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Biomedical subjects

G Simon

Publications and source records attributed to G Simon.

At least 253 records · Page 14Linked to original sources
PubMed1982

Renovascular hypertension with unilateral atherosclerotic renal artery occlusion: diagnostic use of renal vein renins.

Selective renal vein renin studies were performed in seven male patients with severe hypertension and atherosclerotic occlusion of a main renal artery. In five patients, peripheral plasma renin activity was increased, and there was evidence for hypersecretion of renin from the affected kidney and suppression of renin release from the opposite kidney. In one patient, who had occlusion of one renal artery and a high-degree stenosis of the contralateral renal artery, the two kidneys appeared to contribute equally to the high circulating plasma renin activity. Removal of the atrophic, ischemic kidney from these patients, plus bypass of the contralateral renal artery in one patient, resulted in cure or improvement of their hypertension. In one patient, despite hypersecretion of renin from the atrophic kidney, surgery was not recommended because his systemic blood plasma renin activity was not elevated. Histologic examination of the excised kidneys revealed moderate glomerular scarring and tubular atrophy. The findings indicate that the same criteria, derived from renal vein renin studies, that have been used to predict the outcome of surgical repair of renal artery stenosis in hypertensive patients can be applied to the evaluation of patients with hypertension and complete occlusion of a main renal artery.

Arteriosclerosis↗
PubMed1982

Echocardiographic assessment of left ventricular hypertrophy and function in renal hypertensive dogs.

To investigate the performance of the hypertrophied left ventricle, M-mode echocardiographic measurements were performed 2 to 3 times weekly on 8 unanesthetized dogs for several weeks before and for 6 months after the induction of perinephritic hypertension. Four dogs with sham-wrapping and contralateral nephrectomy served as the controls. From a baseline value of 7.7 +/- 0.4 mm (mean +/- SD), left ventricular wall thickness increased to 9.0 +/- 0.6 mm (p less than 0.001) by the 4th week after the induction of hypertension and reached a plateau of 10.2 +/- 1.2 mm (p less than 0.001) by week 10. Fractional shortening of left ventricular dimension (% delta D) increased during early left ventricular hypertrophy and remained elevated for 6 months in the surviving 6 hypertensive dogs. In hypertensive dogs, left ventricular concentric hypertrophy became detectable by week 6 of hypertension. Control dogs did not show these changes. At autopsy, the left ventricular weight of hypertensive and normotensive control dogs was (6.2 +/- 1.4 g/kg and 4.3 +/- 0.5 g/kg (p less than 0.05). In summary, during the early stage of left ventricular hypertrophy in renal hypertensive dogs cardiac performance increased. There is no evidence for deterioration of left ventricular performance as concentric left ventricular hypertrophy develops and becomes chronic.

Animals↗
PubMed1982

Increased serum N-acetyl-beta-D-glucosaminidase activity in human hypertension.

Compared to values obtained in healthy normotensive control subjects, serum activity of the lysosomal enzyme N-acetyl-beta-D-glucosaminidase (NAG) was found to be elevated in patients with untreated or treated essential hypertension and in patients with renovascular hypertension. Increased NAG activity in hypertension could not be ascribed to tissue necrosis because the serum levels of several commonly measured cytosolic enzymes were within normal limits. The kidney is a likely but unproven source of the enzyme elevation in hypertension.

Acetylglucosaminidase↗
PubMed1981

Comparative echocardiographic examinations in sitting and supine position at rest and during dynamic exercise.

Echocardiograms of 12 healthy male subjects in the supine and sitting positions were obtained. The end-diastolic (EDD) and end-systolic (ESD) diameters of the left ventricle were measured, and the stroke volume was calculated as the cube of the diameter. A significantly (P less than 0.001) smaller stroke volume was found in the sitting rest position (67.1 ml) compared to the supine rest position (92.3 ml). During dynamic exercise, the stroke volume increase in the sitting position (29.7%) was considerably higher than in the supine position (13%). The shortening fraction showed no difference in the sitting and supine positions at rest and during dynamic exercise. The results demonstrate good agreement between the echocardiographic method and other noninvasive procedures.

Adult↗
PubMed1981

Effect of sympathectomy on arterial and venous changes in renal hypertensive rats.

Arterial pressure-flow and venous pressure-volume relationships were measured at maximal vasodilatation in the denervated pump-perfused hindquarters of four groups of rats: 1) neonatally sympathectomized (guanethidine-injected and adrenal-demedullated), one-kidney, one-clip hypertensive (n = 9); 2) sympathectomized, sham-operated, unilaterally nephrectomized control (n = 10); 3) sham-sympathectomized, one-kidney, one-clip hypertensive (n = 8); and 4) sham-sympathectomized, sham-operated, unilaterally nephrectomized control (n = 9). Dry defatted weight of anatomically defined segments of the aorta and vena cava in the four groups of rats also was measured. Significant rises in arterial pressure developed in sympathectomized rats after clipping of the renal artery and contralateral nephrectomy. Arterial pressure-flow curves were shifted toward the pressure axis (P less than 0.01) in clipped rats whether sympathectomized or not. In sympathectomized clipped rats, there was also a shift of the venous pressure-volume curves toward the pressure axis (P less than 0.05). The same degree of hypertrophy of the aorta was found in sympathectomized and sham-sympathectomized clipped rats. The findings indicate that in renal hypertensive rats structural changes of both large arteries and veins may develop in the absence of an intact sympathoadrenergic system.

Animals↗
PubMed1981

Further studies of angiopathic serum factor in perinephritic hypertensive dogs.

The serum of perinephritic hypertensive dogs causes waterlogging and increased sodium (Na) content of rabbit aorta explants in tissue culture. In the present study, we investigated the role of tissue glycosaminoglycans in the pathogenesis of these changes. The effect of ouabain and prostaglandin F2 alpha on the composition of rabbit aorta explants in tissue culture was studied to determine if they produced alterations that were similar to those produced by the serum of hypertensive dogs. Rabbit aortic media explants were cultured in tissue culture medium supplemented (15-20%) with serum obtained from 12 dogs during a pre-hypertension control period and after induction of one-kidney, one-wrapped hypertension. After 3 weeks of culture, the explants were harvested, and their Na, potassium (K) and hexosamine content was measured. Compared to the composition of explants cultured in pre-hypertension control serum, the water and Na content of explants cultured in the serum of hypertensive dogs was increased (p less than 0.02, and p less than 0.01). There were no differences in the K and hexosamine content of explants cultured in the two sera. There was a dose-dependent increase in the NA content and a reduction in the K content of explants cultured in the presence of ouabain (5 X 10-8 to 5 X 10-7 M) and PGF2 alpha (1 microgram/ml). The findings of this study provide further evidence for angiopathic serum factor(s) in perinephritic hypertensive dogs. The excess Na of explants cultured in the serum of hypertensive dogs does not appear to be bound to glycosaminoglycans, The accumulation of excess Na is not due to an ouabain-like mechanism.

Animals↗