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Contribution of Leukocytes to Capillary Hemostasis in the Spontaneously Hypertensive Rat
Author(s) -
Tran Edward D,
SchmidSchonbein Geert W
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.732.5
Subject(s) - medicine , endocrinology , dexamethasone , glucocorticoid , blood stasis , blood pressure , venous stasis , chemistry , pathology , alternative medicine , traditional chinese medicine
Our recent evidence suggests that leukocytes in hypertensives are involved in capillary stasis, which may lead to capillary rarefaction. Because the spontaneously hypertensive rats (SHR), a glucocorticoid‐dependent form of hypertension, have more activated circulating leukocytes with pseudopods, we hypothesize in SHR glucocorticoids impair normal leukocyte passage through capillaries and causes stasis. The objective of this study was to examine the effect of glucocorticoids on circulating leukocytes of the SHR and the normotensive Wistar‐Kyoto (WKY) rat and capillary blood flow. Small aliquots of blood (about 8% of blood volume) from SHR or WKY were incubated with or without supplement of dexamethasone (DEX 5 μM in 2 hours). The cells were fluorescently labeled, and transfused into SHRs, WKYs, or Wistar rats. Selected mesenteric networks were continuously observed over 2 hours. The labeled cells were traced with digital fluorescent microscopy. Without central pressure reduction, capillary stasis was initiated by immobilized leukocytes. Untreated SHR and WKY leukocytes did not increase stasis, but DEX‐treated leukocytes increased stasis significantly. DEX‐treated SHR leukocytes induced higher levels of stasis than DEX‐treated WKY leukocytes. These results suggest that the abnormal leukocyte response to glucocorticoids may serve as mechanisms for capillary stasis in SHR. Supported by HL10881.