Biomedical subjects

J Tarnow

Publications and source records attributed to J Tarnow.

At least 91 records · Page 5Linked to original sources

PubMed1976

[The effects of sodiumnitroprusside and trimethaphan induced hypotension on haemodynamics and myocardial oxygen consumption (author's transl)].

The influence of controlled hypotension (mean arterial pressure 60 mmHg) induced by sodium nitroprusside and trimethaphan on systemic circulation and myocardial oxygen consumption was studied in 7 anaesthetized closed chest dogs. The hypotensive effect of both drugs was primarily mediated by a reduction in total peripheral resistance. No change in cardiac output was observed. Stroke volume decreased in the presence of tachycardia. Left ventricular max dp/dt remained unaffected during sodium nitroprusside hypotension and was reduced by trimethaphan. Max dp/dt, load data and heart rate indicated that trimetaphan possesses negative inotropic properties. Sodium nitroprusside induced a hyperperfusion of the heart with a marked decrease in myocardial arteriovenous difference in oxygen. Myocardial oxygen consumption remained unchanged. Trimethaphan, on the other hand, induced only small increments in coronary blood flow and a rise in the arteriovenous difference in oxygen of the heart. This resulted in a higher myocardial oxygen consumption (+16%). Cardiac efficiency was lessened by trimethaphan and remained unaffected in the presence of sodium nitroprusside. As sodium nitroprusside neither affects myocardial oxygen consumption nor alters myocardial contractility, we conclude that sodium nitroprusside has advantages over trimethaphan in the management of controlled hypotension and in the therapy of hypertensive crisis and cardiogenic shock.

Animals↗

PubMed1976

[Effect of high dosages of fentanyl and piritramide upon haemodynamics, coronary blood flow and myocardial oxygen consumption (author's transl)].

High dosages of narcotic analgesics are frequently utilized as the sole anaesthetic agents for patients requiring open-heart surgery. The purpose of this study was to investigate the effect of high dosages of fentanyl and piritramide upon the cardiovascular system. In anaesthetized dogs (N2O:O2=2:1; 0.5 vol% halothane) 0.03 mg/kg fentanyl (=8) and 1.5 mg/kg piritramide (n=8) respectively were given intravenously as a bolus. After the administration of fentanyl there was a slight decrease in blood pressure (10%). The hypotension was the result of a decrease in cardiac output (thermodilution technique) by 13% due to bradycardia. Total peripheral resistance and myocardial contractility remained unaffected. Similar effects were only found late after injection of piritramide, since there was an initial cardiovascular response to piritramide characterized by a marked fall in blood pressure (29%). The major cause of arterial hypotension was peripheral vasodilatation. Load data and the decrease in max dp/dt however indicated also a slight myocardial depression. The altered haemodynamics led to a decrease in myocardial oxygen consumption with both narcotics, which was nearly paralleled by a reduction in coronary blood flow. The narrowing of arteriovenous oxygen difference of the heart proved coronary dilatatory properties of fentanyl and especially of piritramide. This study indicated that high dosages of fentanyl have advantages in comparison to high dosages of piritramide. The clinical implications of the results are discussed.

Animals↗

PubMed1975

Effect of althesin on renal perfusion in anaesthetized dogs.

Since Althesin affects not only the systemic circulation but also certain regional blood flows autoregulated by intrinsic mechanisms, such as cerebral and coronary blood flow, the purpose of this study was to investigate the effect of Althesin upon renal blood flow. After an injection of 2.0 mg/kg Althesin, heart rate (63 per cent) and cardiac output (21 per cent) increased, while total peripheral resistance (25 per cent), mean aortic pressure (9 per cent) and the maximum rate of change of left ventricular pressure (31 per cent) decreased. In spite of the large renal fraction of cardiac output (17.4 per cent) the renal blood flow remained unchanged. Althesin is believed not to be contra-indicated in the presence of renal dysfunction.

Alfaxalone Alfadolone Mixture↗

PubMed1975

[Anaesthetic management of patients with hyperdynamic circulation in hepatic cirrhosis (author's transl)].

