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Biomedical subjects

D Goldwater

Publications and source records attributed to D Goldwater.

8 recordsLinked to original sources
PubMed1994

Influence of suspension on the oxidative burst by rat neutrophils.

The influence of spaceflight on the oxidative burst of neutrophils is not known. The present study was designed to evaluate the influence of antiorthostatic suspension, a ground-based modeling system designed to simulate certain aspects of weightlessness that occur after spaceflight, on the capacity of rat neutrophils to express the oxidative burst, an important host defense mechanism against microbial pathogens. Rats were suspended in whole body harnesses in the antiorthostatic orientation for a 3- or 7-day period. Control rats were suspended orthostatically or allowed to remain in vivarium cages without the attachment of any suspension materials. After suspension, peripheral blood was harvested and neutrophils were isolated by density gradient centrifugation. The enriched neutrophil preparations were stimulated with N-formyl-methionyl-leucine-phenylalanine and phorbol myristic acid to induce the oxidative burst. It was found that neutrophils isolated from suspended animals released the same levels of superoxide anion as did vivarium control animals that were not suspended, indicating that whole body suspension did not alter this aspect of rat neutrophil function.

Animals↗
PubMed1986

Atropine unmasks bed-rest effect: a spectral analysis of cardiac interbeat intervals.

Bed-rest deconditioning is suspected to reduce cardiac reserve, possibly by impairing autonomic function. Heart rate response in normal subjects reveals considerable variability, reflected by a relatively broadband interbeat interval power spectrum. A reduction in this autonomically modulated variability would be predicted to cause a narrowing of the spectrum. We retrospectively analyzed data from 10 aerobically conditioned men (age range 35-49 yr) who had undergone orthostatic tolerance testing with lower body negative pressure pre-bed rest and after 7-10 days of bed rest, while on placebo and after intravenous atropine. Spectra were derived by Fourier analysis of 128 interbeat interval data sets. Spectral power was estimated by computing the root-mean-square (rms) values (mean +/- SD) for the band encompassing the 2nd to 64th harmonics from subjects with a sufficient number of beats: placebo rms is 93 +/- 33 ms for pre-bed rest and 84 +/- 38 ms for bed rest (NS, n = 6); atropine rms is 63 +/- 24 ms for pre-bed rest and 40 +/- 23 ms for bed rest (P less than 0.01; n = 7). These data suggest that atropine "unmasks" a deconditioning effect of bed rest in athletic men, evidenced by a reduction in interbeat interval spectral power not apparent with placebo. Spectral analysis offers a useful means of quantitating the effects of bed-rest deconditioning and autonomic perturbations on cardiac dynamics.

Adult↗
PubMed1986

Plasma viscosity elevations with simulated weightlessness.

Bed rest studies which simulate weightlessness have demonstrated marked changes in the state of hydration of subjects as well as decrements in aerobic capacity. These two phenomena may be linked through increases in blood viscosity which is altered by a loss of free water and which, in turn, influences blood flow needed for aerobic muscular work. This study examines changes in the rheologic properties of blood which attend changes in plasma volume with bed rest in humans and correlates these changes with alterations in aerobic capacity. Eight healthy human subjects were studied on the 6th day of bed rest during two consecutive 10-d bed rest periods separated by a 14-d recovery interval designed to simulate the flight-layover schedule of shuttle astronauts. Plasma viscosity was measured with a Wells-Brookfield viscometer, plasma volume by dye dilution, and maximal aerobic capacity (VO2max) by recumbent cycle ergometry. Bed rest resulted in significant increases in hematocrit and in total plasma protein concentration and fibrinogen concentration, both of which contribute to an elevation in plasma viscosity. The greater than 20% increase in fibrinogen concentration was much greater than could be explained by hemoconcentration. VO2max decreased significantly in the first but not the second bed rest cycle. In many individuals, a decrease in plasma volume and aerobic capacity was coupled with elevated plasma viscosity and hematocrit; however, significant correlations between these variables were lacking. Although significant rheologic perturbations do occur with bed rest, in this study, blood viscosity elevation failed to directly correlate with the reduction in VO2max.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Mechanisms for decreased exercise capacity after bed rest in normal middle-aged men.

