Role of platelets in myocardial ischemia-reperfusion injury in dogs.
We investigated the involvement of circulating platelets in myocardial ischemia-reperfusion injury in canine autoperfused heart-lung preparations using filters to deplete platelets and/or leukocytes. The left anterior descending (LAD) coronary artery was occluded for 40 min, followed by 40 min reperfusion, in 3 groups: a leukocyte-platelet-depleted (LPD) group, in which both leukocytes and platelets were depleted; a leukocyte-depleted (LD) group, in which leukocytes alone were depleted; and a control group. There were no differences in hemodynamics or arrhythmias among groups before or during coronary occlusion. After reperfusion, the maximum rate of change in left ventricular pressure during systole and diastole was significantly higher in the LPD group than in the control and LD groups. The LPD group also showed gradual recovery of regional myocardial function and a decrease in the frequency of premature ventricular contractions. The LD group showed a slight improvement in cardiac function and arrhythmias compared with the control group. Although there was no significant difference in the pulmonary arterial plasma level of thromboxane B2 at any stage among groups, the control group showed an increase after reperfusion. These results suggest that platelets are important in reperfusion injury and that the depletion of both leukocytes and platelets effectively protects against reperfusion injury.
Shimada
Y
Y
Third Department of Internal Medicine, Fukui Medical School, Japan.
Kutsumi
Y
Y
Nishio
H
H
Asazuma
K
K
Tada
H
H
Hayashi
T
T
Nakai
T
T
Morioka
K
K
D000818:Animals; D001792:Blood Platelets / Q000502:physiology*; D004285:Dogs; D006439:Hemodynamics / Q000502:physiology; D007958:Leukocyte Count; D007962:Leukocytes / Q000502:physiology; D009130:Muscle, Smooth / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D010976:Platelet Count; D011651:Pulmonary Artery / Q000378:metabolism; D013929:Thromboxane B2 / Q000097:blood; D018879:Ventricular Premature Complexes / Q000209:etiology
D013929:Thromboxane B2