Lee H. Cooperman

Control of the splanchnic circulation in man. Role of beta-adrenergic receptors.

Some effects of the β-adrenergic receptor blocker, propranolol, were studied in 20 normal, fasting, conscious men. The measurements made included cardiac output, splanchnic blood flow and oxygen consumption, arterial and hepatic venous blood pressure, and heart rate. The intravenous administration of propranolol (0.13 mg/kg) was followed by significant reductions in splanchnic blood flow and oxygen consumption, in cardiac output and in heart rate. Splanchnic perfusion pressure was unchanged; the splanchnic vascular resistance was significantly elevated. Previous treatment with glucose did not alter these findings. Phenoxybenzamine pretreatment lessened the increase in splanchnic vascular resistance which propranolol ordinarily caused. Ganglion-ic blockade with hexamethonium prevented all of the changes which propranolol produced in untreated individuals. These results may best be explained by assuming that the splanchnic circulation in man is influenced both by α receptors, which cause vasoconstriction when activated, and by β receptors, which when activated caused vasodilatation and increase oxygen consumption.

Pulmonary Hemodynamics during General Anesthesia in Man

Pulmonary hemodynamic effects of halothane, halothane–nitrous oxide, and cyclopropane anesthesia were studied in healthy young men. Cardiac output, pulmonary artery and wedge pressures, and arterial and venous oxygen contents were measured. During halothane and halothane–N2O anesthesia there were no significant changes in pulmonary arterial and wedge pressures or in pulmonary vascular resistance. A marked decrease in left ventricular stroke work during halothane anesthesia, with unchanged wedge pressure, suggested myocardial depression. Administration of cyclopropane caused a marked increase in pulmonary arterial and wedge pressures and in pulmonary vascular resistance. The increase in wedge pressure reflected an increase in cardiac work. Increased physiologic shunting occurred with all anesthetic mixtures, but the contribution of maldistribution to the shunt was greater during spontaneous than during controlled respiration. Neither halothane nor cyclopropane prevented changes in pulmonary vascular resistance associated with altered inspired oxygen tension.

Splanchnic Circulation During Nitrous Oxide Anesthesia and Hypocarbia in Normal Man

Circulatory effects of nitrous oxide-d-tubocurarine anesthesia with hyperventilation were studied in healthy, young men. Cardiac output, mean arterial blood pressure, and splanchnic blood flow were measured. During anesthesia and hyperventilation with normal Pco2 (CO2 added to the inspired gases), splanchnic vascular resistance was elevated significantly and the blood flow reduced, but oxygen consumption was unaltered from control values. Cardiac output and total peripheral resistance were unchanged. When Paco2 was not maintained at the normal level, total peripheral resistance and splanchnic vascular resistance were reduced and the respective blood flows augmented compared with the normocarbic period. However, the demand of the splanchnic viscera for oxygen was increased out of proportion to the increase in flow. It is suggested that the nitrous oxide-curarehyperventilation technique may be a poor choice for patients with marginal levels of splanchnic blood flow.

Splanchnic Circulation in Man during Methoxyflurane Anesthesia

The effects of methoxyflurane were determined in 12 healthy fasting male volunteers. Arterial and hepatic venous blood pressures and electrocardiogram were recorded directly and continuously. Cardiac output, splanchnic blood flow and oxygen consumption, splanchnic vascular resistance and blood volume, arteriovenous lactate and pyruvate concentrations, and total peripheral resistance were determined intermittently. During anesthesia, Paco2 Pao2 and body temperature were maintaned at normal levels. Methoxyflurane in an end-expired concentration of 0.2 per cent reduced splanchnic blood flow by 50 per cent and hepatic venous oxygen tension by 30 per cent. Splanchnic was no biochemical evidence of ischemic hypoxia. The reduction in blood flow was caused by arterial hypotension and increased splanchnic vascular resistance. Arteriograms made during methoxyflurane anesthesia indicated that vasoconstriction was limited to the hepatic artery. Cardiac output was unchanged, while total peripheral resistance diminished.

Anesthesia and the Liver

Recent advances in understanding the hepatic effects of anesthesia have influenced surgical thinking. This article will examine three pertinent areas: anesthetic effects on hepatic function, anesthetic problems presented by the patient with liver disease, and anesthetic hepatoxicity.

Time-dependent Circulatory Effects of Methoxyflurane in Man

Methoxyflurane was administered to eight healthy male volunteers over a three-hour period during which myocardial contractility, cardiac output, oxygen consumption, and total peripheral resistance were measured serially. Myocardial contractile force initially decreased, but returned toward control with time. Cardiac output remained unchanged. Total peripheral resistance, reduced at one hour in most cases, did not decrease further during the next two hours. Oxygen consumption remained directly related to cardiac output. It was concluded that some “adaptation” or “recovery” occurs when methoxyflurane is administered for an extended period, but recovery was not as marked as that observed with halothane.