The mechanisms responsible for the decrease in exercise capacity after bed rest were assessed in 12 apparently healthy men aged 50 +/- 4 years who underwent equilibrium gated blood pool scintigraphy during supine and upright multistage bicycle ergometry before and after 10 days of bed rest. After bed rest, echocardiographically measured supine resting left ventricular end-diastolic volume decreased by 16% (p less than 0.05). Peak oxygen uptake during supine effort after bed rest was diminished by 6% (p = not significant [NS]), whereas peak oxygen uptake during upright effort declined by 15% (p less than 0.05). After bed rest, increases in heart rate were also greater during exercise in the upright than in the supine position (p less than 0.05). Values of left ventricular ejection fraction increased normally during both supine and upright effort after bed rest and were higher than corresponding values before bed rest (p less than 0.05). After bed rest, increased left ventricular ejection fraction and heart rate largely compensated for the reduced cardiac volume during supine effort, but these mechanisms were insufficient to maintain oxygen transport capacity at levels during upright effort before bed rest. These results indicate that orthostatically induced cardiac underfilling, not physical deconditioning or left ventricular dysfunction, is the major cause of reduced effort tolerance after 10 days of bed rest in normal middle-aged men.

Bed Rest↗
PubMed1983

Exercise conditioning in middle-aged men after 10 days of bed rest.

Of 12 healthy men with a mean age 50 +/- 4 years who had been at bed rest for 10 days, six were randomly assigned to perform individually prescribed physical exercise daily for 60 days after bed rest (exercise group) and six simply resumed their customary activities (control group). Exercise group subjects were significantly more active than control subjects during this interval (p less than .05). Two classic training effects observed in the 60 days after bed rest were significantly larger among exercise than among control group subjects; compared with values immediately after bed rest, heart rate at a constant submaximal workload declined by 36 +/- 11 beats/min in the exercise group vs 16 +/- 8 beats/min in the control group and peak oxygen consumption increased by 4.8 +/- 4.2 vs 2.2 +/- 5.0 ml/kg/min (both p less than .05). Despite these differences in the cardiovascular response to exercise, peak oxygen consumption in both groups returned to before-bed rest levels by 30 days after bed rest, and this was accompanied by significant (p less than .05) and similar increases in resting left ventricular end-diastolic and stroke volumes in both groups. Simple resumption of usual physical activities after bed rest was as effective as formal exercise conditioning in restoring functional capacity to before-bed rest levels.

Bed Rest↗
PubMed1982

Cardiovascular responses to exercise in middle-aged men after 10 days of bedrest.

The cardiorespiratory response to 10 days of continuous recumbency was assessed in 12 healthy men, age 50 +/- 4 years, who underwent supine and upright graded maximal exercise testing before and after bedrest. The decrease in peak oxygen uptake after bedrest was greater during upright exercise (15.1%, p less than 0.05) than during supine exercise (6.1%, NS): from 25.8 +/- 5.2 to 21.9 +/- 4.5 ml/kg/min and from 24.6 +/- 5.2 to 23.1 +/- 4.8 ml/kg/min. The decrease in submaximal work was also greater in the upright than in the supine position ( p less than 0.05). Ventilation volume was significantly elevated (p less than 0.05) after bedrest during maximal and submaximal effort in both the supine and upright positions. After bedrest, peak heart rate increased 5.7% and 5.9% during supine and upright testing, respectively (p less than 0.05). The increases in rate-pressure product after bedrest were significantly larger (p less than 0.05) during upright than during supine exercise. These results indicate that orthostatic stress is the most important factor limiting exercise tolerance after bedrest in normal middle-aged men. This mechanism also increases the myocardial oxygen demands during submaximal effort after bedrest. Intermittent exposure to gravitational stress during the bedrest stage of hospital convalescence may obviate much of the deterioration in cardiovascular performance that follows myocardial infarction.

Bed Rest↗
PubMed1980

Influence of prolonged recumbency on drug disposition.

The disposition of lidocaine and penicillin was studied in normal subjects before and after 7 days of total recumbency. Penicillin (1,000,000 U) and lidocaine (100 mg) were administered intravenously. Lidocaine protein binding was also followed. Total body clearance, elimination half-life, and volume of distribution were calculated. There were no statistically significant differences in these disposition parameters before and after 7 days of recumbency. The binding of lidocaine also was not changed after bed rest. We conclude that the physiologic changes that occur during prolonged bed rest do not affect distribution or elimination of lidocaine or penicillin.

Bed Rest↗