss of glucose-6-phosphatase activity.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Verapamil may have application in the field of obstetrics for treatment of maternal and fetal tachyarrhythmias. This study was performed to assess the maternal and fetal hemodynamic effects of this drug, as well as to determine its placental transfer and effects on maternal and fetal atrioventricular conduction in the pregnant ewe. Verapamil, 0.2 mg/kg, administered intravenously over 3 min, resulted in a transient decrease in maternal mean and diastolic blood pressures. There was, however, no significant change in fetal systolic, diastolic, and mean blood pressures. Maternal and fetal heart rates also were unchanged throughout the experiment. Atrioventricular conduction, assessed by measurement of PR intervals, was prolonged in both the ewe (41%) and the fetus (78%). Placental transfer of verapamil was limited, as shown by the umbilical vein to uterine artery drug concentration ratios of 0.35–0.45 throughout most of the experiment. Fetal hepatic extraction of the drug appeared to be substantial, since the drug concentration in the fetal carotid artery was less than that of the umbilical vein at 1, 3, and 5 min after drug injection.

ISSN:0003-3022    

出版商:OVID    

年代:1985

数据来源: OVID