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Biomedical subjects

J M Fritsch

Publications and source records attributed to J M Fritsch.

23 records · Page 2Linked to original sources
PubMed1986

Arterial pressure ramps provoke linear increases of heart period in humans.

A variety of methods has been used experimentally to increase baroreceptor activity and provoke transient, vagally mediated cardiac slowing in humans. We studied baroreceptor-cardiac reflex physiology in eight resting volunteers by measuring R-R interval changes during and after spontaneous brief elevations of arterial pressure, preceded by bursts of muscle sympathetic nerve activity. Arterial pressure was measured with a catheter in a brachial artery, and muscle sympathetic activity was measured with a microelectrode positioned transcutaneously in a peroneal nerve. R-R intervals were related to preceding systolic pressures with linear regression analysis. When systolic pressures were correlated with R-R intervals of the next cardiac cycle, slopes (+/- SE) averaged 12.4 +/- 2.2 ms/mmHg and correlation coefficients averaged 0.81 +/- 0.09. Baroreflex slopes were inversely related to base-line systolic pressures. These results are similar to those obtained when baroreceptors are stimulated experimentally; they suggest that elevations of arterial pressure, which are preceded by bursts of muscle sympathetic activity, trigger with one heart-beat latency highly linear increases of efferent vagal-cardiac nerve activity.

Blood Pressure↗
PubMed1986

Baroreflex control of plasma norepinephrine and heart period in healthy subjects and diabetic patients.

Resting diabetic patients may have excessively rapid heart rates, reduced heart rate variability, and subnormal plasma catecholamine levels. Although all of these abnormalities may relate in some way to baroreceptor reflex function, there have been surprisingly few attempts to evaluate systematically baroreflex mechanisms in diabetic patients. Accordingly, we studied autonomic responses over a range of pharmacologically induced arterial pressure changes in 10 unselected young adult insulin-dependent diabetic patients who had no symptoms of autonomic neuropathy, and 12 age-matched nondiabetic subjects. Sympathetic responses were estimated from antecubital vein plasma norepinephrine levels, and parasympathetic responses were estimated from electrocardiographic R-R intervals and their variability (standard deviation). Both were correlated with other noninvasive indexes of peripheral and central nervous system function. Multiple derangements of baroreflex function were found in the diabetic patients studied. Sympathetic abnormalities included subnormal baseline norepinephrine levels, virtual absence of changes of norepinephrine levels during changes of arterial pressure, and supranormal pressor responses to phenylephrine infusions. Parasympathetic abnormalities included subnormal baseline standard deviations of R-R intervals, and R-R interval prolongations during elevations of arterial pressure which were unmistakably present, but subnormal. Our data suggest that in diabetic patients, subnormal baseline plasma norepinephrine levels may signify profound, possibly structural defects of sympathetic pathways. Subnormal resting levels of respiratory sinus arrhythmia may have different implications, however, since vagal, unlike sympathetic reflex abnormalities, can be reversed partly by arterial pressure elevations.

Adult↗