Role of cortisol ion cardiac glucose metabolism in vivo.

Little is known about how physiological concentrations of glucocorticoid relate to cardiac metabolism in vivo. Healthy conscious dogs with catheters implanted for blood sampling and glucose infusion were studied. The range of blood glucose values produced by glucose infusion was 3700 to 74,400 mumol/liter. Arterial glucose concentration (Ca) was not significantly correlated with the arterial-coronary sinus difference in concentration of glucose, Ca-cs glucose (N = 50, r = 0.23). However, at or above glucose infusion rates of 2120 mumol/min, significant increases in cardiac glucose extractions were seen. The range of plasma cortisol values was 13 to 438 nmol/liter. Cortisol immunoreactivity in arterial plasma (Ia cortisol) was significantly and negatively correlated with Ca-cs glucose (N = 50, r = -0.37, P < 0.01). Nonparametric analysis confirmed this association (Spearman rank correlation coefficient, rs = -0.44, P < 0.01). The heart took up and released cortisol in relation to Ia cortisol (N = 50, r = 0.75, P < 0.001; rs = 0.58, P < 0.001). The range of Ia-cs cortisol was -31 to 138 nmol/liter (mean +/- SEM, 12 +/- 4, P < 0.01). The Ca-cs glucose was negatively correlated with Ia-cs cortisol (N = 50, r = -0.43, P < 0.01; rs = 0.50, P < 0.001). Thus, higher plasma cortisol immunoreactivity may lead to greater myocardial cortisol extraction and suppression of myocardial glucose extraction in vivo. At the same time arterial insulin immunoreactivity had a significant positive relationship to myocardial glucose extraction (N = 50, r = 0.37, P < 0.05; rs = 0.38, P < 0.01) and arterial plasma free fatty acids a negative relationship (N = 50, rs = -0.30, P < 0.05).

Effects of beta 2-adrenoceptor stimulation on cardiac metabolism in the conscious dog.

1 The effects of the beta 2-adrenoceptor stimulant, salbutamol, on cardiac metabolism have been studied in conscious mongrel dogs. The potential effects of anaesthesia on the study of cardiac metabolism have been avoided by prior implantation of arterial (A) and coronary sinus (CS) catheters for blood sampling and a central venous catheter for infusion. Extraction of substrates for myocardial energy metabolism (CA-CS) was assessed 3 to 24 days post-operatively. A 100 micrograms bolus of salbutamol was given followed by an infusion of 3 micrograms/min for 1 h. 2 Although heart rate increased significantly from 106 to 165 beats/min, fractional extraction of oxygen tended to fall from 84% to 77%. Thus an increase in coronary blood flow rather than in oxygen extraction must have maintained an oxygen supply commensurate with the salbutamol-induced tachycardia. 3 Neither CA-CS glucose nor fractional glucose extraction altered significantly during salbutamol infusion despite increases in arterial concentration (CA) of glucose and arterial insulin immunoreactivity and a decrease in CA of free fatty acids (FFA). This suggests that an insulin-antagonistic action accompanies the infusion of salbutamol. 4 The fractional extraction of lactate increased during salbutamol infusion. In part, this may have been a reflection of a decreased myocardial extraction of FFA with salbutamol in this model.

Cardiac effects of salbutamol-induced hypokalaemia in the conscious dog.

1. Infusion of salbutamol (3.0 microgram/min after a bolus injection of 100 microgram) produced hypokalaemia in conscious dogs. 2. Measurement of arterial and coronary sinus potassium differences revealed no significant potassium loss from the heart with established hypokalaemia. 3. Shortly after the initial salbutamol bolus and before steady-state hypokalaemia had been achieved during salbutamol infusion, a prolongation of QTc occurred; this corresponded to a significant myocardial potassium of -0.12 mmol/l plasma. 4. Urinary electrolyte excretions indicated that the hypokalaemia was not due to urinary potassium loss. 5. It was deduced that potassium had moved intracellularly. No change in hydrogen ion status occurred to account for this. Pronounced rises in plasma insulin immunoreactivities during salbutamol infusions suggested this as one mechanism for potassium shifts.

Effects of fentanyl and droperidol on canine left ventricular performance.

The effects of fentanyl and droperidol on left ventricular performance were evaluated in the neurally intact dog right-heart-bypass preparation under conditions of constant cardiac output, arterial pressure, and heart rate. Fentanyl, .01 and .02 mg/kg body weight, and droperidol, 0.5 mg/kg, did not affect left ventricular performance. However 1.0 mg/kg droperidol caused a significant (P less than .05) increase in left ventricular end-diastolic pressure and a small decrease in maximum left ventricular dP/dt (.05 less than P less than .10). No significant change in myocardial oxygen consumption was observed. This study indicates that large doses of droperidol may depress left ventricular performance and may account for a portion of the hypotension observed after its administration in man. (Key words: Anesthetics, intravenous, fentanyl; Anesthetics; intravenous, droperidol; Heart, function, fentanyl; Heart, function, droperidol.).