摘要:

Exposure of triiodothyronine (T3-pretreated rats to 1.3% isoflurane 1.8% enflurane, or 1% halothane in 21% oxygen (air) for two hours resulted in hepatic centrilobular necrosis. The incidence of the liver lesion was 28, 24, and 92% after exposure to isoflurane, enflurane, and halothane, respectively. Histopathologic grading indicated that the necrosis was more severe after halothane than after isoflurane or enflurane anesthesia. No lesion was observed in livers prepared from non-anesthetized T3-pretreated rats or in livers prepared from rats which were pretreated with the vehicle for T3and then anesthetized with either isoflurane, enflurane, or halothane. Hepatic necrosis was not observed in vehicle-treated rats exposed to isoflurane in 12% oxygen or in vehicle-treated rats that were deprived of food for 12 hours prior to exposure to isoflurane under hypoxic conditions. Food restriction to maintain the body weight gain of vehicle-treated rats similar to that of T3-treated rats did not result in hepatotoxicity after exposure to halothane in 21% oxygen. Liver necrosis did not occur in pentobarbital anesthetized (40 mg/kg, intraperitoneally) T3-pretreated rats. These results indicate that isoflurane and enflurane, like halothane, can induce hepatic centrilobular necrosis in T3-pretreated rats. The mechanism for liver toxicity of these volatile anesthetic agents in this model remains to be determined.

ISSN:0003-3022    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The characteristics of the neuromuscular blockade produced by prolonged Succinylcholine infusion were compared in 40 patients anesthetized with either nitrous-oxide-isoflurane (0.75–1.50% inspired) or nitrous-oxide-fentanyl. Neuromuscular transmission was monitored using (rain-of-four stimulation and the infusion rate was adjusted to keep the first twitch at 10–15% of its control value.Initially, all patients exhibited a depolarizing-type block, and the infusion rates were similar in the isoflurane (61 μg·kg-1· min-1) and fentanyl (57 μg · kg-1· min-1) groups. Tachyphylaxis developed in both groups and correlated well with the onset of non-depolarizing (phase II) block. Both occurred sooner and at a lower cumulative dose in the isoflurane group. After 90 min, infusion rates were similar in both groups (isoflurane: 107 μg·kg-1· min-1; fentanyl: 93 μg·kg-1· min-1). After the infusion was stopped, the recovery of the train-of-four ratio was inversely related to the dose and duration of exposure to succinylcholine, and was slower with nitrous-oxide-isoflurane anesthesia. After 10 min of recovery, patients receiving isoflurane exhibited train-of-four ratios of 0.5 or less after 8.5 mg/kg succinylcholine and 103 min. Corresponding figures for fentanyl patients were 13 mg/kg and 171 min. The block in all 13 patients (eight with isoflurane, five with fentanyl) who did not recover spontaneously was antagonized successfully with alropine and neostigmlneIt was concluded that with succinylcholine infusion of 90 min or less, isoflurane accelerates the onset of tachyphylaxis and phase II neuromuscular block without affecting succinylcholine requirements. These results, with isofiurane, were similar to those reported previously with enflurane or halothane.

ISSN:0003-3022    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Thiosulfate concentrations and pharmacokinetics were studied in relation to sodium nitroprusside before, during, and after anesthesia. Normal thiosulfate concentrations were 1.13 ± 0.11 mg/dl and 0.28 ± 0.02 mg/dl in plasma and urine, respectively. Cholecystectomy patients had similar concentrations during surgery, with bile thiosulfate concentration of 13.72 ± 2,95 mg/dl. Fasting patients and children had significantly higher plasma and urine thiosulfate concentrations. Over 99% of endogenous filtered thiosulfate was reabsorbed by the kidney in the average case. Coronary bypass patients had decreased plasma thiosulfate levels and increased excretion postoperatively. Disappearance of injected thiosulfate was biphasic; the distribution phase was dependent on the initial rate of injection, and the elimination phase depended on extracellular fluid turnover and renal excretion. Cholecystectomy patients on diurectics had a markedly increased rate of excretion, 56% within 100 min,versusnormal subjects who excreted less than 50% in up to 18 h. In children, plasma thiosulfate did not change significantly, while blood cyanide concentration increased significantly during sodium nitroprusside administration and surgery. Thiosulfate did not change during recovery while cyanide decreased. Normal production of thiosulfate in humans may be limited; hence, continuous thiosulfate infusion may be required during sodium nitroprusside administration.

