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Biomedical subjects

H W Overbeck

Publications and source records attributed to H W Overbeck.

At least 55 records · Page 3Linked to original sources
PubMed1969

Continuous infusion indicator dilution measurement of limb blood flow and vascular response to magnesium sulfate in normotensive and hypotensive men.

A constant infusion, indicator dilution technique for blood flow measurements in the forearm and hand of man was tested and validated in vitro and in vivo. This technique employs jet injection to improve mixing of indicator with arterial blood. The mixing characteristics of the jet injection system were studied in vitro in tubing simulating the brachial artery of man. In addition, actual blood flows in the isolated pump-perfused forelimbs of five dogs were compared with constant infusion, indicator dilution calculated flows. Measurements were also made of mixing and of blood flow in the forearm and hand of man. The technique was used to compare forearm and hand vascular responses with constant intrabrachial arterial infusions of magnesium sulfate in 13 normotensive and 13 essential hypertensive men. In vitro and in vivo the jet injection system significantly improved mixing of indicator with blood, as compared with mixing produced by standard infusion techniques, without causing hemolysis. In 30 measurements in isolated, perfused dog forelimbs the correlation coefficient between actual and calculated blood flow was 0.992. Resting limb vascular resistance in the hypertensive group was significantly higher than in the normotensive group. Limb vascular resistance in all 26 men decreased in response to intrabrachial-arterial infusion of 0.25% magnesium sulfate (8 ml/min). Rate of infusion of Mg(++) was 0.162 mEq/min. There was a significant positive linear correlation between level of initial limb vascular resistance and magnitude of response to magnesium sulfate. Vascular response data adjusted for this source of variation were similar in hypertensives and normotensives.The data suggest that this constant infusion, indicator dilution technique allows accurate calculation of total limb blood flow in man, provided that anomalous bifurcation of the brachial artery is not present. The data also suggest that the jet injection system improves mixing of substances with arterial blood. Thus, use of this system should especially aid reliability of studies of limb vascular responses to vasoactive agents infused into the brachial artery.

Adult↗
PubMedDate not supplied

Increased resistance and impaired maximal vasodilation in normotensive vascular beds of rats with coarctation hypertension.

To study the resistance of normotensive vascular beds in coarctation hypertension, we measured perfusion pressures of pump-perfused (blood), innervated, isolated hindlimbs of 12 rats (Group A) with 4 weeks of hypertension due to partial contriction of the abdominal aorta above the renal arteries, and of three control groups: 11 normotensive rats (Group B) with aorta sham-constricted, nine normotensive rats (Group C) with slight (5%) hindquarters atrophy due to partial constriction of the abdominal aorta below the renal arteries, and six rats with two-kidney, one clip Goldblatt hypertension (Group D). After aortic constriction, measured femoral arterial pressures in Group A rats remained normotensive. In hypertensive rats of Groups A and D, compared to normotensive Group B or C rats, hindlimb pressure-flow curves were displaced toward the pressure axis (p < 0.05). Compared to normotensive rats, drop in hindlimb resistance after acute local nerve section was increased in rats with coarctation hypertension. Residual resistance after maximal vasodilation with intraarterial sodium nitroprusside remained elevated in hypertensive rats of Groups A and D (p < 0.05), as compared to normotensive Group B or C rats; compared to Group B rats, this residual resistance in the coarcted rats of Group A was increased by 9%. Thus, in normotensive vascular beds of rats with chronic hypertension caused by aortic coarctation, resistance is elevated. The neurogenic component contributes to this high resistance, and structural vascular changes, indicated by impaired maximal vasodilation, may also contribute to the elevated resistance. It is most unlikely that these resistance changes are attributable to elevated hindlimb intravascular pressures.

Animals↗
PubMedDate not supplied

Pressure-independent increases in vascular resistance in hypertension: role of sympathoadrenergic influences.

