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Biomedical subjects

G A Meininger

Publications and source records attributed to G A Meininger.

59 records · Page 4Linked to original sources
PubMed1980

Model for antiorthostatic hypokinesia: head-down tilt effects on water and salt excretion.

Water and electrolyte excretion was investigated in antiorthostatic hypokinetic and orthostatic hypokinetic and control rats in metabolic cages. Significant (t test, P < 0.05), diuresis, natriuresis, and kaliuresis occurred in the antiorthostatic hypokinetic subjects but did not occur in either the orthostatic hypokinetic or controls. Recovery from antiorthostatic hypokinesia was characterized by retention of water, sodium, and potassium. Patterns of changes in body weight and food and water orthostatic hypokinetic rats and thus could not account for the differences in renal handling of water and electrolytes. Also, differences in ingestion of food and water in controls could not account for differences in excretion of water and electrolytes between these and antiorthostatic hypokinetic rats. It was concluded that the antiorthostatic position was responsible for the diuresis and natriuresis and that the antiorthostatic hypokinetic rat appears to be a good model for the study of water and electrolyte excretion during conditions such as bed rest, water immersion, and exposure to weightlessness.

Animals↗
PubMedDate not supplied

Distributions of microvascular pressure in skeletal muscle of one-kidney, one clip, two-kidney, one clip, and deoxycorticosterone-salt hypertensive rats.

Studies were performed on the cremaster skeletal muscle in rats to investigate the microvascular changes that are associated with established one-kidney, one clip (1K1C) and two-kidney, one clip (2K1C) Goldblatt hypertension and with deoxycorticosterone (DOC)-salt hypertension. Rats were anesthetized with urethane and chloralose; and cremaster muscles with intact circulation and innervation were suspended in a controlled Krebs bath. Microvascular pressures and vessel diameters were measured at three consecutive arteriolar (A) and venular (V) branch levels. Arteriolar diameters (means +/- SEM) in normotensive (NT) rats were 119 +/- 7, 86 +/- 5, and 31 +/- 3 micron respectively for 1A, 2A, and 3A arterioles; and venule diameters were 218 +/- 12, 141 +/- 15, and 53 +/- 7 micron respectively for 1V, 2V, and 3V venules. As compared to NT rats, there was a selective decrease in lumen size (percent reduction from control) for 1A and 2A (23% to 38%) in 1K1C and 2K1C rats and for 1A, 2A, and 3A (42% to 44%) in DOC rats. Venule diameters were not significantly different between normotensive and hypertensive animals at any branch level. Femoral artery pressures were significantly elevated (greater than or equal to 43%) in all three forms of hypertension; however, this increase in pressure was not proportionally transmitted throughout the microcirculation. This was evidenced by normal pressure in 3A arterioles and in all venules for 1K1C and 2K1C rats and by normal pressures in 3V and larger venules for DOC rats. Our findings indicate that elevated arterial pressure in chronic renal hypertension is not transmitted uniformly across all microvascular segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMedDate not supplied

Autoregulation and vasoconstriction in the intestine during acute renal hypertension.

The purpose of this study was to investigate whether local mechanisms of blood flow autoregulation mediate vasoconstriction during the early development of renal hypertension. Anesthetized rats were instrumented with Doppler flow probes on the celiac (CA), superior mesenteric (SMA), and renal arteries to measure flow velocity in these vessels. Acute two-kidney, one clip renal hypertension was produced by inflating a pneumatic occluder on the left renal artery to reduce flow velocity by 50%. Two hours after renal artery stenosis (RAS), femoral artery pressure (AP) was increased by 35%, CA resistance by 45%, and SMA resistance by 57%. No increases were observed in AP or in CA and SMA resistances for sham-operated, control rats. To determine if autoregulation contributed to the increase in SMA resistance, we protected the SMA vasculature from the increased arterial pressure by servocontrolled inflation of a pneumatic cuff implanted around the SMA. Although normalizing SMA pressure with the protective cuff significantly reduced (p less than 0.05) the increase in SMA resistance that occurred after RAS, SMA resistance remained elevated above control levels. These results suggest that (1) reduced intensity of SMA constriction produced by protection of the SMA is due to inhibition of a local autoregulatory mechanism that is contributing to the increase in SMA resistance during the acute development of renal hypertension, and (2) maintenance of elevated SMA resistance during protection from increased AP is the result of pressure-independent mechanisms that are activated subsequent to renal artery stenosis.

Animals↗