Increased Renal Function in Patients with Acute Left Ventricular Failure: A Possible Homeostatic Mechanism

Abstract

1.Creatinine clearance and urine excretion have been measured in fifty-five patients admitted with suspected myocardial infarction. Patients were grouped on the basis of their radiological report on the first day, irrespective of their diagnosis. The first group consisted of twenty-six patients with normal chest X-rays, the second group of twenty-two patients with radiological evidence of upper zone vessel dilatation and the third group of seven patients with radiological evidence of pulmonary oedema, who were significantly older.2. The mean creatinine clearance on the first day in patients with upper zone vessel dilatation was significantly higher than the creatinine clearance in patients with normal radiographs. By the third and fourth days the clearances were similar in both groups. The patients with pulmonary oedema had low creatinine clearances on all 4 days.3. Glomerular filtration rate was measured with 51Cr-labelled EDTA on twenty occasions, and the results correlated well with the creatinine clearance values obtained on the same day.4. The mean urine volumes on day 1 (2245 f 286 m1/24 h) and day 2 (2219 f232 d/24 h) in patients with upper zone vessel dilatation who had not received diuretics, were significantly higher (P< 0.01) than the urine volumes on day 1 (1652f 145 d/24 h) and day2(1713 f 118 d/ 24 h) in patients with normal radiographs. All the patients with pulmonary oedema had 43 received diuretics during the study and were therefore excluded from this analysis.5. It is concluded that patients with radiological evidence of upper zone vessel dilatation show an elevation of glomerular filtration rate and an increase in urinary output. It is suggested that these responses are mediated via the stimulation of receptors in the left side of the heart and fulfil a homeostaticfunction, to unload an overdistended heart.

Reflex Inhibition of Renal Sympathetic Nerve Activity during Myocardial Ischemia Mediated by Left Ventricular Receptors with Vagal Afferents in Dogs

“…Thus, it has been shown that other vascular beds behave differently from skeletal muscle during myocardial ischemia than has been previously observed for skeletal muscle beds (5,11). In this regard, it has recently been reported that patients with acute myocardial infarction and evidence of elevated left-sided filling pressures have higher creatinine clearance, urine volume, atid sodium excretion than do patients with myocardial infarction and normal filling pressures (12). It is possible that this acute elevation of cardiac filling pressu're may have activated sensory endings in the left atrium and left ventricle.…”

Role of cardiac vagal c-fibers in cardiovascular control

“…In contrast, hemorrhagic shock induces a marked vasoconstriction in the kidney (Gorfinkel et al, 1972), and the vasoconstriction contributes to the development of acute renal failure. Studies by Bennet et al (1977Bennet et al ( , 1978 are also of great interest in this respect. These authors examined the renal function in patients with acute myocardial infarction and moderate left ventricular failure as showed by radiologic measurement of the heart size.…”

“…Interestingly enough, patients with myocardial infarction and acute congestive heart failure show increased urine flow and glomerular filtration rate despite the fall in arterial blood pressure (Efendigil et al, 1975;Bennet et al, 1977). Several of these patients also showed an increased sodium output (Bennet et al, 1978).…”

“…Several of these patients also showed an increased sodium output (Bennet et al, 1978). This increased renal function was most pronounced in patients with radiologic signs of elevated left atrial pressure (Bennet et at., 1977). A logical but of course speculative explanation for these findings is that an acute rise in left atrial pressure increases the activity in left atrial and ventricular C-fiber endings, and hence a reflex inhibition of renal sympathetic outflow occurs.…”

Blood volume in angina pectoris.

“…In man, Bennett et al (1977) have shown that there is an unexpected diuresis in the acute and early stage of left ventricular failure after myocardial infarction, but this does not persist. It might, therefore, be argued that in patients with angina who do not show a chronic rise in enddiastolic pressure or an enlarged heart, the constant short-lasting acute pressure rises associated with angina might lead to diuresis and hence to a reduction in blood volume (Sleight and Widdicombe, 1965).…”