Quantitative electrocardiography during extended space flight

Smith, Raymond A.; Stanton, Kathleen; Stoop, D.; Brown, Danielle; King, Paul H.

doi:10.1016/0094-5765(75)90046-6

Cited by 10 publications

(7 citation statements)

References 4 publications

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“…By comparison, the autonomic nervous system would seem to adapt fairly well to the absence of gravity. Only a small decrease in resting heart rate was observed during the Skylab mission [1]. Studies of shuttle astronauts also showed lower heart rates and diastolic pressures during flight [2].…”

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confidence: 94%

Baroreflex dysfunction induced by microgravity: potential relevance to postflight orthostatic intolerance

Ertl

Diedrich

Biaggioni

2000

Clinical Autonomic Research

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Microgravity imposes adaptive changes in the human body. This review focuses on the changes in baroreflex function produced by actual spaceflight, or by experimental models that simulate microgravity, e.g., bed rest. We will analyze separately studies involving baroreflexes arising from carotid sinus and aortic arch afferents ("high-pressure baroreceptors"), and cardiopulmonary afferents ("low-pressure receptors"). Studies from unrelated laboratories using different techniques have concluded that actual or simulated exposure to microgravity reduces baroreflex function arising from carotid sinus afferents ("carotic-cardiac baroreflex"). The techniques used to study the carotid-cardiac baroreflex, using neck suction and compression to simulate changes in blood pressure, have been extensively validated. In contrast, it is more difficult to selectively study aortic arch or cardiopulmonary baroreceptors. Nonetheless, studies that have examined these baroreceptors suggest that microgravity produces the opposite effect, ie, an increase in the gain of aortic arch and cardiopulmonary baroreflexes. Furthermore, most studies have focus on instantaneous changes in heart rate, which almost exclusively examines the vagal limb of the baroreflex. In comparison, there is limited information about the effect of microgravity on sympathetic function. A substantial proportion of subjects exposed to microgravity develop transient orthostatic intolerance. It has been proposed that alterations in baroreflex function play a role in the orthostatic intolerance induced by microgravity. The evidence in favor and against this hypothesis is reviewed.

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confidence: 94%

Baroreflex dysfunction induced by microgravity: potential relevance to postflight orthostatic intolerance

Ertl

Diedrich

Biaggioni

2000

Clinical Autonomic Research

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“…In the present study, we quantified changes in vagal activity by measuring the PR interval of the electrocardiogram (ECG). Vagal stimulation increases atrioventricular conduction time and thus directly increases the duration of the PR interval (Kinoshita and Konishi, 1989;Levy and Zieske, 1969;Smith et al, 1976). Elongation of the PR interval can be obtained by either an increase in vagal activity and/or a decrease in sympathetic activity.…”

Section: Introductionmentioning

confidence: 99%

Facilitation of Cardiac Vagal Activity by CRF-R1 Antagonists during Swim Stress in Rats

Wood

Verhoeven

Savit

et al. 2006

Neuropsychopharmacol

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Exposure to stressors that elicit fear and feelings of hopelessness can cause severe vagal activation leading to bradycardia, syncope, and sudden death. These phenomena though documented, are difficult to diagnose, treat clinically, and prevent. Therefore, an animal model incorporating these cardiovascular conditions could be useful. The present study examined 'sinking' during a 2-h swim stress, a phenomenon that occurs in 50% of rats during 251C water exposure. Concurrent measurements of body temperature, immobility, heart rate (HR), and PR interval (a measure of vagal activity) were made. Neither decreases in immobility nor variations in hypothermia during swim were correlated with sinking. Bradycardia was more severe in sinking rats (average minimum HR7SEM; 143713 vs 247714; po0.01), and PR interval was elevated (po0.0001). To examine potential modulation of vagal activity during stress, corticotropinrelasing factor (CRF) receptor antagonists (antalarmin, R121919 and astressin B), a glucocorticoid receptor antagonist (RU486), and a peripherally acting cholinergic antagonist (methylatropine nitrate) were administered. The centrally acting CRF antagonist, antalarmin (32 mg/kg), produced elongation of the PR interval (po0.0001), robust bradycardia (135718; po0.001), and increased sinking (92%; po0.05), and methylatropine nitrate (3.2 mg/kg) blocked these effects. Corroborating these data, two different CRF antagonists, R121919 (30 mg/kg) and astressin B (intracerebroventricular (i.c.v.), 0.03 mg/rat) increased sinking to 100%. RU486 (20 mg/kg) blocked HPA axis negative feedback and decreased percent sinking to 25%. From these studies, we concluded that sinking during a 2-h water exposure was a result of extreme vagal hyperactivity. Furthermore, stress-induced CRF release may serve to protect against elevated cardiac vagal activity.

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“…Bigger animals have a longer P-R interval than the smaller ones (17,20). Elongation of P-R interval can be obtained by either an increase in vagal activity and/or a decrease in sympathetic activity (11,14,25). P-R interval duration may lengthen in a wide range of pathological states: disturbances of water and electrolyte balance, hormonal imbalance, and during antiarrhythmic therapy (5,12,25).…”

Section: Introductionmentioning

confidence: 99%

“…Elongation of P-R interval can be obtained by either an increase in vagal activity and/or a decrease in sympathetic activity (11,14,25). P-R interval duration may lengthen in a wide range of pathological states: disturbances of water and electrolyte balance, hormonal imbalance, and during antiarrhythmic therapy (5,12,25). The other cause of P-R interval prolongation may be electrical remodelling due to rapid rhythms, both spontaneous, and pacing induced.…”

Section: Introductionmentioning

confidence: 99%

P-R interval in porcine model of chronic tachycardia-induced cardiomyopathy

Skrzypczak¹,

Zyśko

Pasławska³

et al. 2013

Bulletin of the Veterinary Institute in Pulawy

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The aim of the study was to assess the atrioventricular conduction in the model of porcine pacing induced tachycardiomyopathy. Fifty-one swine were examined: 27 were paced and 24 served as a control group. Every 4 weeks, the animals were anaesthetised for 1 h and an ECG Holter was performed. Thirty minutes after the onset of anaesthesia, P-R and R-R intervals were measured. Each result was assigned to the subgroup according to the animal’s weight and the presence or absence of previous pacing. P-R interval was longer in animals after at least 4 weeks of rapid ventricular stimulation than in adjusted group of the animals according to the body mass. Multivariate analysis has showed that longer P-R interval was related to male gender, higher body mass, slower heart rate, and history of previous pacing. Chronic ventricular pacing led to the slowing of atrioventricular conduction. The presence of differences in the duration of R-R intervals between groups was only found in swine weighing 120-139 kg. The R-R interval was shorter in paced animals, whereas PR interval was longer in that group, indicating that PR prolongation is related to electrical or structural remodelling of the cardiac conductive tissue but not increased sympathetic nervous system activity, which is expected to produce corresponding changes in PR and R-R intervals.

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Quantitative electrocardiography during extended space flight

Cited by 10 publications

References 4 publications

Baroreflex dysfunction induced by microgravity: potential relevance to postflight orthostatic intolerance

Baroreflex dysfunction induced by microgravity: potential relevance to postflight orthostatic intolerance

Facilitation of Cardiac Vagal Activity by CRF-R1 Antagonists during Swim Stress in Rats

P-R interval in porcine model of chronic tachycardia-induced cardiomyopathy

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