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Microvessel diameter changes during hemorrhagic shock in unanesthetized hamsters

Authors :
A. Colantuoni
S. Bertuglia
Marcos Intaglietta
Colantuoni, Antonio
Bertuglia, S.
Intaglietta, M.
Source :
Microvascular Research. 30:133-142
Publication Year :
1985
Publisher :
Elsevier BV, 1985.

Abstract

The effects of hypovolemic shock on the time-dependent diameter changes of small arteries and arterioles were studied in the hamster skin fold window preparation. This experimental model permits the visualization of the microvasculature without the effects of acute surgery, anesthesia, and exposure. In these conditions, all the arterial microvessels showed vasomotion, while the venules and small veins, that were also studied, did not show rhythmic diameter changes. Hemorrhage was induced by the withdrawal of blood through a chronically implanted arterial catheter. The mean arterial blood pressure was reduced to 40 mm Hg in 20 min, and was maintained at this value for an additional 30-min period. Reinfusion of the withdrawn blood was made at 50 min. During the shock period, vasomotion disappeared in all arterial vessels. The small arteries and arterioles, A1 (70-100 micron, mean diameter), A2 (40-70 micron, md), and A3 (15-40 micron, md), contracted by 20 +/- 7, 33 +/- 10, and 34 +/- 11% of the control mean diameter, respectively. A4 terminal arterioles (less than 15 micron, md) dilated after the onset of bleeding; their rhythmic diameter changes subsequently stopped and their mean diameter increased by 75 +/- 7% of the original value. V1 small veins (150-200 micron, md) contracted during shock, while V2 (35-55 micron, md), V3 (25-35 micron, md), and V4 (15-25 micron, md) venous vessels did not show any significant change. Reinfusion of shed blood caused the reappearance of vasomotion; control vasomotion patterns recovered after reinfusion. Our results indicate that the microcirculatory responses to hypovolemic shock are dependent on the vessel type; this inhomogeneous reactivity may be due to the different responsiveness of microvessels to the mechanisms elicited by hemorrhage.

Details

ISSN :
00262862
Volume :
30
Database :
OpenAIRE
Journal :
Microvascular Research
Accession number :
edsair.doi.dedup.....e2928210b19bd58f7b4da5dad9b37ae0
Full Text :
https://doi.org/10.1016/0026-2862(85)90045-7