ISSN:0003-3022    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The impact of tolerance on the metabolism of the whole body, skeletal muscle, brain, kidneys, splanchnic region, and heart during prolonged pentobarbital anesthesia was evaluated in 80 dogs. Oxygen consumption (&OV0312;o2) for each organ system and whole body was calculated from measured blood flow rate and the difference in blood oxygen content between arterial and venous blood during four periods of continuous and unvarying deep pentobarbital anesthesia: 0–3 h, 3–6 h, 12–15 h, and 21–24 h.&OV0312;o2increased with time in whole body (12%), gastrocnemius muscle (83%), calculated entire skeletal muscle (15%), brain (27%), kidneys (20%), and splanchnic area (10%); it decreased in the heart (20%). In all studies, the electroencephalogram indicated a constant deep burst-suppression level of 2–6 bursts/min and blood pentobarbital levels ranged from 4.5–6 mg/dl. About one-fifth of the increase in gastrocnemius &OV0312;o2could be accounted for by the effect of a continuous infusion of succinylcholine, and about two-thirds of the rise in renal &OV0312;o2by increased renal function. The decrease in heart &OV0312;o2was associated with increased cardiac output and decreased systemic vascular resistance.The sustained increase in metabolism was significant and otherwise unexplained in whole body, skeletal muscle, and the brain; it occurred after 3 h and continued through 24 h of pentobarbital anesthesia. This was presumably due to tolerance, and was manifested as increased metabolism during steady deep anesthesia with unchanged blood levels of pentobarbital rather than as a greater requirement for pentobarbital.

ISSN:0003-3022    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The effects of 150 min halothane (1% inspired in 100% O2) anesthesia on cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRo2), cerebral vascular resistance (CVR), cardiac output (CO), and cerebral autoregulation of blood flow (CA) were determined in normal goats and in goats following alpha- and beta-receptor blockade. In normal goats, CBF increased significantly from an awake value of 65 ± 5 ml · min-1· 100 g-1to 135 ± 12 ml · min-1· 100 g-1following 30 min of halothane anesthesia. After approximately 30 min, CBF began to decrease and approached pre-inhalation levels at 150 min. Cerebral vascular resistance and CMRo2decreased during the first 30 min of inhalation, but significantly increased over the next 120 min of anesthesia. Cardiac output decreased significantly with induction of anesthesia, remained below awake values throughout the 150 min of halothane inhalation, and returned to pre-inhalation levels following anesthesia. Mean arterial blood pressure (MABP) increased slightly, but not significantly after halothane was terminated.Alpha- and beta-receptor blockade with phentolamine and pro-pronolol failed to alter the. course of CBF, CVR, and CMRo2throughout the entire experimental period as compared with control values. However, CO failed to return to pre-inhalation levels upon emergence from anesthesia. In addition, MABP was significantly lower than the nontreated goats upon emergence from anesthesia.Arterial injections of angiotensin (1 μg) were administered periodically during the 150 min of anesthesia in order to challenge CA. Cerebral blood flow increased significantly in both normal and receptor-blocked animals with each angiotensin injection indicating a loss of CA to rapid increases in MABP.Results from this study indicate that the initial rise in CBF usually associated with halothane inhalation is a transient phenomenon after which CBF gradually returns to control levels over a protracted period of time. The return of CBF to control values is unrelated to CA and is not influenced by alpha- and beta-adrenergic receptor blockade.

