Jm. Reynolds et Pf. Mcdonagh, PLATELETS DO NOT MODULATE LEUKOCYTE-MEDIATED CORONARY MICROVASCULAR DAMAGE DURING EARLY REPERFUSION, The American journal of physiology, 266(1), 1994, pp. 80000171-80000181
Several studies indicate that leukocytes and platelets exacerbate the
compromise of myocardial function that occurs after ischemia-reperfusi
on (I/R). However, it is unclear whether both leukocytes and platelets
must be present to mediate coronary microvascular damage early during
reperfusion after ischemia. To examine the effects of leukocytes and
platelets on microvascular damage after I/R, we measured transcoronary
albumin extravasation (O/I), perfused coronary capillary density (Cap
s), and transcoronary albumin extravasation per perfused capillary [(O
/I)/Caps] in isolated rat hearts perfused with a Krebs-albumin-red blo
od cell solution [K(S)RBC], whole rat blood diluted with Krebs buffer
(DWB), leukocyte-free, platelet-rich DWB (LFB), or leukocyte-rich, pla
telet-free DWB (LRB) before and after a 30-min period of global, no-fl
ow ischemia. We found that in isolated hearts perfused with K(B)RBC be
fore ischemia, O/I values were significantly increased (+68%, P < 0.01
) and Caps values were significantly decreased (-25%, P < 0.05) after
25 min of reperfusion. A similar pattern of O/I values (+72%, P < 0.01
) and Caps values (-40%, P < 0.05) was observed in hearts perfused wit
h LFB. These effects were exacerbated in hearts perfused with DWB or L
RB. O/I values were increased 90% (P < 0.01), and Caps values were dec
reased 62% (P < 0.01) in the DWB-perfused hearts. Similar increases in
O/I values (+82%, P < 0.01) and decreases in Caps values (-65%, P < 0
.01) were measured in the LRB-perfused hearts. Additionally, (O/I)/Cap
s values were significantly increased in the hearts perfused with DWB
(+93%, P < 0.01) and LRB (+84%, P < 0.01) compared with the hearts per
fused with K(2)RBC or LFB. These results suggest that interactions bet
ween leukocytes and platelets are not requisite for the development of
coronary microvascular damage early during reperfusion after ischemia
.