Pure ethanol has been shown to inhibit platelet aggregation in vitro, ex vivo, and in vivo, although a blood alcohol content (BAC) of > or = 0.2 g/dL is usually required. The BAC of dogs administered the red wine-saline solution intravenously was 0.028 g/dL, much less than is usually necessary for platelet inhibition with pure ethanol. Because red wine and grape juice, but not white wine, abolished the CFRs, this suggests there are compounds present in red wine and grape juice that are not present or are present in a lower concentration in white wine. Wine and grape juice contain a wide variety of naturally occurring compounds, including fungicides, tannins, anthocyanins, and phenolic flavonoids (including flavonols and flavones). These compounds have shown platelet inhibition in vitro by a variety of proposed mechanisms. Perhaps the biological activity of these compounds can explain the platelet-inhibitory properties of red wine and grape juice that are observed without high levels of ethanol.

We investigated: 1) the mechanism of the hypotensive effect of a single bout of dynamic exercise in hypertensive subjects by measuring hemodynamic parameters before and for 2 h after treadmill exercise, and 2) the duration of the effect using ambulatory blood pressure (BP) monitoring once the subjects left the test site. Ten minutes after exercise there was a significant decrease from baseline systolic pressure (SP; -14 +/- 3 mm Hg), mean arterial pressure (MAP; -7 +/- 2 mm Hg), total peripheral resistance (TPR; -3.7 +/- 1.2 units), calf vascular resistance (CVR; -25.4 +/- 4.1 units), and an increase in HR (19 +/- 2 bpm). The changes in SP, DP, MAP, and HR were maintained during the 2 h of post-exercise monitoring; CVR remained decreased for 1 h; TPR returned to baseline within 20 min and then tended to be slightly elevated. CO was significantly decreased at 50, 60, and 120 min after exercise. We conclude that the early decline in BP after dynamic exercise in hypertensive subjects follows a biphasic pattern: 1) an initial decrease in total and regional vascular resistance with maintained CO, 2) followed by increasing resistance and decrease CO. Pre-exercise hypertensive BP values returned during subsequent ambulatory monitoring.

Background-Squatting produces a prompt increase in cardiac output and arterial blood pressure which is accompanied by an immediate decrease in heart rate and forearm vascular resistance. The rise in cardiac output and blood pressure has been attributed to augmented venous return from compression of leg veins, while the decreases in heart rate and forearm vascular resistance are probably due to activation of cardiopulmonary and arterial baroreflexes. Haemodynamic patterns in nine normal men and six heart transplant recipients during 2 min of squatting were examined to determine the role of cardiac innervation in the mediation of these responses. Methods-Stroke volume was monitored by ensemble averaged thoracic impedance cardiography and blood pressure was determined with an Ohmeda fingertip plethysmograph. These techniques provided continuous measurements which were capable of detecting transient and non-steady state changes. Forearm blood flow was measured with venous occlusion plethysmography. Measurements were obtained after 3 min of quiet standing, immediately after squatting, and at 20, 60, and 120 s of sustained squatting. Results-Both groups exhibited similar increases in stroke volume index (normal individuals 10 5 mu/m2; heart transplant recipients 10-3 mu/m2) and mean arterial pressure (normal individuals 8-5 mm Hg; heart transplant recipients 5 0 mm Hg) which were sustained throughout squatting. Each group also showed an initial decrease in peripheral resistance (normal individuals 3*6 units; heart transplant recipients 7-7 units) followed by a return to baseline values after 20 s. Heart rate decreased in normal individuals (10 beats/min) but was unchanged or minimally increased (2 beats/min) in heart transplant recipients. Forearm vascular resistance was conspicuously decreased in normal individuals (47.8 units) but only minimally (20-9 units) and not significantly in heart transplant recipients. Conclusions-The major haemodynamic responses to squatting (increased cardiac output and blood pressure) are similar in normal individuals and heart transplant recipients. These responses are primarily due to augmented venous return and are not altered by cardiac denervation. Both groups also exhibited a transient decline in peripheral vascular resistance which is most likely mediated by arterial baroreflexes activated by the acute rise in arterial blood pressure. The absence of a significant decrease in forearm vascular resistance in heart transplant recipients suggests that this response is partially mediated by cardiopulmonary or ventricular baroreflexes or that local forearm flow mediated vasodilatation remains impaired after heart transplantation.(Br Heart _J 1995;74:154-158)

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