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Biomedical subjects

S C Malpas

Publications and source records attributed to S C Malpas.

47 records · Page 3Linked to original sources
PubMed1992

The amplitude and periodicity of synchronized renal sympathetic nerve discharges in anesthetized cats: differential effect of baroreceptor activity.

We applied a computerized peak detection algorithm to recordings of synchronized sympathetic nerve discharges from anesthetized cats to retrieve information about the characteristics of renal nerve activity (RNA) during changes in baroreceptor activity. The algorithm scanned the series of RNA voltages for significant increases followed by significant decreases in a small cluster of voltage values. Once each synchronized RNA peak had been detected, its corresponding amplitude, width and peak-to-peak interval were calculated. The peak-to-peak interval periodicity showed two modes of synchronized discharge, one between 200-500 ms accounting for 47% of intervals, and a higher 20-180 ms frequency (49% of intervals). Baroreceptor stimulation decreased the occurrence of the high frequencies while increasing the probability of the lower frequency components. The overall occurrence of synchronized peaks per second fell linearly to zero with increases in blood pressure. The peak amplitude of RNA was unimodally distributed and was not affected by baroreceptor stimulation until an increase in mean arterial pressure reached a threshold (mean 142 +/- 5 mmHg) whereupon it fell quickly to zero. Sino-aortic vagal denervation did not affect the distribution of peak height. The width of synchronized discharges was also unimodal, mean 82 +/- 1 ms, and was almost unchanged during baroreflex stimulation acting in parallel with changes in the peak amplitude and decreasing at high blood pressures. Sino-aortic vagal denervation did not affect the synchronized width. There was no relationship between the periodicity and amplitude or width of synchronized discharges under all conditions. The results indicate that the periodicity and amplitude of renal synchronized discharges appear to be independent of each other and are differentially affected by baroreceptor input.

Animals↗
PubMed1992

Effect of asphyxia on the frequency and amplitude modulation of synchronized renal nerve activity in the cat.

A computerized peak detection algorithm was used to retrieve new information about changes in the characteristics of renal nerve activity (RNA) with asphyxia in anesthetized cats. The algorithm scanned the series of RNA voltages for significant increases followed by significant decreases in a small cluster of voltage values. Once each synchronized RNA peak had been detected, its corresponding amplitude, width, and peak-to-peak interval were calculated. The peak-to-peak interval showed two rhythms of synchronized discharge: one between 200-500 ms accounting for 38 +/- 3% of intervals and a higher 20-180 ms frequency (52 +/- 5% of intervals). Asphyxia did not change the periodicity distribution despite increases in arterial pressure. The peak amplitude of RNA, reflecting the number of active fibers, was unimodally distributed and was increased 39 +/- 9% with asphyxia. The shape of the distribution was unchanged. The width of the synchronized activity was also unimodally distributed, mean 79 +/- 3 ms, and increased by asphyxia to 99 +/- 5 ms. The results indicate that the control of the periodicity and amplitude of synchronized discharge appear to be independent and are differentially affected by chemoreceptor input.

Animals↗
PubMed1992

A new approach to analysis of synchronized sympathetic nerve activity.

Renal sympathetic nerve activity (RSNA) recorded from the multifiber preparation is a continuously fluctuating variable in terms of period and amplitude, reflecting a coordinated tonic level of output from the vasomotor center. Yet current methods of analysis cannot simultaneously measure both of these parameters. A new accurate technique for assessing changes in global sympathetic activity is required. We made a novel application of a computerized peak detection algorithm (Cluster program) to recordings of synchronized sympathetic nerve discharges. The procedure was applied to this new area to retrieve information about the characteristics of synchronized RSNA. Peaks in synchronized RSNA activity were detected from short-term (20 ms) integrated recordings in which voltage changes had been digitized at 200 Hz and stored on computer. The program scanned the data series for significant increases followed by significant decreases in a small cluster of voltage values. The program permits the input of the cluster sample sizes for the test peaks and pre- and postpeak nadirs and also the minimum height to be defined as a peak. Once each synchronized RSNA peak had been detected, its corresponding amplitude, width, and peak-to-peak interval were calculated. The program successfully characterized RSNA in a group of eight cats and yielded results comparable to other analysis techniques. The peak-to-peak interval period showed two modes of synchronized discharge, one related to the cardiac cycle and a faster 8- to 14-Hz frequency. The synchronized peak amplitude and width showed unimodal frequency distributions. The relationship between each of the three variables was examined; only the peak height and width were significantly related to each other.(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗
PubMed1991

