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Biomedical subjects

G H Anderson

Publications and source records attributed to G H Anderson.

At least 19 recordsLinked to original sources
PubMed1979

Effects of a portacaval or peritoneovenous shunt on renin in the hepatorenal syndrome.

Ten patients with hepatorenal syndrome were evaluated before and after creation of a side-to-side portacaval shunt or insertion of a peritoneovenous shunt, procedures which produced an increase in plasma volume and cardiac output. In the seven patients who survived surgery, renal function improved significantly, plasma renin activity fell from high to normal levels, and low levels of plasma renin substrate increased. Prior to surgery, blockade of angiotension II by saralasin produced hypotension and an increase in plasma renin activity, whereas after surgery, saralasin had no effect on blood pressure or renin. Our findings suggest that decreased "effective" plasma volume may be important in the stimulation of renin release and possibly in the pathophysiology of renal failure in the hepatorenal syndrome.

Angiotensinogen↗
PubMed1979

Effect of mineral mixture in diet on protein intake regulation in the weanling rat.

Weanling rats fed a choice of two diets varying only in protein concentration (10 and 60% casein) select a lower proportion of dietary energy as protein when the dietary minerals are supplied by a mineral mixture high in Na, K, and Cl but low in P and Cu (Hi Cl) than when the diets contain the Bernhart-Tomarelli (BT) mineral mixture. The addition of Na and/or K as acetate salts to the BT mineral mixture, to levels in the Hi Cl mixture, had no effect on regulation of protein intake. However, the addition of Na and/or K as chloride salts to the BT mineral mixture resulted in the rats selecting a protein concentration equivalent to the Hi Cl fed group. Weight gains and energy consumption were similar for all groups. It was therefore concluded that dietary chloride affects protein feeding behavior.

Acetates↗
PubMed1979

Diabetes, dietary tryptophan, and protein intake regulation in weanling rats.

The effects of streptozotocin-induced diabetes and tryptophan content of the protein fed on protein intake regulation by weanling rats selecting from 10 and 60% casein diets were evaluated. In uncompensated diabetes the ratio of tryptophan to other selected neutral amino acids in plasma and brain tryptophan were reduced, protein intake per unit of body weight was increased, and serotonin, 5-hydroxyindoleacetic acid, and norepinephrine were unaffected. Enrichment of the tryptophan content of the ingested protein caused a decrease in protein, but not energy consumption of both diabetic and nondiabetic rats. The reduction in protein intake correlated inversely with increases in the tryptophan content relative to the neutral amino acids in plasma and with increases in brain tryptophan and serotonin levels in both diabetic and nondiabetic rats. The data suggest that protein-feeding behavior is regulated by a mechanism that includes brain serotonergic activity with insulin, through its influence on circulating amino acids, determining the quantity of protein consumed in relation to body weight.

Animal Population Groups↗
PubMed1978

Renin angiotensin involvement in transient hypertension after renal injury.

Transient hypertension occurred in 3 patients shortly after blunt injury to the abdomen. Renal trauma was suspected in all 3 patients and radiological evidence for renal injury was present in 2. Plasma renin activity definitely was elevated in 1 patient and probably was elevated in another. There was a decrease in blood pressure in all 3 patients during infusion of the angiotensin II analogue--saralasin--showing that the hypertension in these patients was angiotensin-mediated. Renal function as reflected by the blood urea nitrogen, creatinine and electrolytes was not impaired significantly. Thus, acute hypertension after blunt abdominal trauma may be angiotensinogenic and is not necessarily sustained.

Adult↗
PubMed1978

Evidence for an angiotensinogenic mechanism of the hypertension of Cushing's syndrome.

The blood pressure response to the angiotensin II analog 1-sar-8-ala-angiotensin II, or saralasin, was studied in five patients with clinical and laboratory evidence of Cushing's syndrome. Plasma renin activity, plasma renin substrate, and plasma renin concentration were measured in all five patients. The renin system and the response to saralasin were measured after furosemide administration. Plasma aldosterone was measured after infusion of 2 liters normal saline. All patients studied showed a hypotensive response to saralasin, the mean BP changing from 163/108 mm Hg to 130/85 mm Hg (P less than 0.02). There was a significant elevation of the plasma renin activity and plasma renin concentration in the patients compared to normal subjects, although plasma renin substrate was not significantly different from normal values. There was normal suppression of plasma aldosterone after the infusion of 0.9% saline. The findings indicate that the hypertension of these patients with Cushing's syndrome was mediated in large part by angiotensin II.

Adrenal Glands↗
PubMed1978

Role of angiotensin II in the aldosterone secretory response to adrenocorticotropin in sodium-restricted normal human subjects.

A study was performed to determine the possible role of angiotensin II (AII) in mediating the increased adrenal aldosterone response to infused alpha 1-24-ACTH, induced by sodium deprivation. Nine normal subjects, aged 18-31 yr. received 8-h infusions of 1) alpha 1-24-ACTH (0.5 U given over 8 h) while on a diet with unrestricted sodium content; 2) saralasin at 0.5 micrograms/kg/min or ACTH alone (0.5 U over 8 h) on the 7th day of a 10 meq sodium diet; and 3) ACTH and saralasin together on the 8th day while still on sodium restriction. AII was administered for the last 2 h of infusion 3. Plasma cortisol and aldosterone concentrations were measured at hourly intervals during the infusions and plasma renin activity was measured at 2 hourly intervals. ACTH infusion produced an increase in the plasma aldosterone concentration which was significantly greater during sodium restriction than when sodium intake was unlimited. This increase was not associated with an ACTH-induced rise in the plasma renin activity and was not significantly altered when ACTH was administered with saralasin. The rise in plasma cortisol concentration induced by ACTH was not significantly different when the normal subjects were on liberal and restricted sodium intakes. It is concluded that AII plays little if any acute role in increasing the stimulatory action of ACTH on aldosterone secretion during sodium restriction.

Adolescent↗
PubMed1978

Platelet lysis and aggregation in shear fields.

A rotational viscometer was used to study the effects of shear stress on platelets in human platelet-rich plasma (PRP). For 5-min exposure times, shear stresses above 160 dynes/cm2 induced platelet lysis (as determined by release of platelet lactic dehydrogenase). For 30-s exposure times, shear stresses greater than 600 dynes/cm2 were required to induce platelet lysis. The platelet counts of sheared PRP were decreased to as low as one-fifth the original count due largely to shear-induced aggregation. The count is a minimum at intermediate stress levels (200-400 dynes/cm2). Higher stresses induce disaggregation as well as lysis. The diminution in the counts was partially reversed in 2 h incubation after cessation of shearing. Experiments were carried out with three different viscometer configurations so that the shear stress and the solid surface area access could be varied independently. Surface access was not a significant variable in the conditions of the experiments. Thus aggregation and lysis may be induced by stress effects alone as well as by solid surface effects. The results also show that the response of platelets to shear stress is strongly dependent on exposure time. Platelets are much less resistant to shear stress than red cells for relatively long exposure times. However, the converse is true for very short exposure times.

Blood Platelets↗