The autonomic nervous system drives variability in heart rate, vascular tone, cardiac ejection, and arterial pressure, but gender differences in autonomic regulation of the latter three parameters are not well documented. In addition to mean values, we used spectral analysis to calculate variability in arterial pressure, heart rate (R-R interval, RRI), stroke volume, and total peripheral resistance (TPR) and measured circulating levels of catecholamines and pancreatic polypeptide in two groups of 25 +/- 1.2-yr-old, healthy men and healthy follicular-phase women (40 total subjects, 10 men and 10 women per group). Group 1 subjects were studied supine, before and after beta- and muscarinic autonomic blockades, administered singly and together on separate days of study. Group 2 subjects were studied supine and drug free with the additional measurement of skin perfusion. In the unblocked state, we found that circulating levels of epinephrine and total spectral power of stroke volume, TPR, and skin perfusion ranged from two to six times greater in men than in women. The difference (men > women) in spectral power of TPR was maintained after beta- and muscarinic blockades, suggesting that the greater oscillations of vascular resistance in men may be alpha-adrenergically mediated. Men exhibited muscarinic buffering of mean TPR whereas women exhibited beta-adrenergic buffering of mean TPR as well as TPR and heart rate oscillations. Women had a greater distribution of RRI power in the breathing frequency range and a less negative slope of ln RRI power vs. ln frequency, both indicators that parasympathetic stimuli were the dominant influence on women's heart rate variability. The results of our study suggest a predominance of sympathetic vascular regulation in men compared with a dominant parasympathetic influence on heart rate regulation in women.

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We studied 15 men (8 treatment, 7 control) before and after 21 days of 6º head-down tilt to determine whether daily, 1-h exposures to 1.0 G(z) (at the heart) artificial gravity (AG) would prevent bed rest-induced cardiovascular deconditioning. Testing included echocardiographic analysis of cardiac function, plasma volume (PV), aerobic power (VO(2)pk) and cardiovascular and neuroendocrine responses to 80º head-up tilt (HUT). Data collected during HUT were ECG, stroke volume (SV), blood pressure (BP) and blood for catecholamines and vasoactive hormones. Heart rate (HR), cardiac output (CO), total peripheral resistance, and spectral power of BP and HR were calculated. Bed rest decreased PV, supine and HUT SV, and indices of cardiac function in both groups. Although PV was decreased in control and AG after bed rest, AG attenuated the decrease in orthostatic tolerance [pre- to post-bed rest change; control: -11.8 ± 2.0, AG: -6.0 ± 2.8 min (p = 0.012)] and VO(2)pk [pre- to post-bed rest change; control: -0.39 ± 0.11, AG: -0.17 ± 0.06 L/min (p = 0.041)]. AG prevented increases in pre-tilt levels of plasma renin activity [pre- to post-bed rest change; control: 1.53 ± 0.23, AG: -0.07 ± 0.34 ng/mL/h (p = 0.001)] and angiotensin II [pre- to post-bed rest change; control: 3.00 ± 1.04, AG: -0.63 ± 0.81 pg/mL (p = 0.009)] and increased HUT aldosterone [post-bed rest; control: 107 ± 30 pg/mL, AG: 229 ± 68 pg/mL (p = 0.045)] and norepinephrine [post-bed rest; control: 453 ± 107, AG: 732 ± 131 pg/mL (p = 0.003)]. We conclude that AG can mitigate some aspects of bed rest-induced cardiovascular deconditioning, including orthostatic intolerance and aerobic power. Mechanisms of improvement were not cardiac-mediated, but likely through improved sympathetic responsiveness to orthostatic stress.

1. Stroke volume and cardiac output were measured using the Doppler ultrasound technique in 16 normal subjects immersed to the neck in water at 33 degrees C, 35 degrees C, 37 degrees C and 39 degrees C. A standard aortic diameter was assumed and results were expressed as percentage changes from pre-immersion resting values. 2. Cardiac output rose progressively at higher temperatures, increasing by 30% at 33 degrees C and by 121% at 39 degrees C. At thermoneutral temperatures (33 degrees C and 35 degrees C) this was achieved by an increase in stroke volume of 50% despite a significant decrease in heart rate. There was a further rise in stroke volume and pulse rate at higher temperatures and a mean tachycardia of 109 +/- 4 beats/min was noted at 39 degrees C. Calculated peripheral resistance reduced progressively with increasing temperature of immersion. 3. This non-invasive and simple technique may provide a non-exercise-related cardiovascular stress test to study cardiovascular responses in a variety of pathophysiological states.

SUMMARY A duplex scanner which consists of a real time two dimensional scanner and a pulsed Doppler flowmeter was used to measure superior mesenteric blood flow in 70 healthy subjects. By processing the Doppler shift signals, the instantaneous average Doppler shift frequency and then the instantaneous average velocity of the flow rate were calculated. Both diameter of the vessel and angle between vessel and beam were measured from real time imaging. The mean (+ standard error of the mean) of the superior mesenteric blood flow was 517±19 ml/min. There was neither significant difference in flow between sexes, nor correlation between flow and age (r=0.042). The mean of coefficients of variability were 6-8% over the short term, and 8.2% in long term studies.The superior mesenteric artery supplies blood to the duodenum -except for its superior portion -and also to the whole of the small bowel and the right half of the colon. Little information is available concerning superior mesenteric artery blood flow (SMABF)