Heart rate variability and cardiac autonomic function in men with chronic alcohol dependence.

Cardiac autonomic function was studied in 23 alcohol dependent men by standard tests of autonomic function and measurement of 24 hour heart rate variability. In all there was peripheral or central nervous system damage or both. Standard tests of autonomic function showed vagal neuropathy in seven. The remainder had normal autonomic function tests. Twenty four hour heart rate variability was measured as the standard deviation of the successive differences between RR intervals from an ambulatory electrocardiogram recording. Twenty four hour heart rate variability was significantly lower in both alcohol dependent groups than in controls, but the results in the two alcohol dependent groups were not significantly different from each other. The results of standard tests of autonomic function did not distinguish between the alcohol dependent men with normal autonomic function and controls. The differences in heart rate variability between this group and the controls may have been the result of the ability of this method to detect small changes in autonomic integrity. Cardiomyopathy may also account for some of these differences and such abnormalities should be excluded before results are to be regarded as a reflection of vagal function. Twenty four hour measurement of heart rate variability may be a more useful index of cardiac vagal neuropathy than currently available tests of autonomic function.

Adult↗
PubMed1990

Circadian variation of heart rate variability.

STUDY OBJECTIVE: The aim of the study was to examine the circadian variation in heart rate variability and to test the hypothesis that the variation is due to vagal influence. DESIGN: Human subjects, some with vagal neuropathy, underwent ambulatory 24 h electrocardiographic monitoring, the recordings being played back through an analyser which identified and timed successive pulse (R-R) intervals. Heart rate variability was measured for each 30 min period over 24 h as the standard deviation of the successive differences between R-R intervals, which filtered out low frequency components of heart rate variability that were not autonomic in origin. Modelled curves of heart rate variability were compared using analysis of variance. SUBJECTS: The subjects were aged between 33 and 65 years and were matched in three groups for age and sex. There were 11 healthy controls, 12 insulin dependent diabetics and seven alcoholics with vagal neuropathy. RESULTS: A significant circadian variation in heart rate variability was present, characterised by a rise during sleep. Mean heart rate variation was significantly reduced in groups with vagal neuropathy, although the amplitude of the cycle and time of peak variability was not significantly different. The circadian variation was sustained regardless of the degree of vagal neuropathy. CONCLUSIONS: The cycle of heart rate variability is not dependent on vagal interaction. It may be due to fluctuations in sympathetic activity affecting beat to beat variability.

Adult↗
PubMed1990

Mechanism of ethanol-induced vasodilation.

The mechanism by which ethanol ingestion causes dermal vasodilation is unclear, but it may result from a direct action on central vascular control mechanisms. Forearm blood flow and peripheral skin temperatures were examined in five quadriplegics (lesions above T7) and five control subjects, before and after the ingestion of ethanol (0.75 ml/kg body wt). The lack of vasomotor efferent function was confirmed in the quadriplegics by the absence of vasodilation in response to radiant heating of the torso. There were no significant changes in peripheral temperatures or forearm blood flow after ethanol in the quadriplegics. The control subjects had a significant increase in forearm blood flow (1.12 +/- 0.2 ml.min-1.100 ml-1) and skin temperature (finger 2.4 +/- 0.4 degrees C, toe 3.4 +/- 0.3 degrees C) after ethanol. These data suggest that ethanol may induce peripheral vasodilation by modulation of central vasomotor control mechanisms.

