Abstract
We assessed a kallikrein-like amidase activity probably related to the kallikrein-kinin system, as well as the participation of leukocyte infiltration in renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min of ischemia and to different periods of reperfusion. A control group consisted of sham-operated mice, under similar conditions, except for ischemia induction. Kallikrein-like amidase activity, Evans blue extravasation and myeloperoxidase activity were measured in kidney homogenates, previously perfused with 0.9% NaCl. Plasma creatinine concentration increased only in the 60-min ischemic group. After 20 min of ischemia and 1 or 24 h of reperfusion, no change in kallikrein-like amidase activity or Evans blue extravasation was observed. In the mice subjected to 20 min of ischemia, edema was evident at 1 h of reperfusion, but kidney water content returned to basal levels after 24 h of reperfusion. In the 60-min ischemic group, kallikrein-like amidase activity and Evans blue extravasation showed a similar significant increase along reperfusion time. Kallikrein-like amidase activity increased from 4 nmol PNA mg protein-1 min-1 in the basal condition to 15 nmol PNA mg protein-1 min-1 at 10 h of reperfusion. For dye extravasation the concentration measured was near 200 microg of Evans blue/g dry tissue in the basal condition and 1750 microg of Evans blue/g dry tissue at 10 h of reperfusion. No variation could be detected in the control group. A significant increase from 5 to 40 units of DeltaAbs 655 nm g wet tissue-1 min-1 in the activity of the enzyme myeloperoxidase was observed in the 60-min ischemic group, when it was evaluated after 24 h of reperfusion. Histological analysis of the kidneys showed migration of polymorphonuclear leukocytes from the vascular bed to the interstitial tissue in the 60-min ischemic group after 24 h of reperfusion. We conclude that the duration of ischemia is critical for the development of damage during reperfusion and that the increase in renal cortex kallikrein-like amidase activity probably released from both the kidney and leukocytes may be responsible, at least in part, for the observed effects, probably through direct induction of increased vascular permeability.
Highlights
Damage produced by ischemic disorders has been recently studied in different organs but some of the alterations described have not been strictly attributed to the ischemia suffered by the organ [1,2,3,4]
Separate groups of five or six mice each were subjected to a specific pair of conditions, and amidase activity, Evans blue extravasation, kidney water content and myeloperoxidase activity were determined for each situation
Kallikrein-like amidase activity, plasma creatinine concentration and tissue water content were studied after different periods of ischemia (20 or 60 min) and reperfusion (1 or 24 h)
Summary
Damage produced by ischemic disorders has been recently studied in different organs but some of the alterations described have not been strictly attributed to the ischemia suffered by the organ [1,2,3,4]. The role of neutrophils in post-ischemic damage has been studied in myocardium [5], kidney [1], intestine [2], brain [6] and pancreas [4]. Cell membrane disintegration is the consequence of both the formation of biologically dangerous free radicals through an enhanced activity of xanthine oxidase and leukocyte interaction with the microvascular endothelial cells in the intestine [2]. Experiments involving ischemia and reperfusion of coronary arteries revealed that the endothelium was activated. Under these conditions, endothelial cells were able to release several factors such as interleukin-8 and platelet activating factor, that act as either chemotactic or activating factors for neutrophils [5,8,9]. Several studies have demonstrated that NO concentration increases during ischemia and decreases upon reperfusion, facilitating the binding of neutrophils to the endothelium during the latter period [5,10]
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Schedule a callMore From: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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