Ischemic time-dependent microvascular changes and reperfusion injury in the rat small intestine.
The significance of the reperfusion period in the pathophysiology of complete occlusion of the intestinal circulation is controversial. Our study was designed to evaluate the exact magnitude of reperfusion-induced intestinal mucosal damage in a standardized rat model of complete segmental arterial ischemia as a function of the occlusion time. Intestinal ischemia was maintained for 15, 30, or 60 min, or ischemia was followed by a 30-min reperfusion period. Intraarterial India ink perfusion was applied to visualize the mucosal vascularity changes induced by ischemia or ischemia-reperfusion. The height of the distributing arterioles of the villi and the average mucosal thickness were recorded by an image analysis system, and the degree of mucosal damage was established on a semiquantitative 0 to 5 grade scale. Ischemia induced erythrocyte obstructions at the villus tip, a progressive decrease in carbon-filled arteriole height, and a concomitant 7, 23, or 35% reduction of the mucosal thickness. The percentage decrease in perfused arteriole height/percentage mucosal thickness reduction ratio was 2.2, 1.5, or 1 during the 15-, 30-, or 60-min ischemia, respectively. Extravasation of the carbon tracer was observed in the 60-min ischemia group. During reperfusion, the mucosal layer was reduced by 27, 38, or 57%, respectively, compared with the baseline values. The arteriole height reduction/mucosal thickness reduction ratio was 1:1 in all ischemic-reperfused groups. The degree of mucosal damage was significantly increased during reperfusion after the 15-min ischemia. Microvessel obstruction is initiated at the villus tip following the onset of arterial occlusion, with subsequent destruction of the surrounding tissues during reperfusion. The reperfusion component of the net mucosal damage may be very significant in early forms of complete occlusion of the mesenteric circulation.
Boros
M
M
National Cardiovascular Center Research Institute, Osaka, Japan.
Takaichi
S
S
Hatanaka
K
K
D000818:Animals; D001158:Arteries / Q000473:pathology / Q000502:physiology; D007413:Intestinal Mucosa / Q000098:blood supply / Q000473:pathology; D007421:Intestine, Small / Q000098:blood supply* / Q000473:pathology; D008297:Male; D008833:Microcirculation; D008854:Microscopy, Electron; D008871:Microvilli / Q000502:physiology / Q000648:ultrastructure; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology*; D012720:Severity of Illness Index; D013997:Time Factors; D014661:Vasoconstriction / Q000502:physiology