Use of the gastroepiploic vessels as recipient or donor vessels in the free transfer of composite flaps by microvascular anastomoses.
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The utero-ovarian vein and ovarian artery in surgical specimens were cannulated and perfused in a countercurrent manner with isotonic, buffered solutions, fortified on the venous side with progesterone or radiolabelled methylantipyrine. Both substances were gradually transferred from the vein into the artery in the majority of the experiments while albumin was not exchanged. The results point to the existence of a countercurrent exchange mechanism in the human ovarian pedicle. Hardly detectable amounts of methylantipyrine were transferred from femoral vein to artery in the cat.
Prostaglandin release from microvessels isolated from the rabbit cerebral cortex was determined under three different atmospheric conditions: 100% O2 ("O2") room air, and 95% N2:5% CO2 ("N2-CO2"). Initial studies with homogenates prepared from rabbit cerebral microvessels (RCMV) indicated two pathways of enzymatic PGH2 transformation, namely PGI2 synthase and GSH-dependent PGH-PGE isomerase. We measured the release of the principal products of these pathways, 6-keto PGF1 alpha and PGE2 from freshly prepared RCMV. The release of 6-keto PGF1 alpha exceeded that of PGE2 in all three protocols. RCMV incubated in "N2-CO2" exhibited a reduction in the release of 6-keto PGF1 alpha compared to room air or "O2" incubated RCMV, evident at 30-60 min of incubation. No significant differences in the release of PGE2 were observed among the three incubation protocols. In all three incubation protocols the ratio of 6-keto PGF1 alpha to PGE2 did not differ during the initial 10 minutes of each incubation. After 30 to 60 min of incubation, this ratio did not change from the "O2" or room air treated RCMV, but decreased significantly for the "N2-CO2" treated group. To determine the reversibility of the apparent "N2-CO2" induced decline in 6-keto PGF1 alpha release, microvessels were removed from the nitrogen atmosphere and incubated in room air. Release was measured during the initial 10 min following reintroduction to room air and was compared to room air pretreated controls treated in an identical manner.(ABSTRACT TRUNCATED AT 250 WORDS)
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