Early in reperfusion, leukocytes alter perfused coronary capillarity and vascular resistance.
Myocardial no-reflow is a critical consequence of myocardial ischemia-reperfusion (I/R). Recent studies indicate that formed blood elements (e.g., leukocytes and platelets) contribute greatly to the compromise of myocardial blood flow that occurs after I/R. To assess the contributions of leukocytes and platelets to alterations in microvascular perfusion, we measured total coronary vascular resistance and perfused coronary capillary density before and after a 30-min period of no-flow ischemia in isolated rat hearts perfused with either 1) a Krebs-albumin-red cell solution [K(2)RBC]; 2) diluted whole blood (DWB) with Krebs (1:1); or 3) leukocyte-free DWB (LFB). We found that hearts perfused with K(2)RBC before ischemia demonstrated a significant decrease in perfused capillarity (-25%, P less than 0.05) after 25 min of reperfusion. Hearts perfused with LFB before ischemia exhibited a similar decrease in perfused capillarity (-33%, P less than 0.05) during reperfusion. However, in the DWB-perfused hearts, there was a 62% decrease in perfused capillarity (-62%, P less than 0.01) during reperfusion. Moreover, during reperfusion, total coronary vascular resistance was elevated significantly (+76%, P less than 0.01) in the DWB-perfused hearts but not in either the K(2)RBC or LFB groups. These results indicate that 1) platelets do not play a major role in alterations of microvascular perfusion after ischemia; 2) leukocytes are not requisite for the development of microvascular no-reflow early in reperfusion but their presence further exacerbates this deleterious effect; and 3) a relationship exists between perfused capillarity and vascular resistance in the isolated rat heart after global ischemia.
Reynolds
J M
JM
Department of Physiology, Texas Tech University Health Sciences Center, Lubbock 79430.
McDonagh
P F
PF
D000818:Animals; D001792:Blood Platelets / Q000502:physiology; D002199:Capillary Permeability; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000503:physiopathology*; D007962:Leukocytes / Q000502:physiology*; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D014655:Vascular Resistance