Study on glucocorticoid receptors during intestinal ischemia shock and septic shock.
Glucocorticoid receptors (GCRs) were studied by the radioligand binding assay in peripheral leukocytes obtained from dogs during intestinal ischemia shock and obtained from patients with septic shock. Sixteen healthy adult mongrel dogs were divided into two groups at random. The model of intestinal ischemia shock was made by occluding both superior mesenteric artery and vein in the occlusion group. Leukocytic GCRs and plasma cortisol were measured just at the time when mean arterial pressure (MAP) was 13.3 kPa (100 mmHg), 6.6 kPa (50 mmHg), and 3.3 kPa (25 mmHg). Clinically leukocytic GCRs were measured in ten patients in septic shock during hypotensive period and in ten normal volunteers used as control subjects. The results showed that in the occlusion group of animals, the levels of GCRs decreased progressively after shock; there was a significant positive correlation between the extent of reduction of MAP and that of GCRs. Leukocytes from the occlusion group contained significantly lower levels of GCRs than those from controls. The results of clinical observation confirmed the reduction of GCR levels in patients with septic shock. This paper reports for the first time the finding of secondary disorder of GCRs during septic shock, advances a new hypothesis concerning the pathophysiology of shock at the receptor level, and offers the experimental evidence for early use of massive doses of glucocorticoid (GC) in dealing with septic shock.
Huang
Z H
ZH
Department of General Surgery, Chang Zheng Hospital, Shanghai, China.
Gao
H
H
Xu
R B
RB
D000293:Adolescent; D000328:Adult; D000368:Aged; D000818:Animals; D003907:Dexamethasone / Q000097:blood; D004285:Dogs; D005260:Female; D006801:Humans; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000378:metabolism* / Q000503:physiopathology; D007962:Leukocytes / Q000032:analysis; D008297:Male; D008875:Middle Aged; D011869:Radioligand Assay; D011965:Receptors, Glucocorticoid / Q000032:analysis*; D012769:Shock / Q000378:metabolism* / Q000503:physiopathology; D012772:Shock, Septic / Q000378:metabolism* / Q000503:physiopathology
D011965:Receptors, Glucocorticoid; D003907:Dexamethasone