ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Hemodynamic and blood-gas variables were studied before and after pentolinium tartrate administration in six patients anesthetized with nitrous oxide–halothane and maintained at PaCO235–40 torr. Measurements were made prior to induction of anesthesia; before and 10, 20, and 60 minutes after administration of pentolinium (0.3 mg/kg); 15 minutes after return of arterial blood pressure to control values. Mean arterial blood pressure (MAP) was significantly decreased at 20 (P< 0.02) and 60 (P< 0.001) minutes, in association with significant decreases in systemic vascular resistance (SVR) (P< 0.05 andP< 0.005). At 60 minutes MAP was significantly lower than that at 10 minutes (P< 0.01). Cardiac output (CO) was increased (P< 0.05) after 10 minutes secondary to a significant increase in heart rate. Neither variable changed significantly thereafter. CO and HR were significantly lower (P< 0.01) 60 minutes after pentolinium than at 10 minutes; both returned to 10-minute values after intravenous administration of atropine. Changes in stroke volume (SV) and mean right atrial pressure (MRAP) were not significant. Whole-body O2uptake (&OV0312;O2) was not significantly altered by pentolinium. However, a substantial diminution of myocardial O2consumption (M&OV0312;O2) was deduced from a significant decrease in the heart rate–arterial systolic pressure product (HR × ASP). Fifteen minutes after return of MAP to control levels, SVR was 11.5 per cent lower, while CO was still significantly higher (P< 0.02) than control values. Following ganglionic blockade with pentolinium during halothane–N2O anesthesia, HR is a valuable index of changes in CO, while the HR × ASP index may be utilized to evaluate changes in M&OV0312;O2. Assessment of myocardial performance during controlled hypotension is possible by the use of routinely available measurements.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Inhalation of 40 per cent N2O by nine patients who had occlusive disease in two or more coronary arteries with elevation of left ventricular end-diastolic pressures (LVEDP) significantly decreased arterial pressure (average 5 per cent) and myocardial contractility as measured by dP/dt/CPIP (average 14 per cent), and increased LVEDP (average 21 per cent). N2O had no significant effect in four patients who had angina without angiographically demonstrable coronary arterial disease. It is concluded that N2O depresses myocardial function in patients who have occlusion of the coronary arteries and impaired left ventricular function.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

The effects of sodium nitroprusside (SNP) on total, ipsilateral cerebral blood flow (CBF) in the unanesthetized and anesthetized goat was evaluated under four conditions: 1) bolus injection of SNP into the cerebral circulation via the temporal artery; 2) continuous infusion of SNP into the temporal artery in amounts too small to affect the peripheral circulation (0.57–1.14 µg/kg/min); 3) intravenous infusion of SNP; 4) continuous intravenous infusion of SNP with a bolus injection of angiotensin. Small doses (20, 40, and 80 µg) of SNP injected directly in the cerebral circulation of the awake goat produced immediate increases of 21 ± 8, 36 ± 8, and 48 ± 10 per cent, respectively, in CBF lasting 1 to 3 min without causing peripheral cardiovascular changes. The effects of SNP were attenuated by 1.5 per cent halothane anesthesia. Continuous infusion of SNP into the temporal artery in amounts too small to cause peripheral cardiovascular effects produced sustained increases in CBF averaging 31 ± 8 per cent; CBF returned to preinfusion values upon cessation of infusion. Intravenous infusion of SNP in both anesthetized and unanesthetized animals in recommended clinical dosages (3–8 µg/kg/min) produced hypotension but did not significantly alter CBF. However, upon injection of angiotensin (1.43 µg/kg), both peripheral blood pressure and CBF increased sharply, suggesting that SNP may impair autoregulation of CBF. The results of this study indicate that SNP dilates the cerebral vascular system in a way that is probably similar to its effects on other vascular beds.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

To study the cerebral protective effects of hypothermia in arterial hypoxia, anesthetized (70 per cent N2O), mechanically ventilated rats were cooled to a body temperature of 27 C. Hypoxia was induced by decreasing the oxygen content in the inspired gas mixture either to 6–7 per cent or to 2.5–3 per cent. This reduced mean PaO2to about 25 and 11–12 torr, respectively. At PaO225 torr, there was no change in cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), or labile tissue metabolites. The absence of signs of cerebral hypoxia could be attributed to an effect of temperature andpH on the hemoglobin–oxygen dissociation curve. Thus, at 27 C with a PaO2of 25 torr the total oxygen content (TO2) of arterial blood remained >15 ml (100 ml)-1, about three times the value obtained at this PO2in normothermic rats. At PaO211–12 torr, arterial TO2was reduced to about 5 ml (100 ml)−1. The hypoxia induced no change in CMRO2, a threefold increase in CBF, a moderate lactacidosis in the tissue, and a small decrease in phosphocreatine content, but no change in ATP, ADP, or AMP. These changes are less marked than those occurring at the same arterial TO2in normothermic rats. It is concluded that hypothermia exerts a pronounced protective effect on the brain in hypoxic hypoxia, and that two mechanisms are involved. First, since hypothermia shifts the oxyhemoglobin-dissociation curve towards the left, and prevents or minimizes a rightward shift due to acidosis, it maintains a high TO2in arterial blood at a given PaO2. Second, by reducing CMRO2, and thereby presumably also cellular energy requirements, hypothermia exerts a protective effect at the cellular level.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Metabolic, hemodynamic and neuroendocrine responses to halothane were measured in five normal and five malignant hyperthermia-susceptible (MHS) swine. Constant-volume ventilation was used. There was no therapeutic intervention. In MHS animals, blood lactate concentrations increased first, and the initial increases appeared to be non-hypoxic in origin. Lactate concentrations increased progressively to more than 20 µm/ml. Whole-body oxygen consumption increased almost twofold, and hind limb muscle oxygen consumption increased almost threefold. Extrapolated increases in muscle oxygen consumption accounted for about 55 per cent of the increase in whole-body oxygen consumption. Respiratory and metabolic acidosis, marked hyperkalemia, and increases in catecholamines and temperature occurred secondarily and were accompanied by progressive circulatory failure.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

The metabolism and renal effects of enflurane were studied during and after anesthesia in ten surgical patients without renal disease; ten control patients received halothane. Enflurane was metabolized to inorganic fluoride with a mean peak serum level of 22.2 ± 2.8 µM four hours after anesthesia. Urinary inorganic and organic fluoride excretions were increased but oxalic acid excretion was not. suggesting that the latter is not an enflurane metabolite. Postanesthetic renal function, including the response to vasopressin, was normal in both groups. During enflurane anesthesia renal blood flow, glomerular filtration rate, and urinary flow rate were 77, 79, and 67 per cent of control values, respectively. In this study of patients without renal disease, metabolism of enflurane to inorganic fluoride was insufficient to cause clinically significant renal dysfunction.

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1976

数据来源: OVID