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We investigated the influence of aging on cardiac baroreflex function during dynamic exercise in seven young (22 [+ or -] 1 yr) and eight older middle-aged (59 [+ or 1] 2 yr) healthy subjects. Carotid-cardiac baroreflex function was assessed at rest and during moderate-intensity steady-state cycling performed at 50% heart rate reserve (HRR). Five-second pulses of neck pressure and neck suction from +40 to -80 Torr were applied to determine the operating point gain ([G.sub.OP]) and maximal gain ([G.sub.MAX]) of the full carotid-cardiac baroreflex function curve and examine baroreflex resetting during exercise. At rest, mean arterial pressure (MAP) and heart rate were similar between the younger and older subjects. In contrast, the resting [G.sub.OP] and [G.sub.MAX] were significantly lower in the older subjects. The increase in MAP from rest to exercise was greater in the older subjects ([DELTA] +20 [+ or 1] 2 older vs. [DELTA] +6 [+ or 1] 3 younger mmHg; P < 0.001). However, the [G.sub.OP] was similar in both groups during exercise because of a reduction in the younger subjects. In contrast, [G.sub.MAX] was unchanged from rest and therefore remained lower in older subjects (-0.19 [+ or 1] 0.05 older vs. -0.42 [+ or 1] 0.05 younger beats x [min.sup.-l] x [mmHg.sup.-1]; 50% HRR; P < 0.001). Furthermore, exercise resulted in an upward and rightward resetting of the cardiac baroreflex function curve in both groups. Collectively, these findings suggest that the cardiac baroreflex function curve appropriately resets during exercise in older subjects but operates at a reduced [G.sub.MAX] primarily because of age-related reductions in carotid-cardiac control manifest at rest. arterial baroreceptors; aging; heart rate doi:10.1152/ajpregu.00199.2007

Intravital microscopic techniques were used to examine the mechanisms underlying bradykinin-induced leukocyte/endothelial cell adhesive interactions (LECA) and venular protein leakage (VPL) in single postcapillary venules of the rat mesentery. The effects of bradykinin superfusion to increase LECA and VPL were prevented by coincident topical application of either a bradykinin-B[sub 2] receptor antagonist, a cell-permeant superoxide dismutase (SOD) mimetic or antioxidant, or inhibitors of cytochrome P-450 epoxygenase (CYPE) or protein kinase C (PKC) but not by concomitant treatment with either SOD, a mast cell stabilizer, or inhibitors of nitric oxide synthase, cyclooxygenase, xanthine oxidase, NADPH oxidase, or platelet-activating factor. Immunoneutralizing P-selectin or intercellular adhesion molecule-1 (ICAM-1) completely prevented bradykinin-induced leukocyte adhesion and emigration but did not affect VPL. On the other hand, stabilization of F-actin with phalloidin prevented bradykinininduced leukocyte emigration and VPL but did not alter leukocyte adhesion. These data indicate that bradykinin induces LECA in rat mesenteric venules via a B[sub 2]-receptor-initiated, CYPE-, oxidant- and PKC-mediated, P-selectin- and ICAM-1dependent mechanism. Bradykinin also produced VPL, an effect that was initiated by stimulation of B[sub 2] receptors and involved CYPE and PKC activation, oxidant generation, and cytoskeletal reorganization but was independent of leukocyte adherence and emigration. [ABSTRACT FROM AUTHOR]

Reports that preconditioning with ethanol prevents postischemic leukocyte-endothelial cell adhesive interactions. Mean arterial blood pressures; Time course for changes in plasma ethanol concentration after gastric instillation; Changes in the number of rolling and adherent leukocytes.

Presents information on a study which examined the mechanism of action of ischemic preconditioning in preventing prolonged ischemia and reperfusion in the small intestine. Methodology; Results; Discussion on the results.

Focuses on a study which investigated the role of a proline/arginine-rich antimicrobial peptide PR-39 in the prevention of postischemic microvascular dysfunction. Effect of PR-39 treatment on neutrophil-endothelial cell interactions; Effect of PR-39 on oxidant production and microvascular barrier integrity.

Determines whether ischemic preconditioning (IPC) would prevent leukocyte adhesion and emigration in postischemic skeletal muscle. Examination of whether production of adenosine during IPC versus reperfusion after prolonged ischemia plays a role in the IPC-induced reductions in postischemic leukocyte adhesion and emigration.

It is now recognized that reperfusion after a prolonged period of reduced or absent blood flow, although necessary to salvage ischemic tissue, initiates a complex series of deleterious reactions which ultimately induce the same effects as ischemia per se, i.e., cell injury and necrosis. Work conducted over the past 15 years has uncovered the fact that post-ischemic leukocyte infiltration plays a major role in the reperfusion component of ischemia/reperfusion (I/R) injury. This discovery has led to a concerted research effort directed at identifying interventions that prevent post-ischemic leukocyte adhesion and emigration. Recent work indicates that flavonoids are particularly effective anti-inflammatory agents in the setting of I/R. While the mechanisms underlying the powerful protective effects of these compounds is uncertain, a growing body of evidence indicates that flavonoids are potent anti-oxidants that also act to inhibit the activity of key regulatory enzymes involved in the activation of pro-inflammatory signaling cascades. In addition, it appears that these compounds prevent the expression of specific adhesion molecules involved in leukocyte recruitment, observations which provide the molecular basis for the anti-adhesive properties of these compounds.