ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The effect of sodium nitroprusside (SNP) on the pulmonary vasoconstrictor response to alveolar hypoxia was assessed by measuring the redistribution of blood flow in response to unilateral hypoxia. Ten dogs were anesthetized with thiopental and pentobarbital and a double-lumen endotracheal tube was inserted to permit separate ventilation of right and left lungs. Tidal volumes were maintained constant and redistribution of blood flow to each lung was followed by recording the radioactivity of mixed expired gas during the continuous intravenous infusion of133Xe.The pulmonary vasoconstrictor response was tested by ventilating the left lung with oxygen, 7 per cent, followed by 100 per cent nitrogen before, during and after an intravenous infusion of SNP. The experimental sequence was then repeated. Unilateral hypoxia consistently decreased blood flow to the hypoxic lung (P<0.02), and there was no significant difference in flows during nonhypoxic conditions. Following infusion of SNP at a rate sufficient to decrease the mean arterial pressure to 80 torr there was a significant increase in flow (P<0.01) to the nonhypoxic lung in response to both degrees of hypoxia. The second infusion of SNP blunted the pulmonary vasoconstrictor response to anoxia (P<0.001), but the first infusion produced no significant blunting of response to either level of hypoxia. Arterial oxygen tension values increased significantly (P<0.05) during hypoxic conditions following SNP infusion and were significantly decreased (P<0.05) during the second infusion of SNP.These results suggest that SNP may increase arterial hypoxemia by depressing the homeostatic diversion of blood flow away from hypoxic areas of the lung; on discontinuation of SNP, there may be an increased protective response to hypoxia.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

This study was designed to investigate the mechanism by which sodium nitroprusside (SNP) decreases oxygenation by determining its effects on venous admixture (&OV0422;VA/&OV0422;t) and ventilation— perfusion distribution (&OV0312;A/&OV0422;) in animals with normal and abnormal lungs. SNP was infused into seven dogs anesthetized with pentobarbital. Mean blood pressure was decreased by 40 per cent during normal lung function and again after the production of diffuse pulmonary edema by intravenous administration of oleic acid. Measurements of blood-gas values, &OV0422;VA/&OV0422;tand &OV0312;A/&OV0422; by the inert-gas-elimination method were taken before, during, and after SNP infusion during ventilation with air and then during ventilation with 100 per cent oxygen in each pulmonary condition. SNP caused no change in cardiac output (&OV0422;t) during normal lung function or after the production of pulmonary edema. SNP had no effect on pulmonary gas exchange during normal lung function. During pulmonary edema and ventilation with air, SNP decreased Pao2from 71 ± 7 torr (mean ± 1 SD) to 61 ± 11 torr (P<.01), and increased &OV0422;VA/&OV0422;t(oxygen method) from 20 ± 8 to 38 ± 18 per cent (P<.01). The increase in &OV0422;VA/&OV0422;tcorrelated well with a 28 per cent decrease in pulmonary vascular resistance (PVR) (r =-.863). During pulmonary edema with air and ventilation SNP increased &OV0312;A/&OV0422; maldistribution, but during ventilation with oxygen, SNP caused no significant change in &OV0422;V/&OV0422;t, PVR, or &OV0312;A/&OV0422;. The increase in &OV0422;V/&OV0422;tand increases in perfusion to low &OV0312;A/&OV0422; regions seen only in animals with pulmonary edema during ventilation with air are compatible with the hypothesis that nitroprusside impairs pulmonary gas exchange by inhibiting hypoxic vasoconstriction, thus increasing &OV0312;A/&OV0422; maldistribution.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Following the observation that mice manifest a characteristic withdrawal syndrome after an hour of exposure to nitrous oxide, the authors reasoned that there might be a very rapidly developing tolerance to nitrous oxide. Thus, they determined the inspired concentrations that cause loss of the righting reflex in mice (i.e., the ED50), in the presence of 1 atm of oxygen, of: 1) nitrous oxide alone; 2) cyclopropane alone; 3) nitrous oxide plus 13.6 atm helium; 4) ethylene plus 13.6 atm helium. In each instance the ED5U was determined after averages of 6,34 and 64 min. of exposure to the anesthetic agents. For nitrous oxide alone the ED50at 6 min was 1.18 ± 0.049 atm, increasing to 1.39 ± 0.061 atm at 64 min. For ethylene plus helium the ED50increased from 1.21 ± 0.033 atm at 6 min to 1.31 ± 0.039 atm at 64 min, indicating the development of acute tolerance. Neither cyclopropane alone nor nitrous oxide plus helium caused acute tolerance. This absence of tolerance may have resulted from a slower development of an alveolar anesthetic concentration.