| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Research Abstract |
1. Object
In oder to study of endotoxin shock and hypoxic condition on the microcirculation, we observed continuously the mesentrium of Wistar strain rats under a transmitting microscope with an irrigation system.
2. Method
(1) Recording the images of the mesenterium on the high speed video, and measuring the velocity of blood and the diameters of vessels. (2) Measuring the continuous change of the diameters of microvessels using an image splitter, and recording on a polygraph. Also measuring and recording the arterial pressure.
3. Results
In normal rats as control, the intravenous injection of urinasttin (UST); anti-shock agent, casued shortening of vasoconstrictive periods induced by topical norepinephrine(NE) of 1 g. These shortening were notable during the recovery periods. In cont-rast with this, in the rats of endotoxin shock, UST caused less shortening of recovery periods. So we supposed that USt may affect anything to the abnormal vascular action with endotoxin.
The rats under endotoxin shock with UST treatment kept more higher arterial pressure than not treated ones. These facts were co-operated with the results of the change in the diameter of microarteriole.
Next, we compared the two groups of rats under endotoxin shock. One group rats were treated by UST, before endotoxin injection, the others were treated by UST after endotoxin. The former kept high arterial pressure and blood velocity, although vasoconstriction of mesenterium was less than the latter. From above results, we concluded that pre-treatment by UST softened the symptoms of endotoxin shock.
Under hypoxic condition (F_<102>=0.15), the micro-circulation of mesenterial vessels of rats under endotoxin shock was extended of its diameter of vessels gradually, and became to constract more sensitively by topical of NE(1 g), and the hypoxic vasoconstriction was also promoted during the endotoxin shock.
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