Cirrhosis of the liver is frequently associated with arterial hypoxaemia and a hyperdynamic state of the systemic circulation. The hypoxaemia and the circulatory changes probably have a common aetiology, namely, shynting in the systemic and pulmonary vascular beds. Experiences in two well-documented cases suggest that anaesthetic agents may increase arteriovenous shunting and hypoxaemia in patients with hepatic cirrhosis. A plan for preanaesthetic identification and anaesthetic management in this type of patients is outlined.

Adult↗

PubMed1975

[Cardiovascular effects of the new inhalation anaesthetic isoflurane in man (author's transl)].

Cardiovascular responses to isoflurane (forane)-nitrous oxide-oxygen anaesthesia were studied in seven older premedicated patients. Anaesthesia was induced with the new non-barbiturate induction agen etomidate. All patients were intubated and mechanically ventilated to maintain normal PaCO2. Clinical concentrations of isoflurane (0.75 and 1.5 vol.-% inspiratory) decreased mean arterial pressure 22%-42%. Only small reductions in cardiac output and stroke volume were seen. Heart rate, central venous and pulmonary artery pressure remained nearly unaffected. The major cause of the arterial hypotension was a fall in total peripheral resistance by 36% as anaesthesia deepened. Left ventricular maximum dp/dt and load data indicated that isoflurane also possesses negative inotropic properties. Tension-time-index and total body oxygen consumption decreased by 47% and 20% respectively. AVDO2 values remained within the normal range. We take this to mean that the oxygen supply was adequate to meet the metabolic demands of the body as a whole. This was corroborated by the finding that base excess did not change significantly. Conclusions considering the use of isoflurane in patients with diminished cardiovascular reserve are drawn.

Adult↗

PubMed1975

[The effect of ketamine on haemodynamics and myocardial oxygen consumption in anaesthetized dogs (author's transl)].

Ketamine is an induction agent. This experimental study was designed to investigate the immediate effects of ketamine upon haemodynamics, inotropism and myocardial oxygen consumption during induction. In a circulatory steady state of a piritramide - nitrous oxide - oxygen basic anaesthesia normoventilated dogs (n = 8) received intravenous injections of 5.0 and 10.0 mg/kg ketamine within 30 sec at random. Immediately after administration of 10.0 mg/kg ketamine the cardiac output (thermo dilution method) rose (27%) on account of tachycardia while the total peripheral resistance (40%) and the mean arterial pressure (23%) decreased. The decrease in stroke volume (37%) and the inotropic parameter dp/dt max (42%) as well as the increase in the end-diastolic left ventricular pressure (31%) and in the pressure of the pulmonary artery (11%) suggest considerable myocardial depressor properties of ketamine. The change in haemodynamics was paralleled with an increase in myocardial oxygen consumption (47%), which was initially met by an increase in coronary blood flow (25%) and an additional oxygen utilization (20%). The increase in arterio-coronary venous oxygen difference is believed to be due to a constriction of the coronary arteries after ketamine. Since external cardiac work remained unchanged,while myocardial contractility and myocardial wall tension (Psyst) decreased, the increase in heart rate (63%) explains the rise in myocardial oxygen consumption. The efficiency of cardiac work, which is defined as the ratio of myocardial displacement work to myocardial energy demand, decreased (31%) and illustrated the uneconomic work of the heart under the influence of ketamine. The clinical utilization of the data obtained from this study are discussed.

Animals↗

PubMed1975

[Effects of glucagon on systemic circulation, coronary blood flow and myocardial oxygen consumption in the anesthetized dog (author's transl)].

The systemic and coronary hemodynamic effects of 10, 20, 40 and 80 mug/kg glucagon have been studied in 9 anesthetized normoventilated closed-chest dogs. Intravenous administration of this agent produced a dose-related increase in the average coronary blood flow between 19% (10 mug/kg) and 49% (80 mug/kg). Coronary vascular resistance decreased by between 16% (10 mug/kg) and 39% (80 mug/kg). A--V O2 difference 1 min after the administration of glucagon no changes in myocardial oxygen extraction were observed after 5, 10 and 20 min. The calculated myocardial oxygen consumption rose up to 50% after 80 mug/kg glucagon. We conclude that the increase in coronary blood flow and the decrease in coronary resistance are mainly secondary to the metabolic effects of the increased myocardial contractility and heart rate, and that there is only an initial direct vasodilating effect on the coronary vessels.

Animals↗

PubMed1974