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The authors previously had found that mice exposed to an anesthetizing concentration of nitrous oxide (1.45 atm) for only one to two hours would convulse when picked up by the tail following anesthesia.1In the present study they examined seven other anesthetics to discover whether this withdrawal (dependence) phenomenon was unique to nitrous oxide. Groups of mice were exposed to an ED50of each agent for different periods of time and were tested for the incidence of withdrawal convulsions until they disappeared. Withdrawal convulsions occurred after 4-15 min of exposure to nitrous oxide, ethylene, and cyclopropane and (to a very slight extent), diethyl ether, and disappeared within 90 min in every instance. Convulsions were not elicited following exposure to halothane, enflurane, isoflurane, or fluroxene. The withdrawal syndrome following exposure to nitrous oxide was not changed by pretreatment with either α -methyldopa or reserpine, and thus a possible relationship between sympathomimetic action of the agents and the production of dependence appears unlikely.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Mice continuously exposed to nitrous oxide, 50 per cent, for two to three weeks become tolerant to anesthesia, as evidenced by an increase in the concentration of nitrous oxide necessary to abolish the righting reflex from 1.49 ± 0.045 atm to 1.67 ± 0.053 atm after three weeks (auto-tolerance). Also, there was an increase in the concentration of a second anesthetic (cyclopropane or isoflurane) necessary to abolish the righting reflex (cross-tolerance). Cyclopropane ED50increased from 0.130 ± 0.0068 atm to 0.148 ± 0.0044 atm after two weeks of exposure to nitrous oxide, 50 per cent. Isoflurane ED50increased from 0.00570 ± 0.000163 atm to 0.00622 ± 0.000200 atm after three weeks of exposure to nitrous oxide, 50 per cent. Mice continuously exposed to isoflurane, 0.15 or 0.3 per cent, manifested neither auto- nor cross-tolerance. After three weeks of exposure, 69 per cent of mice removed from nitrous oxide, 50 per cent, convulsed when gently suspended by the tail (i.e., manifested a stimulus-elicited withdrawal syndrome indicating dependence on nitrous oxide). After three weeks of exposure, 43 per cent of mice convulsed when removed from isoflurane, 0.15 per cent. However, only 4 per cent of mice convulsed after six or nine weeks of exposure to this concentration of isoflurane.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Halothane was investigated for its mutagenic effects inDrosophila melanogaster. The induction of sex-linked recessive lethals was used as an indicator of genetic damage. Adult male flies were exposed to halothane either for 14 days at 1,000 or 1,600 ppm (v/v) or for one or two days in 2,100 or 20,000 ppm. In several experiments slight increases of the mutation frequency were observed. For the pooled data of the 14 day-exposure experiments, the increase amounted to a doubling of the spontaneous rate, just reaching the level of 5 per cent significance. The authors consider this a borderline result, indicating, with a fair degree of probability, that halothane has weak mutagenic activity, under the conditions studied.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The effects on gastric fluidpH of a single dose of milk of magnesia given at various intervals prior to induction of general anesthesia in 115 parturients needing emergency operative delivery with general anesthesia were studied. In addition, the responses of rat lungs to tracheally injected gastric contents from parturients treated with orally administered milk of magnesia and untreated were compared. Stomach contents from parturients were removed by orogastric sump tube as soon as possible after induction of anesthesia. Single doses of milk of magnesia were given at various intervals prior to induction to 