Journal of applied physiology
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To test for an active vasodilator system in human hand and finger skin, seven subjects had a small area of dorsal hand, palm, or dorsal finger pretreated with bretylium (BT) to block adrenergic vasoconstriction. Skin blood flow was monitored at a BT-treated site, a comparable untreated site, and the forearm by laser-Doppler flowmetry. Cutaneous vascular conductance (CVC) was evaluated from the ratio of blood flow to arterial pressure. ⋯ With body heating, increases in CVC at untreated sites of forearm, palm, dorsal hand, and dorsal finger were 881 +/- 165, 779 +/- 368, 423 +/- 115, and 1,430 +/- 716%, respectively (all P < 0.05). At BT-treated sites of palm, dorsal hand, and dorsal finger, increases were 35 +/- 15, 342 +/- 107, and 343 +/- 34%, respectively (palm not significant, others P < 0.05). Increased CVC at the palm began after 1.2 +/- 0.2 min of heating, significantly earlier than forearm (11.8 +/- 2.5 min), dorsal hand (16.4 +/- 3.4 min), or dorsal finger (15.6 +/- 3.6 min), which did not differ significantly from one another.(ABSTRACT TRUNCATED AT 250 WORDS)
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The peripheral vascular response to sepsis is characterized by a vasodilatation of the systemic arterial vessels. Pulmonary hypertension with an increase in resistance and back pressure to flow defined by pressure-flow (P-Q) relationships has been reported in experimental sepsis. We hypothesized that endotoxin can induce differential alterations in resistance and back pressure to flow in the liver venous and arterial beds. ⋯ Raising Pout from 0 to 15 mmHg decreased PV slope in the endotoxin group to a greater degree than in controls (P < 0.05). In the HA, endotoxin caused a decrease in slope but did not alter Pback. The simultaneous increase in the PV Pback and slope that occurs with endotoxemia decreases splanchnic venous return, pooling blood in the splanchnic compartment for a given total blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)