Biomedical subjects

C C Coonts

Publications and source records attributed to C C Coonts.

3 recordsLinked to original sources

PubMed1999

The heart is not necessarily empty at syncope.

BACKGROUND: Although extensively investigated, the mechanism(s) of post-spaceflight orthostatic intolerance has not been elucidated. Several researchers have proposed that the "trigger" for syncope is an empty ventricle, initiated when a hypercontractile state, possibly due to a sudden surge in epinephrine, causes the walls of the left ventricle to touch leading to a profound sympatho-inhibition and intense vagal stimulation. HYPOTHESIS: A markedly reduced left ventricular end systolic volume (LVESV) achieved during progressive, presyncopal-limited lower body negative pressure (LBNP) is the trigger for syncope. METHODS: Eight healthy men, age 25.1+/-1.3 yr, volunteered for the study. Changes in left ventricular end-diastolic volume and LVESV were measured, using two-dimensional echocardiography, at each stage of LBNP from rest up to presyncope (PS). Plasma venous catecholamine concentrations were measured at the end of each stage by high performance liquid chromatography (HPLC) with electrochemical detection. RESULTS: All subjects reached PS. Three men became bradycardic at presyncope while five remained tachycardic. LVESV decreased by 28% at PS with no evidence of ventricular cavity obliteration. Norepinephrine increased by 44% from rest to PS, but no epinephrine surge was detected (35% increase from rest to PS). CONCLUSION: These data indicate that it is possible to initiate syncope with only a 28% decrease in LVESV, and that sympatho-inhibition and bradycardia are not required elements for syncope to occur.

Adult↗

PubMed1999

Moderate sodium restriction does not alter lower body negative pressure tolerance.

HYPOTHESIS: Space travel with exposure to microgravity leads to a significant reduction in orthostatic tolerance on return to Earth, for which countermeasures are only partially successful. The purpose of this study was to examine the effect of moderate dietary sodium restriction on tolerance to LBNP. METHODS: Eight healthy men, age 25.1+/-1.3 yr, volunteered for the study. Subjects were exposed to presyncopal LBNP after consuming their "typical" diet (C) for 5 d and after consuming a sodium restricted (SR) diet for 5 d. Diet sequence was randomized and adherence was verified by 24-h urine collection on the 4th and 5th days of each diet. RESULTS: All subjects reached presyncope during the LBNP, regardless of diet. Urinary sodium excretion was 3390+/-950 mg on the C diet and 1174+/-560 mg on the SR diet. Urinary potassium was not different between the diets. Cumulative stress index scores were 655+/-460 (mm Hg x min) on the C diet and 639+/-388 (mm Hg x min) during SR. Cardiac volumes, BP and total peripheral resistance were not different at any stage of the LBNP between the diets, nor were catecholamines. Plasma renin activity, determined by radioimmunoassay, was significantly higher during SR at rest, and during all stages of LBNP in comparison with the control diet. CONCLUSION: Moderate dietary sodium restriction is not detrimental to orthostatic tolerance.

Adult↗

PubMed1999

Validation of impedance cardiography during lower body negative pressure.

BACKGROUND: Both echocardiographic and impedance cardiographic techniques have been used individually for the determination of stroke volume (SV) during lower body negative pressure (LBNP). Impedance cardiography has not been validated during LBNP. HYPOTHESIS: The purpose of this study was to determine both the absolute values for SV and the change in SV for each stage of LBNP using both impedance and echocardiographic techniques during staged LBNP to presyncope. The hypothesis was that there would be no difference between the two techniques for either the absolute values of SV or for the change in SV with each stage of LBNP. METHODS: There were 16 men who volunteered to undergo LBNP. LBNP was lowered in 10 mmHg stages for 5 min per stage until presyncope was reached. Left ventricular SV was determined by two-dimensional echocardiography and impedance cardiography. Both the absolute values for SV and the change in SV from baseline at each stage of LBNP were compared for the two methods. RESULTS: There were no significant differences between the two techniques for the measurement of either the absolute SV or the change in SV with LBNP. The two methods correlated highly with r = 0.89 for the absolute SV values and r = 0.93 for the change in SV. Graphical analysis with the Bland-Altman analysis showed little bias in the impedance measurement for SV (-0.031 ml) and the change in SV (-2.7 ml). CONCLUSIONS: Impedance cardiography was a reliable measure of SV, as well as the change in SV, during LBNP stress to presyncope.

Adult↗