摘要:

Lung volumes, deadspace, ventilation, and ventilatory response to CO2challenge were studied on the day before and for the first three days after corrective cardiac surgery. Ten patients underwent coronary artery bypass grafting and ten patients had mitral valve prostheses inserted. Half of the patients in each group received halothane as the major anesthetic, and the other half received morphine sulfate (1–2 mg/kg). Mitral valvereplacement patients anesthetized with morphine showed lower CO2sensitivity on the first postoperative day than those who received halothane. Patients who had coronary artery bypass grafts tended to hyperventilate during the postoperative period, but this did not occur on the first postoperative day in those who received morphine anesthesia.Respiratory rate was always higher postoperatively, most markedly in patients who received halothane for coronary artery bypass grafts. Vital capacity was diminished by 67 per cent in all groups postoperatively. VD/VTtended to increase during the first and second postoperative days and then decrease toward control values on the third postoperative day in all groups except valvereplacement patients who received morphine. Morphine anesthesia may increase the period of mechanical ventilation necessary after cardiac surgery partly as a result of impaired CO2sensitivity.

ISSN:0003-3022    

出版商:OVID    

年代:1975

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

The effects of repeated doses of decamethonium or succinlcheline in mureles of the cat, dog, and rabbit have been examined. In particular, the relation of degree of neuromuscular block to intersity of the electrical change at the end-plate region has been found to be more consistent when the peak spatial gradient of depolarization is used as a measure of electrical effect than when the peak depolarization is used: the reason for this difference is discussed. A plot of twitch height against electrical change provides a convenient frame of reference for following the development of phase II block quantitatively. Examples presented show that the extent and kinetics of phase II block can vary considerably among species or among muscles in a given species.

ISSN:0003-3022    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

The effects of methoxyflurane, trichloroethylene, chloroform, halothane and diethyl ether on the division of Chinese hamster fibroblasts in spinner culture have been studied. All agents caused dose-dependent inhibition of cell multiplication. Halothane increased the cell cycle time roughly in accordance with its effect on multiplication rate. There was no evidence that milosis was greatly prolonged, and only small numbers of “cmetaphases“ were seen. However, exposure to halothane resulted in a marked and rapid reduction in the prophase count, suggesting prolongation of G2(the post-synthetic phase). Cine-photomicrography showed frequent delay in division of cytoplasm at mitosis, and many binucleate cells were seen.

ISSN:0003-3022    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

The activities of liver microsomal enzymes were studied in preparations from unanesthetized rats and rats anesthetized for one hour with nitrous oxide, diethyl ether, halothane or chloroform. Most of the enzymes studied were cytochrome P-450-dependent oxygenates that hydroxylate endogenous substrates. The other microsomal enzymes, assayed for comparison, included the cytochrome P-450-dependent aminopyrine demethylase, glucose-6-phosphatase, a dehydrogenase, and NADPH-cytochrome P-450 reductase. No anesthetic was associated with a significant change in activity of any enzyme studied. In rats pretreated with phenobarbital no anesthetic except chloroform changed enzymic activity. All hydroxylations were inhibited markedly by chloroform, as were a microsomal dehydrogenation, hydrolysis of glucose-6-phosphate, and NADPH-cytochrome P-450 reductase activity. Administration of α tocopherol did not prevent the inhibition associated with chloroform in phenobarbital-induced animals.It is concluded that cytochrome P-450-dependent hydroxylations involved in metabolic processes normally proceeding in the endoplasraic reticulum of the liver are not permanently affected by the anesthetics used in this study. The inhibitory effect of chloroform after pretreatment with phenobarbital is unspecific and affects a large number of different microsomal enzymes. Evidence that mechanisms other than lipid peroxidation may be responsible for the toxic effects of chloroform in the liver is presented.

