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Biomedical subjects

J Gaya

Publications and source records attributed to J Gaya.

63 records · Page 4Linked to original sources
PubMed1981

Postsynaptic adrenergic unresponsiveness in hypotensive haemodialysis patients.

In order to ascertain the significance of autonomic dysfunction in hypotensive maintenance haemodialysis patients, plasma norepinephrine (NE) was measured by radioenzymatic assay in 15 nondiabetic uraemic subjects of similar age and time on dialysis, five of them chronically hypotensive and 10 normotensive. Hypotensive patients had: 1) Significantly higher NE levels than their normotensive counterparts, both in basal conditions and after orthostatism and 2) significantly lesser increments in mean arterial blood pressure during a NE infusion than the normotensive group. Rather than implicating a mechanism based on autonomic neuropathy, our results suggest that in haemodialysis patients with chronic hypotension, there is a defect located at the adrenergic postsynaptic level.

Adult↗
PubMedDate not supplied

Renal kallikrein excretion in cirrhotics with ascites: relationship to renal hemodynamics.

To investigate if the renal kallikrein-kinin system may be involved in the homeostasis of renal perfusion in cirrhosis, urinary kallikrein activity was measured in 11 normal subjects, 31 cirrhotics with ascites and preserved renal plasma flow (548.2 +/- 32.2 ml per min) and glomerular filtration rate (85.8 +/- 3.4 ml per min), and 18 cirrhotics with functional renal failure (renal plasma flow: 229.9 +/- 23.4 ml per min; glomerular filtration rate: 34.9 +/- 3.3 ml per min). Plasma renin activity, plasma norepinephrine concentration and the urinary excretion of prostaglandin E2 were also measured in these subjects. Cirrhotics without renal failure showed a significantly higher renin (4.9 +/- 1.1 ng per ml per hr), norepinephrine (458.2 +/- 50.4 pg per ml), urinary kallikrein (15.4 +/- 1.8 pkat per min) and urinary prostaglandin E2 (0.52 +/- 0.08 ng per min) than did normal subjects (1.08 +/- 0.1 ng per ml per hr, 218.1 +/- 18.2 pg per ml; 8.4 +/- 1.4 pkat per min and 0.24 +/- 0.02 ng per min, respectively). Cirrhotics with renal failure showed a significantly higher renin (16.1 +/- 3.4 ng per ml per hr) and norepinephrine (739.4 +/- 79.2 pg per ml), and a significantly lower urinary kallikrein (5.2 +/- 0.6 pkat per min) and urinary prostaglandin E2 (0.15 +/- 0.02 ng per min) than did normal subjects and cirrhotics without renal failure. Glomerular filtration rate correlated (p less than 0.001) with urinary kallikrein (r = 0.53), urinary prostaglandin E2 (r = 0.55), plasma renin (r = -0.41) and norepinephrine (r = -0.44).(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMedDate not supplied

Effects of propranolol on azygos venous blood flow and hepatic and systemic hemodynamics in cirrhosis.

The effects of propranolol on blood flow through gastroesophageal collaterals and on systemic and hepatic hemodynamics were investigated in 23 cirrhotic patients with portal hypertension. Gastroesophageal collateral blood flow was evaluated by the measurement of azygos venous blood flow by continuous thermal dilution. Azygos venous blood flow was markedly increased in these patients (544 +/- 48 ml per min, as compared with 132 +/- 18 ml per min in subjects without portal hypertension (p less than 0.001). Propranolol at doses achieving effective beta-blockage (83 +/- 5 mg) (mean +/- S.E.M.) markedly reduced azygos venous blood flow (to 354 +/- 34 ml per min, p less than 0.001). Reduction of azygos venous blood flow (-34.2 +/- 3.6%) was significantly greater (p less than 0.01) than reductions in cardiac output (-22.6 +/- 1.9%), hepatic venous pressure gradient (-11.5 +/- 2.4%) and hepatic blood flow (-13.4 +/- 7.4%). The hemodynamic effects of propranolol were not related to plasma norepinephrine levels. Reduction of gastroesophageal collateral blood flow may be the mechanism by which oral propranolol therapy reduces the risk of repeated episodes of variceal bleeding in cirrhotic patients with portal hypertension.

Azygos Vein↗
PubMedDate not supplied

Temporal relationship between hyperaldosteronism, sodium retention and ascites formation in rats with experimental cirrhosis.

To investigate the role of aldosterone in sodium retention and ascites in cirrhosis, the urinary sodium excretion, sodium balance and urinary excretion of aldosterone-18-glucuronide (UAldV) were serially measured in 11 rats undergoing cirrhosis induction with carbon tetrachloride (CT) and phenobarbital (CT rats) and in 10 control rats which received phenobarbital. All CT rats developed ascites, seven within the ninth week after starting the program and four within the 10th week. One week before the onset of ascites, CT rats and control rats were different with respect to sodium excretion (1.41 +/- 0.15 vs. 1.82 +/- 0.1 mEq per day), sodium balance (0.57 +/- 0.12 vs. 0.20 +/- 0.09 mEq per day) and UAldV (67.8 +/- 9.5 vs. 25.7 +/- 1.7 ng per day). These differences were more pronounced within the week in which ascites was detected in CT rats. Before these 2 weeks, both groups did not differ with respect to these parameters. In the 132 urine samples obtained in CT rats, there was a correlation between sodium excretion and UAldV (r = -0.53; p less than 0.001). Twenty-one additional CT rats were divided into two groups. Eleven animals were given spironolactone (20 mg per day s.c. in olive oil) from the 6th week, and 10 only received olive oil. Thirteen weeks after starting the program, all rats not treated with spironolactone had sodium retention and ascites (in five rats, ascites appeared within the ninth week and in five within the tenth week); this occurred in only one animal treated with spironolactone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMedDate not supplied

Renal excretion of prostaglandin E2 and plasma renin activity in type I diabetes mellitus: relationship to normoglycemia achieved with artificial pancreas.

To determine the effect of normoglycemia on renal prostaglandin synthesis and renin-angiotensin system activity, prostaglandin E2 (PGE2) urinary excretion, plasma renin activity (PRA), and glomerular filtration rate (GFR) were studied in seven patients with insulin-dependent diabetes mellitus (IDDM) without complications, both in basal conditions and after a 20-h treatment with an artificial pancreas. Normoglycemia induced a significant reduction in PGE2 excretion (88 +/- 23 vs. 55 +/- 25 ng/12 h, P less than .05) and GFR (138 +/- 34 vs. 105 +/- 20 ml X min-1 X 1.73 m-2, P less than .05) and a nonsignificant increment of PRA (0.52 +/- 0.48 vs. 0.83 +/- 0.92 ng X ml-1 X h-1). The results enhance the hypothesis that renal prostaglandins play a role in the renal functional alterations observed in IDDM during hyperglycemia.

Adolescent↗