ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The authors determined cardiovascular, renal, and hormonal responses to increased airway pressure during continuous positive-pressure ventilation (CPPV) and continuous positive airway pressure (CPAP). Nine healthy, hydrated laboratory swine had appropriate catheters placed to allow for measurement of intra-pleural, aortic, inferior vena caval, and left ventricular end-diastolic pressures; cardiac output; and urinary flow. Samples of arterial blood were analyzed for oxygen and carbon dioxide tensions, pH, plasma vasopressin, osmolality, and creatinine and sodium concentrations. Urine was analyzed for osmolality and creatinine and sodium concentrations, and volume was recorded. Intrapleural pressure was subtracted from left ventricular end-diastolic pressure to calculate transmural pressure, a reflection of left ventricular filling pressure. Glomerular filtration rate and urinary free-water and osmolal clearances were also calculated.Expiratory left ventricular filling pressure was decreased equally by CPAP and CPPV. However, inspiratory left ventricular filling pressure and cardiac output were decreased by CPPV only. Urinary flow and glomerular filtration rate were decreased equally by CPAP and CPPV. Sodium excretion was decreased and plasma vasopressin increased by CPPV, but not by CPAP. Urinary free water and osmolal clearances were not changed by either ventilatory pattern. Although many of the renal-function variables were affected similarly by CPPV and CPAP, these alterations were not influenced solely by cardiac output or vasopressin, because only CPPV depressed cardiac output and increased vasopressin levels.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The hemodynamic and renal effects of mechanical ventilation with positive end-expiratory pressure (PEEP) were studied with and without continuous dopamine administration in ten patients who had acute pulmonary failure. The application of 20 cm H2O PEEP during mechanical ventilation resulted in improvements in arterial blood oxygen tension, from 63 ± 6 to 81 ± 12 torr (mean ± SE), and intrapulmonary shunt fraction, from 29 ± 3 to 21 ± 3 per cent, whereas cardiac output, systemic oxygen transport and renal function were impaired by 20, 19 and 47 per cent, respectively. Dopamine infusion at a rate of 5 ± 0.05 μg/ kg/min reversed the deleterious effects of PEEP on cardiovascular and renal function: cardiac output increased from 4.5 ± 0.3 to 6.0 ± 0.51, urinary output from 1.0 ± 0.3 to 1.7 ± 0.4 ml/min, sodium excretion and creatinine clearance by 50 per cent. Systemic oxygen transport was improved from 680 ± 44 to 925 ± 78 ml, arterial oxygen tension from 81 ± 12 to 102 ± 14 torr, and total deadspace to tidal volume ratio from 0.49 ± 0.02 to 0.44 ± 0.03 with dopamine. The authors conclude that the depression of cardiovascular and renal functions that may occur in patients who need high levels of PEEP for the treatment of acute pulmonary failure can be treated successfully with dopamine infusion. This represents a valuable alternative to expansion of blood volume for the improvement of systemic oxygen transport and arterial blood oxygen tension in critically ill patients.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The effects of pentobarbital on survival times of mice exposed to oxygen, 5 per cent, were studied over a large dosage range in normal mice and in mice made tolerant to the effect of barbiturates. Tolerance was induced by pretreatment with phenobarbital, 210 mg/kg, for three days, which increased the median anesthetic dose (AD50) for pentobarbital from 34 to 53 mg/kg. In nontolerant mice there was a dose-related increase in mean survival times for doses between 35 and 60 mg/kg, with a maximum increase to 303 per cent above control. At doses of more than 60 mg/kg survival times progressively decreased toward control. For tolerant mice survival time as a function of pentobarbital dosage was shifted to the right, i.e., protection necessitated higher doses. This shift was not explained by lower brain concentrations of pentobarbital in tolerant animals, but rather parallelled the increased tolerance to the anesthetic effect of the barbiturate. The authors conclude that in this model the protective effect of barbiturate is a function of the anesthetic effect rather than the barbiturate concentration in brain per se. Hypothermia (29 C) resulted in an increase in mean survival time comparable to that in barbiturate-treated animals. This supports the hypothesis that protection is ultimately a function of decreased cerebral metabolism, whether produced by anesthesia or by hypothermia. This model measures only the effect on spontaneous respiration during hypoxia. It is possible that other mechanisms are involved if barbiturates protect in other situations, such as during or after periods of complete ischemia.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Halothane (0.05–1.7 vol per cent end-tidal) in nitrous oxide (N2O), 60 per cent: oxygen (O2), 40 per cent was administered to nonmedicated, closed-chest pigs. Ventricular function was analyzed from cardiac output (thermodilution) and left ventricular (LV) pressure indices. Ventricular volumes and compliance were estimated from single and biplane LV angiography. In separate experiments, the effects of N2O, time, and the angiographic dye injections were shown to be minimal. Halothane caused dose-dependent decreases in aortic blood pressure, cardiac output, peak first derivative of left ventricular pressure (LV dP/dt), the in-vivo maximum velocity of fiber shortening (Vmax), and ejection fraction; non-dose-dependent decreases in heart rate and circumferential fiber shortening rate. Although a pronounced dose-related negative inotropic effect of halothane in the pig heart was demonstrated, there was no definite effect on ventricular pressure-volume relationships (compliance). If there was any such effect of halothane, it was obscured by the cardiac depression produced.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

