Macromolecular permeability increase following incomplete ischemia in the hamster cheek pouch and its inhibition by terbutaline.
The microvascular permeability increase during the reperfusion after incomplete ischemia in the everted hamster cheek pouch preparation was measured by intravital microscopy. FITC-dextran 1500,000 was given i.v. as tracer of macromolecular leakage. Incomplete ischemia of the left cheek pouch was obtained by occlusion of the ipsilateral carotid artery, its external branch and the contralateral external carotid artery. Reperfusion after thirty minutes of incomplete ischemia resulted in a fully reversible increase in the number of FITC-dextran leakage sites (leaks) from 0 to 68 +/- 18 in 7 hamsters. The response to a second period of ischemia, starting one hour after the first ischemia period, was significantly smaller (9 +/- 5 leaks). Local treatment with terbutaline (10(-6) M), a beta 2-receptor agonist, abolished the permeability response to ischemia almost completely (0.5 +/- 0.3 leaks, n = 6). Local application of histamine (2 X 10(-6) M) at the end of the experiments gave a response that was in accordance with that seen in hamsters not subjected to ischemia. These results were compared with those obtained from previous studies in our laboratory with a complete ischemia model and it appears as these two methods, incomplete and complete ischemia, give similar results.
D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects; D002610:Cheek; D006224:Cricetinae; D007511:Ischemia / Q000503:physiopathology*; D008297:Male; D008647:Mesocricetus; D008833:Microcirculation / Q000502:physiology; D013726:Terbutaline / Q000494:pharmacology*
D013726:Terbutaline