Luminal diameter and vasa vasorum response to stent dilation in the rabbit aorta.

RATIONALE AND OBJECTIVES: We examined the changes in luminal diameter and vasa vasorum after stent dilation of the aorta of nonatherosclerotic rabbits. METHODS: Balloon-expandable stents were placed in the aortas of rabbits at the L3 level and were expanded. After 8 weeks, the rabbits were euthanized, perfused with barium sulfate particles, frozen, sectioned, and X-rayed. RESULTS: The luminal intrastent diameter (2.3 +/- 0.23 mm) was significantly different (p < .05) from the expanded stent diameter but was not different from the luminal diameter above (2.3 +/- 0.53 mm) and below (1.9 +/- 0.18 mm) the stent. The number of vasa vasorum at the stent (46 +/- 7.2) was significantly increased compared with above (21 +/- 4.8, p < .001) and below (14.4 +/- 4.6, p < .001) the stent. CONCLUSION: After 8 weeks, luminal diameter was uniform. The increased vasa vasorum in the stented section suggested an increase in blood flow to the aortic wall, which may be important to the remodeling process.

Histamine or adenosine blockade alters intestinal blood flow autoregulation in swine.

The possible role of histamine or adenosine in intestinal blood flow autoregulation in 1-mo-old swine was examined by obtaining pressure-flow relationships before and during intestinal histamine H1- or adenosine-receptor blockade in two groups of fasting animals under anesthesia with pentobarbital sodium (30 mg/kg). Changes in abdominal and thoracic aortic pressures and in superior mesenteric and left renal arterial flows were recorded during controlled aortic compression above the celiac artery. After control intestinal and renal pressure-flow relationships were obtained, a test dose of agonist (0.1 microgram histamine or 0.2 microgram adenosine/kg body wt) was given into the superior mesenteric artery. Then an intra-arterial infusion of blocking agent was started (0.1 mg.kg-1.min-1 chlorpheniramine or 10 mumol/min theophylline). Degree of blockade was assessed with doses of agonist given before and after a second set of intestinal and renal pressure-flow relationships was obtained. Complete blockade of intestinal vascular histamine H1-receptors with chlorpheniramine abolished, and incomplete blockade of adenosine-receptors with theophylline attenuated, intestinal blood flow autoregulation. Renal blood flow autoregulation remained at its control level. These results indicate that both histamine and adenosine are among the physiological vasodilators contributing to intestinal blood flow autoregulation when arterial pressure is decreased in young swine.

Vasoactive compound effects on autoregulating versus nonautoregulating intestinal and renal circulations in young swine.

Vascular resistance changes to single intra-arterial injections of norepinephrine, histamine and adenosine were examined in 12 kidney and 10 jejunum preparations perfused in situ in fasting swine anesthetized with pentobarbital. Threshold doses were higher and other response magnitudes were smaller in the nonautoregulating renal circulation of 1-week-olds and jejunal circulation of 2-week-olds than in autoregulating circulations of 1-month-olds. These results suggest a correlation between maturation of autoregulatory capability and of vasodilator histamine and adenosine receptors.

The synergistic effect of angiotensin II and urea on systemic blood pressure.

The hypertensive synergism of A-II and urea was studied in anesthetized cats. Femoral arterial pressure was measured while test substances were infused in a femoral vein. Dose-response analysis of the A-II + urea interaction suggested that A-II pressor effects and A-II + urea potentiation involve a common mechanism. Methylurea and mannitol + A-II also induce a similar potentiation. While plasma osmolality and plasma volume indicated no systemic changes, intracellular osmotic shifts may be a factor in the synergism. Since inhibition of the potentiation by indomethacin was not replicated, prostaglandins can no longer be considered important. No effect of ganglionic blockade also eliminated CNS influences as a factor. Dual infusion suggested urea-induced A-II changes were not important for the synergism. Since a synergism of A-II with amino acids occurred, alteration of A-II receptors was indicated. Thus, the A-II + urea pressor synergism may involve either intracellular osmotic shifts or a receptor modification so A-II is more accessible.