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Biomedical subjects

M E Olsen

Publications and source records attributed to M E Olsen.

43 records · Page 3Linked to original sources
PubMed1984

The influence of sodium intake on physiological responses to angiotensin II in conscious dogs.

The renin-angiotensin system (RAS) is suppressed either by high sodium intake or by high levels of angiotensin II (A II). Therefore in prior studies it has been difficult to sort out the influence on the cardiovascular homeostases of different levels of A II and different levels of sodium in the diet respectively. The present study examines the quantitative effects of A II on mean arterial blood pressure (MABP), electrolyte excretion and hormone secretion in conscious dogs on low, normal and high sodium intake with the endogenous RAS blocked with continuous intravenous infusion of enalapril (MK-421). Fourteen dogs on three different Na diets, low, normal and high (5, 30 and 250 mmol/day), were infused continuously with enalapril, 4 mg/kg/day and studied with superinfused A II at rates of 0, 1, 3, 6 and 12 ng/kg/min., each period lasting one week. Converting enzyme inhibitor (CEI) decreased MABP equally in dogs on low and normal sodium intake to about 80% of control, but did not have a significant effect in dogs on high sodium intake. The initial infusion of angiotensin II at the lowest rate had a pronounced effect on MABP in the normal and high sodium states, but had no effect on MABP in the sodium depleted dogs. However, at the higher rates of infusion, the angiotensin II increased the pressure to a similar degree at all levels of sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1984

Angiotensin II natriuresis and anti-natriuresis: role of renal artery pressure in anaesthetized dogs.

The aim of this study was to determine the role of changes in renal artery pressure (RAP), renal haemodynamics, and tubular reabsorption in mediating the natriuretic and anti-natriuretic actions of angiotensin II (ANG II). In anaesthetized dogs, endogenous ANG II formation was blocked with SQ-14225 and ANG II was infused intravenously at rates of 5-1215 ng/kg/min while RAP was either servo-controlled at the normal level or permitted to increase. When RAP was servo-controlled to prevent a rise in RAP, ANG II infusion at all rates from 5-1215 ng/kg/min decreased urinary sodium excretion (INaV) and fractional sodium excretion (FENa), while increasing fractional reabsorption of lithium (FRLi), an index of proximal tubule fractional sodium reabsorption (FRDNa). When RAP was permitted to increase, ANG II infusion rates up to 45 ng/kg/min decreased UNaV, and FENam while increasing FRLi and FRDNa greater than However, at 135 ng/kg/min and above UNaV and FENE increased while FRLi and FRDNa decreased when RAP was allowed to rise, even though renal blood flow and filtration fraction were not substantially different from the values observed when RAP was servo-controlled. Filtered sodium load was slightly higher when RAP was permitted to increase during ANG II infusion, compared to the dogs in which RAP was servo-controlled, although the differences were not statistically significant. Thus, even very large doses of ANG II cause anti-natriuresis when RAP is prevented from increasing. The natriuretic effect of high doses of ANG II is caused by increased RAP which decreases fractional sodium reabsorption in proximal and distal tubules and causes slight increase in sodium delivery to the tubules.

Absorption↗
PubMed1983

Hepatic extraction of insulin after carbohydrate hyperalimentation.

Peripheral venous plasma insulin and C-peptide concentrations during oral glucose tolerance tests were measured in 7 normal weight non-diabetic subjects before and after 7 days of sucrose hyperalimentation. This induced a deterioration of the glucose tolerance with higher levels of glucose, insulin and C-peptide. The C-peptide to insulin molar ratio as well as the relation between incremental areas under the plasma curves of the two peptides were used as relative measures of the hepatic insulin extraction. Both estimates of hepatic insulin extraction were unchanged by hyperalimentation, suggesting that the induced decreases in glucose tolerance and insulin receptor function are not followed by a decrease in hepatic insulin extraction as found in obese subjects with similar changes in glucose tolerance and insulin receptor function.

Adult↗
PubMed1982

Gastric inhibitory polypeptide (GIP) and insulin release in response to oral and intravenous glucose in uremic patients.

Eight patients with advanced renal failure of long duration were studied 1 day after hemodialysis. A 50 g oral glucose load (OGTT) and an intravenous glucose infusion (IVGI), giving the same plasma glucose profile as the OGTT, were carried our in order to study the relation between Gastric Inhibitory Polypeptide (GIP) plasma levels after oral glucose and the insulin release during OGTT and IVGI. The plasma GIP increase during OGTT was significantly elevated compared to a group of eight healthy volunteers. The insulin potentiation during OGTT in relation to GIP was significantly depressed in the uremic patients. It is proposed that a factor of intestinal origin is released during intake of carbohydrates, which blocks the B-cell response to the combined glucose-GIP stimulus. Alternatively, the concentrations of plasma GIp measured have included GIp fragments without insulin releasing capability.

Administration, Oral↗
PubMedDate not supplied

Quantitative liquid chromatographic method using fluorescence detection for determining zearalenone and its metabolites in blood plasma and urine.

The liquid chromatographic (LC) method described, suitable for use with both blood plasma and urine, is applicable for determination of zearalenone and alpha-zearalenol at levels as low as 0.5 ng/mL plasma and 5 ng/mL urine. The sample is incubated overnight with beta-glucuronidase to analyze for both conjugated and unconjugated forms of zearalenone. The next day, the sample is acidified with H3PO4, extracted with chloroform, and evaporated to dryness. The residue is dissolved in toluene and loaded onto a silica gel cartridge which is washed with toluene and eluted with toluene-acetone (88 + 12). The eluate is evaporated, and the residue is dissolved in chloroform, extracted with 0.18M NaOH, neutralized with H3PO4, and re-extracted with chloroform. The chloroform extract is evaporated, dissolved in mobile phase for LC, and injected onto a normal phase column under the following chromatographic conditions: mobile phase of water-saturated dichloromethane containing 2% 1-propanol, and fluorescence detector, excitation wave-length 236 nm, and 418 nm cut-off emission filter. Recoveries of zearalenone and its metabolites from blood plasma and urine are 80-89% in the range 2.0-10 ng standard/mL plasma, and 81-90% in the range 10-30 ng standard/mL urine. This method was used to analyze blood and urine samples from a pig fed zearalenone-contaminated feed (5 mg/kg), corresponding to 80 micrograms/kg body weight. Zearalenone was rapidly metabolized to alpha-zearalenol, which appeared in the blood only 30 min after feeding. Almost all zearalenone and alpha-zearalenol was found conjugated with glucuronic acid in both blood plasma and urine.

Animals↗