ISSN:0003-3022    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

Experiments were performed to determine whether depression of venomotor responses with halothane results from interference with sympathetic activation or from an effect on venous smooth muscle cells. Changes in isometric tension of isolated canine saphenous-vein strips were recorded. Adrenergic activation was achieved by transmural electrical stimulation, by addition of tyramine, and by addition of norepinephrine. Halothane (0.5 to 3 per cent) did not significantly alter basal tension. It lessened the reaction of the veins to electrical stimulation but not their response to norepinephrine; it increased the response to tyramine. Since the responses to norepinephriae and tyramine were not decreased, halothane appears to act on the nerve terminal to prevent release of neurotransmitter associated with nerve-terminal depolarization. Thus, halothane causes inhibition of electrically induced venoconstriction in cutaneous veins, probably by interfering with the release of norepinephrine from nerve terminals rather than by an inhibitory effect on the smooth-muscle cells.

ISSN:0003-3022    

出版商:OVID    

年代:1975

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

The effect of halothane on A-V conduction was evaluated in dogs during atrial pacing using the technique of His-bundle electrocardiography. In addition, the effects of lidocaine and diphenylhydantoin (DPH) on A-V conduction were examined during halothane anesthesia. Effects of these drugs on three subintervals of A-V conduction were compared. These included the P-H (stimulus artifact to His-bundle deflection—atrioventricular conduction), H-Q (His-bundle deflection to onset of QRS complex—His-Purkinje conduction), and H-S intervals (His-bundle deflection to end of QRS complex—total intraventricular conduction). Linear regression best described the relationship between duration of interval (P-H, H-V, and H-S) and heart rate during incremental increases in the atrial paced rate. Data from these experiments were fitted to a multiple linear regression model that predicted the effects of increasing concentrations of halothane, lidocaine, and DPH on slope and intercept coefficients. Increasing concentrations of halothane (30 and 45 mg/100 ml arterial) prolonged all three subintervals of A-V conduction to more than control (15 mg/100 ml arterial). Both lidocaine and DPH further depressed conduction at all levels of halothane anesthesia. The P-H interval was particularly sensitive to drug effects. This may represent potentiation of the normal slowing of conduction through the AV node in response to incremental increases in heart rate (fatigue response). We conclude that both lidocaine and DPH fail to reverse the depressant effect of halothane on A-V conduction. This may explain their ineffectiveness in treating certain types of arrhythmias during halothane anesthesia.

ISSN:0003-3022    

出版商:OVID    

年代:1975

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

The effects of nitrous oxide on ventricular performance and pulmonary circulation were studied in 12 patients with angiographically demonstrated coronary-artery disease and normal ventricular contractility who had received 2 mg/kg morphine intravenously. Seventeen studies were performed intraoperatively, five before and 12 after cardiopulmonary bypass and myocardial revascularization. Recordings were obtained during oxygen breathing and during nitrous oxide administration. Fifty per cent nitrous oxide significantly decreased mean arterial pressure (P< 0.05), cardiac index (P< 0.01), stroke index (P< 0.01), left ventricular stroke work index (P< 0.01), peak left ventricular dP/dt (P< 0.05) and dP/dt/P (P< 0.01), and heart rate-systolic arterial pressure product (P< 0.01). Mean pulmonary arterial pressure (P< 0.05), pulmonary artery occluded pressure (P< 0.01). left ventricular end-diastolic pressure (P< 0.01) and pulmonary vascular resistance (P< 0.05) increased. Heart rate, right atrial pressure and systemic vascular resistance remained unchanged. When nitrous oxide was discontinued. all variables returned to control except mean pulmonary arterial pressure and pulmonary vascular resistance. Responses were similar before and after cardiopulmonary bypass and myocardial revascularization. These findings suggest that nitrous oxide depresses left ventricular performance when administered intraoperatively to patients who have received large doses of morphine for coronary-artery surgery. Nitrous oxide also increases pulmonary vascular resistance. possibly via alpha-adrenergic stimulation.

ISSN:0003-3022    

出版商:OVID    

年代:1975

数据来源: OVID