Studies (1-5) of patients with congestive heart failure, decompensated hepatic cirrhosis and nephrosis have provided evidence of increased amounts of aldosterone or aldosterone-like substances in urine during edema or ascites formation. More recently, it has been demonstrated (6) that increased urinary excretion of aldosterone occurs in association with sodium retention in dogs with right heart failure and in dogs with ascites secondary to constriction of the thoracic inferior vena cava. The data in both man and dog imply that the blood level of aldosterone is elevated.Numerous attempts have been made to elucidate the mechanism regulating aldosterone secretion in clinical states associated with the formation of edema, but no data have been reported to show that increased circulating aldosterone results from increased secretion rather than from a decreased rate of inactivation. The purpose of this study was to determine the relative rates of secretion of aldosterone in 1) dogs with cardiac failure produced by stenosis of the pulmonary artery, 2) dogs with thoracic inferior vena cava constriction and ascites, and 3) normal dogs.
METHODSRight heart failure was produced in four dogs by controlled progressive constriction of the main pulmonary artery by a method described previously (7). In three other animals, ascites formed following constriction of the thoracic inferior vena cava. Six normal dogs provided the control material. All animals were female mongrel dogs weighing 15 to 23 kg. The dogs were fed a synthetic diet containing 60 mEq. of sodium and 18 mEq. of potassium per day with two exceptions; one dog with heart failure and one normal dog received 40 mEq. The procedure for isolation of aldosterone from adrenal venous and peripheral blood is shown in Figure 1. An aqueous acetone extract of the blood was concentrated by evaporation in an atmosphere of nitrogen and partitioned twice between petroleum ether and aqueous 70 per cent ethanol. The aqueous ethanol extract was similarly concentrated and then extracted with methylene chloride. This methylene chloride extract was concentrated and 689
Maximum left ventricular systolic pressure response to aortic constriction served as a measure of myocardial contractility in anesthetized euthyroid and hyperthyroid guinea pigs. This response in hyperthyroid guinea pigs (155.4 ± 1.40 mm Hg) was significantly greater than in euthyroid animals (147.3 ± 1.33 mm Hg) (P<.001) and developed at a lower end-diastolic pressure in hyperthyroid (11.27 ±0.418 mm Hg) than in euthyroid guinea pigs (14.15 ±0.521 mm Hg) (P<.001). Beta-adrenergic receptor blockade with propranolol decreased the heart rate in both groups of animals but did not alter the contractile response. After propranolol, the heart rate of the hyperthyroid animals, though decreased, was still greater than that of euthyroid controls. Cardiac stimulation at a rate similar to that of the hyperthyroid animals (430 beats/min) did not change the left ventricular contractile response of normal guinea pigs. It is concluded that myocardial contractility in hyperthyroid guinea pigs is greater than normal. Increased activity of the sympathetic nervous system is probably present in hyperthyroidism, is reflected in the tachycardia, but does not appear to increase myocardial contractility. The increased myocardial contractility therefore is probably due in large part to a direct effect of thyroid hormone on cardiac muscle.
ADDITIONAL KEY WORDSpropranolol hemodvnamic function beta-receptor blockade pressure work tachycardia cardiac stimulation • Many attempts have been made to define the relationship of the sympathetic nervous system to the cardiovascular changes produced by excess thyroid hormone. For years the hyperkinetic circulation of thyrotoxicosis was thought to be related to a hypersensitivity to catecholamines (1). However, recent reports have shown that thyroxine does not
The atrial fibrillation threshold was measured in 10 anesthetized dogs by delivering a series of impulses directly to the right atrium after infusion of 4.5 ml of 5% glucose per kilogram of body weight, and after 1.5 ml of absolute alcohol per kilogram in 3 ml/kg of 5% glucose. There were no changes in the atrial fibrillation threshold after glucose. The mean AFT before alcohol was 6.8 volts. Immediately after alcohol infusion, the arterial blood alcohol concentration (BAC) was 300.7 mg/100 ml, and the AFT increased to 9.75 volts (P less than 0.01); 20 minutes later the BAC was 181.2 mg/100 and the AFT 8.5 (P less than 0.02). There was no rebound decrease in AFT up to 65 minutes. The findings suggest that in anesthetized normal dogs, alcohol may have a direct mild antiarrhythmic effect on the atria. Atrial fibrillation in alcoholics may be due to alcohol indirectly through electrolyte, autonomic, or histologic changes.
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