99 patients. No patient who received milk of magnesia 10 to 80 min prior to sampling was found to have a gastric-fluidpH of less than 2.5 and volume of more than 25 ml. Five parturients who had taken milk of magnesia and had gastric-fluidpH values of less than 2.5 had received the antacid more than 80 min prior to sampling of gastric contents. Of 16 patients who did not receive an antacid, five had gastric-fluidpH values of less than 2.5 and volumes of more than 25 ml.Lung-weight-to-body-weight (LW/BW) ratios were significantly different for the three groups of rats studied. The LW/BW ratio was 8.0 x 10-3for rats that received tracheal instillations of gastric fluid from one parturient who was not treated with milk of magnesia and whose gastric-fluidpH was 1.4. The LW/BW ratio was 6.4 x 10-3in 20 rats that received intratracheal instillations of gastric fluid from one parturient who was treated with milk of magnesia and whose gastric-fluidpH was 8.7. The LW/BW ratio of sham-injected rats was 5.3 x 10-3. The authors conclude that milk of magnesia is an effective preinduction antacid in emergency obstetric anesthesia; that a single dose of 30 ml prior to induction will increase thepH values of gastric contents to more than 2.5 in all patients in the interval from 10 to 80 min after ingestion; and that milk of magnesia-neutralized gastric contents resulted in less severe induced aspiration pneumonitis in rats than did acidic gastric contents.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The disposition of morphine in the serum and in the cerebral cortex during normocarbia and hypocarbia was studied in dogs. Normocarbia was maintained by controlled ventilation with air (pHa, 7.40; Paco2,40 torr) and by controlled hyperventilation with a gas mixture of CO2, 3 per cent, O2, 21 per cent, balance N2(pHa, 7.40; Paco2, 38 torr). Hypocarbia was induced by hyperventilation with air (pHa, 7.57, Paco2, 20 torr). After achievement of a steady acid-base status, morphine sulfate, 2 mg/kg, was injected intravenously. Thereafter, serial samples of serum and cerebral cortex were taken at intervals for four hours and analyzed for morphine concentrations using radioimmunoassay. In dogs with hypocarbia, serum morphine concentrations 15-240 min following intravenous injections were higher; the serum half-life during the elimination phase remained unchanged, 62-65 min. The apparent volume of distribution, Vdand plasma clearance, Clpof morphine were less during hypocarbia. Morphine concentrations in the cerebral cortex were significantly increased at 15-240 min during hypocarbia. Estimated half-lives of morphine in the cerebral cortex were 5.5 hours during normocarbia, and 8.2 hours during hypocarbia. Maintenance of normocarbia during hyperventilation minimized these changes. These results suggest that during hypocarbia the higher serum morphine concentrations, higher drug distribution coefficient in lipid phase and increased ratio of free base: acid salt of morphine facilitated the penetrance of morphine into the brain, in spite of decreased cerebral blood flow. Once in the brain, a greater portion of morphine was probably present in the protonated form in a relatively acidic milieu and thus less able to pass through lipid barriers back to the circulation.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Because maternal stress may adversely affect the fetus, the authors tested the effects of brief episodes (15-60 sec) of maternal stress in 18 awake pregnant ewes. Maternal agitation and stuggling occurred either following non-painful stimuli such as loud noises or sudden movements of personnel (ten animals) or following the brief application to the ewe's skin of a uniform electrical stimulus of 30 volts with a frequency of 167 Hz for 30-60 sec (eight animals). Stimulation of either type produced a 45-50 per cent increase in mean maternal arterial blood pressure and a concomitant 32-52 per cent decrease in uterine blood flow (P<0.05). The decreases in uterine blood flow were brief, lasting less than 3 min, and were not associated with fetal asphyxia. Maternal plasma norepinephrine levels were measured following electrically induced maternal stress and were increased 25 per cent. The authors conclude that maternal stress may decrease uterine blood flow secondary to release of endogenous norepinephrine.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID