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PubMedDate not supplied

Increased leukocyte rolling in newly formed mesenteric vessels in the rat during peritoneal dialysis.

OBJECTIVE: Long-term peritoneal dialysis (PD) is associated with the development of functional and structural alterations of the peritoneal membrane. The present study reports the effects of chronic exposure to PD fluid on mesenteric leukocyte-endothelium interactions, using intravital video microscopy. METHODS: Rats (n = 7) received 10 mL lactate-buffered 3.86% glucose-containing PD fluid daily during a 5-week period via a subcutaneously implanted mini access port that was connected via a catheter to the peritoneal cavity. In a first control group (n = 8), catheters were implanted but no fluid was instilled; a second control group (n = 8) remained untreated. The number of rolling and adherent leukocytes as well as blood flow and other fluid dynamic variables were analyzed in mesenteric postcapillary (diameter 10-25 mu) and collecting (diameter 26-40 mu) venules. Neovascularization was semiquantitatively assessed after inspection of video images and by light and electron microscopy. Using FITC-labeled albumin, microvascular leakage was examined. RESULTS: Rats exposed to PD fluid showed a more than twofold increase in the number of rolling leukocytes (p < 0.01); the number of adherent leukocytes was not changed. Furthermore, exposure to PD fluid induced severe neovascularization in rat mesentery. No microvascular leakage was observed in the various groups. The observed differences could not be explained by differences in systemic or local hemodynamic parameters or peripheral leukocyte counts, but is most likely associated with new vessel formation. CONCLUSIONS: Exposure of rat peritoneal membrane to conventional PD fluid for 5 weeks affected local leukocyte-endothelium interactions. In addition, severe angiogenesis was induced, whereas microvascular permeability remained unaltered.

Animals↗
PubMed1979

Congenital ascites due to mesenteric vessel constriction caused by malrotation of the intestines.

A newborn premature girl with congenital, non-chylous ascites is presented. The ascites recurred although laparocentesis was performed three times. The ascites was probably due to a superior mesenteric vein constriction caused by a malrotation of the intestines. After division of the Ladd-bands no ascites recurred. Non-chylous, congenital ascites may have a surgically treatable cause.

Ascites↗
PubMed1992

Nitric oxide mediates hyporeactivity to vasopressors in mesenteric vessels of portal hypertensive rats.

Increased levels of circulating vasodilators have been claimed to be the causative factor in the hyporesponsiveness to endogenous vasopressors in portal hypertension. To investigate whether this hyporeactivity to vasopressors is also present in an in vitro system perfused with a synthetic medium, the responsiveness to graded concentrations of norepinephrine, arginine-vasopressin, and potassium chloride was tested in perfused superior mesenteric arterial beds of normal rats and rats with portal hypertension induced by partial portal vein ligation (PVL). The same vasopressors were tested after incubation of vessel preparations with the stereo-specific nitric oxide formation inhibitor N omega-nitro-L-arginine (NNA, 10(-4) mol/L). Vessel preparations of PVL compared with normal rats (n = 8 per group and vasopressor) expressed a significant (P less than 0.05) hyporeactivity to norepinephrine, arginine-vasopressin, and potassium chloride over a wide range of concentrations. This hyporesponsiveness was overcome by preincubating vessel preparations with NNA. In summary, portal hypertension is accompanied by a significant in vitro hyporeactivity of splanchnic vessels to norepinephrine, arginine-vasopressin, and potassium chloride, and secretion of nitric oxide in this preparation seems responsible for this blunted response.

Animals↗
PubMed1987

[An experimental study of chemical embolization using conjugated estrogen--ultrastructural observations on rat mesenteric vessels].

We previously reported a new embolization method using conjugated estrogen and also a basic study which demonstrated that conjugated estrogen produced microcirculatory disturbance. To clarify the mechanism of this microcirculatory disturbance following the administration of conjugated estrogen, the changes of vascular endothelial cells and red blood cells were studied. After intra-arterial infusion of conjugated estrogen into rat mesenteric arteries, microcirculatory changes were observed with a biomicroscope, and also ultrastructural changes of vascular endothelial cells and red blood cells were examined. As a result, biomicroscopically, mesenteric microcirculatory disturbance in proportion to the doses of conjugated estrogens was seen and stasis of the microcirculation was finally observed in all rats. Ultrastructural observations revealed an appearance of spherocytes soon after the infusion and injury of vascular endothelial cells perfused with conjugated estrogen. Vascular endothelial cells were injured remarkably, including their plasma membrane, cytoplasm, and nuclei when mesenteric microcirculation showed sludging under the biomicroscope. At the stage of stasis, endothelial cells were severely injured and most of the vessels were filled with spherocytes. From these results, it was presumed that vascular endothelial injury and alterations of red blood cells into spherocytes induced by conjugated estrogen were the major factors of embolization effect of the conjugated estrogen. Furthermore, conjugated estrogen was considered as an effective embolic material because not only main arteries but microcirculations could be occluded by its intraarterial infusion.

Animals↗