ISSN:0003-3022    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Newborn rats were treated with guanethidine sulfate for the first three weeks of life in order to produce a partial permanent peripheral sympathectomy. The rats were allowed to grow to 250–300 granu on a normal sodium diet Using diethyl ether anesthesia, arterial and venous cannulas were placed and the animals allowed to awaken in restraining cages. The rats were divided into four groups: awake (n = 6), halothane 1.3 vol % (n = 8), enflurane 2.2 vol % (n = 8), and ketamine 125 mg/kg, ip (n = 8). The protocol consisted of a one-hour control awake period, one hour of stable anesthesia (one group received no anesthesia), and one-half-hour iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity was measured at the end of each time period. Thirty untreated normal rats were similarly divided into four groups and served as the control. The degree of peripheral sympathectomy was assessed through cardiac norepinephrine concentrations, plasma catecholamines, and response to 50% hemorrhage:Guanethidine treatment resulted in a 78% decrease in cardiac norepinephrine from 189 ± 15 ng/g in the untreated animals compared with 42.4 ± 5 ng/g in the treated animals. The five-fold increase seen in plasma norepinephrine to acute decapitation was completely absent in the treated animals. Hemorrhage of 50% of blood volume resulted in a 75% mortality rate in the treated animals, while there were no deaths 30 min after hemorrhage in the normal animals. Blood pressure for the 30 treated animals during the awake period was 114 ± 2 mmHg, which was significantly less than 124 ± 1 mmHg in the untreated animals (P< 0.05). Likewise, plasma renin activity of 1.58 ± 0.25 ng · ml-1· h-1in the treated group was significantly less than 2.59 ± 0.21 ng · ml-1· h-1in the untreated rats (P< 0.05). With the induction and maintenance of stable anesthesia, blood pressure decreased to 82 ± 2 mmHg with halothane, 92 ± 4 mmHg with enflurane, and 104 ± 4 mmHg with ketamine in the treated animals. Plasma renin activity did not increase in either treated or untreated animals. Similar degrees of blood pressure decreases were seen in untreated animals. With the infusion of saralasin, a further decrease of approximately 20 mmHg in blood pressure was seen, in both the treated and untreated rats anesthetized with halothane. However, in treated rats anesthetized with enflurane or ketamine, no depressor response to saralasin was seen, which is in marked contrast to the response seen in untreated animals. The plasma ratio response in the treated animals also was blunted. Using this animal model, these experiments suggest that partial peripheral sympatbectomy does not result in deleterious effects when rats are anesthetized with halothane, enflurane, or ketamine anesthesia.

ISSN:0003-3022    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

General anesthetics are used to eliminate perception of stimuli, yet there have been few studies of the cerebral metabolic effects of stimulation during anesthesia, and of these studies, the results are discrepant. The authors therefore applied the quantitative 2-[14C]deoxyglucose method in a study of the effects of electrical stimulation (5 volts, 0.5 ms, 10 Hz) of a rat's saphenous nerve on glucose utilization in structures of the sensory pathway after administering pentobarbital or nitrous oxide. Under both conditions, stimulation produced a 75 to 108% increase in glucose utilization in the ipsilateral dorsal horn of the spinal cord, and a 9 to 11% increase in only a small fraction of the contralateral somatosensory cortex. No unilateral metabolic effect was seen in the dorsal column nuclei, ventroposterolateral thalamus, periaqueductal gray matter, dorsal raphe nuclei, or the reticular formation.The results of this study show that during peripheral stimulation, little metabolic response is seen in the brain even if the animal is receiving only nitrous oxide (70%), while the dorsal horn of the cord responds dramatically under the same conditions. Moreover, anesthesia with the potent cerebral metabolic depressant pentobarbital does not substantially alter the metabolic responsiveness of the cord or brain to stimulation. Thus, although there are marked differences between the resting rate of metabolism produced by 70% nitrous oxide and pentobarbital, in terms of their effects on the metabolic response to stimulation, the agents are quite similar.

