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T Musch

Publications and source records attributed to T Musch.

4 recordsLinked to original sources
PubMed1988

The peripheral distribution of cardiac output in heart failure.

There are two sets of compensatory mechanisms activated when the heart fails: cardiac mechanisms that try to maintain a normal cardiac output and peripheral circulatory mechanisms that try to maintain blood pressure to perfuse the heart and the brain. The latter are most important during the stress of exercise. During exercise, two patterns of responses are noted: 1) blood vessels supplying active skeletal muscle fail to dilate normally, and 2) blood vessels supplying other visceral organs constrict excessively. The inability of skeletal muscle resistance vessels to dilate normally to a metabolic stimulus is related to sodium and water accumulation in the vessels and to a deconditioning response. These effects probably are at the small artery level. This results in an abnormal metabolic response to exercise. Vasoconstriction in visceral organs is related to neurogenic (sympathetic adrenergic) and humoral (angiotensin, norepinephrine, and vasopressin) mechanisms. The peripheral sympathetic nervous system is the primary determinant of the high plasma norepinephrine levels seen in heart failure. The role of the sympathetic nervous system is to provide for acute vasoconstriction and the renin-angiotensin system is to provide for chronic visceral vasoconstriction. These circulatory mechanisms operate most effectively over different time frames that are either short (sympathetic nervous system), intermediate (renin-angiotensin system), or long (deconditioning, vascular stiffness). When treatment is successful these systems return to normal over similar time frames.

Cardiac Output↗
PubMed1987

Enhanced metabolic vasodilation secondary to diuretic therapy in decompensated congestive heart failure secondary to coronary artery disease.

Since sodium and water retention have been implicated as major factors limiting maximal metabolic vasodilation in congestive heart failure (CHF), the effect of rigorous diuresis on maximal vasodilatory capacity was studied systematically in 9 subjects hospitalized with decompensated CHF. Peak reactive hyperemic blood flow, measured by strain-gauge plethysmography, was used as an index of maximal vasodilatory capacity. After 24 hours of diuresis and a 2.2-kg weight loss, maximal flow increased from 19.9 to 26.1 ml/min X 100 ml (p less than 0.05). Despite a further 1.4-kg weight loss between 24 and 48 hours, maximal blood flow increased no more (26.1 to 25.8 ml/min X 100 ml). Since blood pressure did not change significantly, minimal forearm resistance and maximal conductance showed similar improvements. It is unlikely that vasoconstrictor hormone changes could account for this effect since a marked decrease in plasma norepinephrine occurred in only 2 of 8 subjects and plasma renin activity decreased in only 1 subject. As a group there was no significant change in norepinephrine level, which remained substantially above normal (1,525 to 1,148 pg/ml), or in plasma renin activity (12.3 to 18.9 ng/ml/hour). Because the improvement in vasodilator capacity reached a plateau by 24 hours despite continued diuresis, and because peak reactive hyperemic blood flow was still 32% below normal, it is suggested that a second mechanism besides sodium and water retention is responsible for a significant portion of the impaired peripheral vasodilation in CHF.

Aged↗
PubMed1987

A 30-day forearm work protocol increases maximal forearm blood flow.

To evaluate the local circulatory changes that accompany chronic localized work, we studied the effects of a 4-wk handgrip work protocol on maximal forearm work-related blood flow (ml X min-1 X 100 ml-1) in the nondominant forearms of six normal subjects. The reactive hyperemic blood flow response (RHBF) was also evaluated pre- and posttraining in both forearms of each subject to determine whether maximal vasodilatory capacity would be enhanced. In addition, maximal O2 consumption (VO2max) was measured. We found that chronic handgrip work led to an increase in work-related blood flow (before, 22.4; after, 32.1; P less than 0.05); a drop in work-related minimal resistance (R) (before, 6.4; after, 4.1; P less than 0.05). RHBF rose in the chronically exercised extremity by 30% (before, 33.5; after, 43.7; P less than 0.05) as minimal R fell (before, 3.2; after, 2.2; P less than 0.05). RHBF and R in the unstimulated dominant forearm remained unchanged (blood flow: before, 33.5; after, 31.0; NS; R before, 3.2; after, 3.2; NS). VO2max (ml X kg-1 X min-1) did not change (before, 35.7; after, 34.0). These findings show that localized skeletal muscle forearm work is associated with a localized increase in vasodilation (RHBF). Thus the vascular system appears to be an independent integral partner in the training process.

Adult↗