Experimental aortic coarctation in rats is accompanied by non-pressure-related increases in hindlimb total vascular resistance and its neurogenic and structural components. To investigate the role of the sympathoadrenergic system, we partially constricted or sham-constricted the abdominal aorta in rats age 6 weeks that had had adrenal demedullation and guanethidine injections to produce peripheral sympathectomy (SYMP rats, N = 13-coarcted, 14-sham-coarcted) and in sham-sympathectomized, sham-demedullated control rats (SHAM rats, n = 14-coarcted, 11-sham-coarcted). In both SHAM and SYMP rats with coarctation, tail and femoral arterial pressures did not increase but carotid pressures rose by 18-25% (p less than 0.01), accompanied by significant increases in heart weight/body weight. However, arterial pressures in SYMP were 30% lower than those in SHAM rats (p less than 0.005). In the pump-perfused (blood, 1 ml/min), innervated, isolated hindlimbs of SYMP, compared to SHAM rats, the effect of acute section of local nerves on resistance was reduced and denervation hypersensitivity was documented. In contrast to SHAM, coarctation in SYMP rats was not accompanied by increases in total hindlimb resistance and its neurogenic component; there were, however, significant rises in the humoral-myogenic (p less than 0.01) and structural (p less than 0.05) components. Thus, the sympatho-adrenergic system influences arterial blood pressure and accounts for the elevated neurogenic component of peripheral vascular resistance in coarctation hypertension rats, but does not account for the elevated structural component of resistance. An unknown humoral factor, or factors, may be incriminated in the latter.

Adrenal Medulla↗
PubMedDate not supplied

Sodium pump activity in arteries of Dahl salt-sensitive rats.

Decreased activity of the electrogenic sodium pump of vascular smooth muscle has been reported in several forms of experimental hypertension and may play an important role in basic disease mechanisms. It has been proposed that such pump suppression may characterize volume-expanded forms of hypertension. The present investigation tested this latter hypothesis. Sodium pump activity was assessed in vitro in sodium-loaded tail artery and thoracic aorta freshly excised from Dahl salt-sensitive (S) and salt-resistant (R) rats on low (0.4%) or high (8%) NaCl diets for 5 to 7 weeks. Rubidium (86Rb) uptake in the absence (total uptake) and presence (ouabain-insensitive uptake) of 1.0mM ouabain was measured and ouabain-sensitive uptake (nmole/mg dry weight/10 min) was calculated. In S rats, salt feeding was accompanied by elevation of arterial pressure, cardiac hypertrophy, increases of 20% to 30% in total blood volume, and increases in the ouabain-sensitive, ouabain-insensitive, and total uptakes in the aorta, but no significant change in uptakes in the tail artery. However, ouabain-sensitive uptake in the tail artery of all S rats exceeded than in R rats. There was no evidence of a decrease in vascular sodium pump activity accompanying hypertension in either artery. Therefore, the results of this study provide no evidence in support of the hypothesis that pump suppression in vascular smooth muscle characterizes volume-expanded forms of hypertension. It is unlikely that the observed increases in vascular pump activity in S rats reflected intracellular sodium concentrations higher than those in the control rats. Rather, increases in the numbers of pump molecules or in their turnover rate are probably involved.

Animals↗
PubMedDate not supplied

Sodium pump activity in arteries of rats with Goldblatt hypertension.

Several laboratories have reported evidence suggesting abnormalities in the activity of the sarcolemmal sodium pump in vascular smooth muscle in hypertension. The present experiments were designed to investigate the relationship of such changes to the status of the renin-angiotensin-aldosterone system and body fluid volumes. We assessed sodium pump activity in vitro in sodium-loaded tail artery and thoracic aorta freshly excised from rats with chronic one-kidney, one clip, and two-kidney, one clip hypertension, and from appropriate normotensive control rats. 86Rb uptake in the absence (total uptake) and presence of 1.0 mM ouabain (ouabain-insensitive uptake) was measured, and ouabain-sensitive uptake (nmole/mg dry weight/18 min) was calculated. There were increases in plasma renin activity in the two-kidney, one clip rats only. In the hypertensive rats there were significant increases (up to +60%) in the ouabain-sensitive and total 86Rb uptakes in both tail artery and aorta. The magnitude of increases in arterial tissue uptakes in the two forms of Goldblatt hypertension, and in one-kidney, one clip hypertensive rats given 0.9% saline to drink for 2 to 3 days before sacrifice, were similar. Further sodium loading of aortas from normotensive control rats did not increase their uptake. The results of this study provide no evidence for decreases in sodium pump activity, instead indicating that there are increases in the activity of the pump in the sarcolemma or arterial smooth muscle studied in vitro. These increases in pump activity do not appear to be related to altered activity of the renin-angiotensin-aldosterone system, to changes in body fluid volumes, or to increases in intracellular concentrations of sodium. Increases in numbers or concentration of sarcolemmal pump molecules or in their turnover rate may be involved. However, in vitro 86Rb uptake by tail artery and aorta may not reflect the status of sodium pump activity in resistance vessels in vivo.

Animals↗