THE EFFECT OF POLYCYTHEMIA ON SKIN BLOOD-FLOW IN HYPERTENSIVE RATS

Citation
Ms. Rendell et al., THE EFFECT OF POLYCYTHEMIA ON SKIN BLOOD-FLOW IN HYPERTENSIVE RATS, Comparative biochemistry and physiology. Part A, Physiology, 112(3-4), 1995, pp. 355-363
Citations number
45
Categorie Soggetti
Physiology,Biology
ISSN journal
10964940
Volume
112
Issue
3-4
Year of publication
1995
Pages
355 - 363
Database
ISI
SICI code
1096-4940(1995)112:3-4<355:TEOPOS>2.0.ZU;2-H
Abstract
Polycythemia has marked effects on blood flow through large arteries, but there has been little study of microvascular flow properties, part icularly in the hypertensive state. We have previously shown that skin blood flow in the rat had properties very similar to those in man. We used laser Doppler techniques to determine the effect of erythropoiet in-induced polycythemia on skin blood how in 12 Spontaneously Hyperten sive Rats (SHR) as compared with 12 normotensive Wistar-Kyoto (WKY) ra ts. We contrasted flow values at the back and base of tail, nutritivel y (NUTR) perfused skin sites, with those at the plantar surface of the paw, a site with substantial arteriovenous anastomotic (AVA) perfusio n. Erythropoietin treatment produced a substantially greater hematocri t response in the SHR rats, rising from 47 +/- 1 to 64 +/- 1, than in the WKY animals, who showed an increase from 46 +/- 1 to 55 +/- 1. Blo od pressure was higher in the EPO-treated WKY and SHR rats: 157 +/- 4 mm Hg as compared to 148 +/- 2 mmg Hg in the WKY animals and 228 +/- 4 mm Hg as compared to 201 +/- 3 mm Hg, respectively (both p < 0.03). E rythropoietin treatment had very little effect on basal skin blood flo w in either WKY or SHR rats. However, there was significantly lower he at-stimulated how at the plantar surface of the paw in the EPO treated rats (WKY: 27.3 +/- 1.9 ml/min/100 gm vs 35.5 +/- 1.5 ml/min/100 gm i n the untreated state; p < 0.02; SHR: 32.7 +/- 2.6 ml/min/100 gm vs 45 .4 +/- 2.3 ml/min/100 gm in the untreated state; p < 0.01), In contras t, there was little difference at the back or tail. We conclude that e rythropoietin-induced polycythemia affects flow in AVA rather than NUT R microvessels. Although raised vascular pressure has produced microva scular flow in our previous studies, the rise in pressure associated w ith high hematocrit appears to result from an increase in microvascula r resistance, decreasing how. Our study helps clarify clinical observa tions on the hemodynamic consequences of hematocrit elevation.