To elucidate the interaction of 4-aminopyridine with neostigmine and pyridostigmine, the authors studied 57 anesthetized surgical patients using a technique of constant infusion of pancuronium to quantitate antagonist activity. 4-Aminopyridine, 0.15 or 0.35 mg/kg, produced no antagonism, while 0.5 mg/kg produced a mean 24 ± 6 per cent (peak) antagonism. The dose that produced 50 per cent antagonism (EDsn) of neostigmine alone was 22 μg/kg; with 0.35 mg/kg 4-aminopyridine, it was 7 μg/kg. The ED50of pyridostigmine alone was 110 μg/kg; with 0.35 mg/kg 4-aminopyridine, it was 27 μg/kg. 4-Aminopyridine prolonged the onset times of both neostigmine and pyridostigmine, but prolonged the duration of action of neostigmine only. At a given level of antagonism of pancuronium, adding 4-aminopyridine 0.35 mg/kg, to neostigmine and to pyridostigmine decreased the amounts of atropine needed to prevent a change in heart rate by 68 and 70 per cent, respectively. The authors conclude that 4-aminopyridine potentiates antagonism of a pancuronium-induced neuromuscular blockade by neostigmine or pyridostigmine. Also, less atropine is needed to prevent cardiac muscarinic stimulation when 4-aminopyridine is used with either neostigmine or pyridostigmine.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The possibility that acute or chronic imipramine administration predisposes to development of cardiac arrhythmias from pancuronium during anesthesia with halothane or enflurane was explored. Acute administration of imipramine, 0.5, 1, 2, or 3 mg/kg, or pancuronium, 10, 40, or 80 μg/kg, caused dose-dependent tachycardia in dogs anesthetized with halothane (n = 5) or enflurane (n = 5) except for the 3 mg/kg dose of imipramine, which decreased heart rate by 11 ± 1 beats/min (P < 0.01). Simultaneous administration of pancuronium and imipramine caused tachycardia in an additive manner in doses of pancuronium to 80 μg/kg and imipramine to 2 mg/kg; at higher doses, the tachycardia became less than additive. Forty additional dogs were given imipramine, 8 (n = 20) or 16 mg/day (n = 20), for 15 days, and then anesthetized with either halothane or enflurane. Pancuronium did not cause cardiac arrhythmias in the dogs anesthetized with enflurane. Although pancuronium, 10 and 40 μg/kg, did not produce arrhythmias in the halothane-anesthetized dogs, the 80 μg/kg dose produced premature ventricular contractions and ventricular tachycardia, which rapidly progressed to ventricular fibrillation and cardiac arrest in two of ten dogs given imipramine, 8 mg/kg/day, and in four of ten dogs given imipramine, 16 mg/kg/day. Although only the dogs that had severe ventricular arrhythmias had significantly increased blood nor-epinephrine concentrations, the norepinephrine concentrations increased before the appearance of ventricular arrhythmias. The authors conclude that severe ventricular arrhythmias may occur as a result of administration of pancuronium in dogs anesthetized with halothane and receiving imipramine chronically. These results suggest that pancuronium should be given with caution to a patient receiving chronic tricyclic antidepressant therapy who is anesthetized with halothane.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

There is sufficient evidence that anesthetics may cause cancer to justify a test of their carcinogenic potential. Baden et al., using the Ames test, a rapid and inexpensive genetic indicator of carcinogenicity, have shown that among currently used anesthetics fluroxene alone caused bacterial mutations. The authors used the sister chromatid exchange (SCE) technique, another rapid assay of mutagenic-carcinogenic potential. The frequency of sister chromatid exchanges in Chinese hamster ovary cells increases when the cell cultures are exposed to mutagcnic-carcinogens, particulary in the presence of a metabolic activating system. With this test system a one-hour exposure to 1 MAC nitrous oxide, diethyl ether, trichloroethylene, halothane, enflurane, isoflurane, methoxyflurane, or chloroform did not increase SCE values. Divinyl ether, fluroxene and ethyl vinyl ether increased SCE values in the same circumstances. Results of this study of mammalian cells suggest that no currently used anesthetic is a mutagen-carcinogen. The results also suggest that anesthetics containing a vinyl moiety may be mutagen-carcinogens.

ISSN:0003-3022    

出版商:OVID    

年代:1979

数据来源: OVID