Adult↗
PubMed1990

Heart-rate variability and cardiac autonomic function in diabetes.

Cardiac autonomic function was measured in 25 subjects with insulin-dependent diabetes mellitus and 11 control subjects. Autonomic integrity was assessed with standard tests of autonomic function and a new technique of measuring heart-rate variability (HRV) for 24 h. All of the diabetic subjects were selected on the basis of peripheral or autonomic neuropathy or long-term poorly controlled diabetes. They were divided into groups according to presence or absence of vagal neuropathy based on the results of standard tests of autonomic function. Thirteen diabetic subjects had normal autonomic function tests (group 1), and vagal neuropathy was detected in 12 diabetic subjects (group 2). All subjects were monitored by ambulatory electrocardiograph, and the recordings were played back through an analyzer that identified and timed successive pulse (R-R) intervals. HRV was measured from the standard deviation of the successive differences between R-R intervals. HRV was significantly reduced in group 1 (mean +/- SE 73 +/- 9 ms) and group 2 (65 +/- 12 ms) diabetic subjects compared with the control group (138 +/- 10 ms). The standard tests of autonomic function did not distinguish the vagal dysfunction noted with HRV monitoring in group 1 diabetic subjects compared with control subjects. Measurement of 24-h HRV can detect small changes in cardiac autonomic function compared with currently available tests.

Circadian Rhythm↗
PubMed1989

Heart rate variability during hypoglycaemia.

A diabetic patient with parasympathetic neuropathy underwent 24-h ECG monitoring. During the 24 hours the patient had a hypoglycaemic event. Heart rate variability was greatly increased during this time, though heart rate was unaltered. The reasons for the sudden increase are unknown but may indicate a fruitful line for further research.

Arrhythmias, Cardiac↗
PubMedDate not supplied

Baroreflex control of heart rate during hypoxia and hypercapnia in chronically hypertensive rabbits.

1. It has been proposed that hypertension alters the respiratory and cardiovascular responses to chemoreceptor stimulation. However, in studies of human hypertension or in genetic animal models of hypertension it has been difficult to unequivocally attribute the changes to hypertension per se, rather than to a genetic predisposition towards an altered chemoreflex response independent of hypertension. 2. In the present study a group of seven rabbits were made hypertensive via a continuous 7 week infusion of angiotensin II (AngII; 50 ng/kg per min, i.v.). Animals were studied twice before AngII treatment commenced, twice during infusion and 48 h after stopping infusion. At each of these times the relationship between heart rate (HR) and mean arterial pressure (MAP) was determined under normoxic, acute hypoxic (10% O2 + 3% CO2) and acute hypercapnic (18% O2 +, 6.5% CO2) conditions for 20 min. A group of six animals also served as time controls. 3. Angiotensin II infusion increased arterial pressure from control levels of 80 +/- 2 to 114 +/- 8 mmHg and maintained it at this level throughout the 7 week period. After 1 week of AngII infusion there was a rightward shift in the heart rate-baroreflex curve, indicating that the baroreflex was now operating at an increased level of pressure. These changes were associated with reductions in the gain from -7.6 +/- 1.6 to -3.0 +/- 0.2 b.p.m./ mmHg, HR range and curvature of the baroreflex. These effects were maintained throughout the 7 weeks of hypertension and were reversed within 2 days of ceasing AngII infusion. Acute hypoxia and hypercapnia in normotensive animals caused a reduction in the HR range of 19 +/- 7 and 15 +/- 7 b.p.m., respectively, but caused no change in the gain (sensitivity) of the baroreflex. Despite the marked changes in the baroreflex produced by the hypertension, the effect of hypoxia or hypercapnia on the HR baroreflex was not different in the hypertensive group. 4. It is concluded that chronic experimental AngII-based hypertension does not alter the HR baroreflex response to hypoxia or hypercapnia and suggests that the altered responses seen in other studies is due to a genetic predisposition as opposed to the effect of raised arterial pressure.

Angiotensin II↗