ISSN:0003-3022    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The effects of halothane and fentanyl anesthesia on responses to ligation of a coronary artery in chronically prepared rats were compared with responses in conscious animals. A total of 86 rats were used; 24 were ligaled under halothane anesthesia, 18 under fentanyl, and 23 were left conscious. Three other groups (each of seven rats) were identically prepared but not ligated. Non-ligated rats were left conscious or anesthetized with halothane or fentanyl. Ligation was performed with the aid of a permanently implanted snare around the left anterior descending coronary artery. The responses to ligation that were measured were: arrhythmias, blood pressure changes, heart rate changes, EGG changes, mortality rate, occluded zone, and infarcted cardiac tissue mass. It was found that 1% halothane anesthesia starting 30 min before and continuing for 4 h after permanent ligation, had an overall beneficial effect, when compared with controls. Fentanyl (200–1,000 μg/kg, iv) had no overall beneficial effect, compared with conscious controls. Halothane reduced arrhythmias and mortality rates, when compared with controls, while fentanyl did not. Halothane produced lower blood pressures, fewer EGG changes, and lower heart rates than those seen in conscious or fentanyl anesthetized rats. The occluded and infarcted zones produced by ligation were not influenced by the two anesthetics.

ISSN:0003-3022    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The effects of enflurane and halothane on contractile force of the right ventricle were compared using the Walton-Brodie strain gage arch and pulmonary artery catheter data in dogs anesthetized with pentobarbital. Twenty mongrel dogs were studied to determine the effects of the two anesthetics on contractile force during a 30-minute exposure to four approximate multiples of MAC: 0.75, 1.0, 1.25, and 2.0, and during a 2-h exposure to 1.0 MAC of each agent. Both anesthetics caused a dose-dependent reduction in contractile force, cardiac output, and mean arterial blood pressure. Enflurane caused greater depression of all variables at all concentrations tested. After a 30-min exposure to 0.75, 1.0, 1.25, and 2.0 MAC, halothane depressed contractile force 33.9%, 37.9%, 46.1%, and 73.4%, respectively, and enflurane depressed contractile force 48.4%, 53.5%, 66.6%, and 81.3%, respectively. The depression produced by enflurane at 1.0 and 1.25 MAC was significantly greater (P< 0.05) than the depression produced by halothane at equal MAC. The reduction of cardiac output by enflurane at 1.25 and 2.0 MAC was significantly greater than that observed with halothane (P< 0.05). The decrease in mean blood pressure produced by enflurane was significantly greater (P< 0.05) than the decrease produced by halothane at 1.0,1.25, and 2.0 MAC No significant differences between groups were found in temperature, arterial Pco2, Po2,pH, or hematocrit levels. No diminution of the differences in effect on contractility between the two agents was observed when the exposure period was lengthened to two hours at 1.0 MAC.

ISSN:0003-3022    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

To determine whether non-invasive measurement of brain electrical activity can predict ischemic brain damage, we recorded the electroencephalogram (EEC) and somatosensory- (SEP) and auditory- (AEP) evoked potentials before, during, and after trimethaphan-induced profound arterial hypotension in dogs. The authors set out to compare the change in electrical activity with the degree of brain damage, as determined by microscopic examination. Dogs were anesthetized with halothane (1.4 vol % inspired), maintained horizontal (head at the level of the heart), and ventilated mechanically (FIo20.50); deviations from normal acid-base status were corrected. Twenty animals received a 1.5-mg/kg intravenous bolus of trimethaphan. Three animals were resistant to the drug. The remaining animals had profound hypotension [mean arterial blood pressure (MABP) at some steady level between 12 and 25 mmHg] for 1 h. Eight of these animals died during or soon after the hypotensive period as a consequence of cardiac arrest (three), intestinal bleeding (three) or unknown causes (two). In all survivors, EEC intensity and the amplitude of the SEP decreased during hypotension; both variables recovered with restoration of MABP. All nine animals surviving hypotension had no apparent neurologic or behavioral deficit nor any histologic evidence of ischemic brain cell injury. We were thus unable to find a MABP threshold for brain injury or to determine what degree of electrical change correlated with mimimal brain injury. Our findings suggest, under the conditions of our experiments, a great margin of tolerance for profound hypotension by the brain in this species. Other organ systems–-the heart, gastrointestinal tract, and liver–-proved to be more susceptible to ischemic damage. Eight of the nine surviving animals had elevations in serum alanine transaminase (SGPT), aspartate trans-aminase (SCOT), and alkaline phosphatase. Animals with the greatest increases in these enzymes showed centrilobular hepatocyte degeneration.

ISSN:0003-3022    

出版商:OVID    

年代:1983

数据来源: OVID