Reynolds J M, McDonagh P F
Department of Pharmacology, Drake University College of Pharmacy, Des Moines, Iowa 50311.
Am J Physiol. 1994 Jan;266(1 Pt 2):H171-81. doi: 10.1152/ajpheart.1994.266.1.H171.
Several studies indicate that leukocytes and platelets exacerbate the compromise of myocardial function that occurs after ischemia-reperfusion (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 (Caps), and transcoronary albumin extravasation per perfused capillary [(O/I)/Caps] in isolated rat hearts perfused with a Krebs-albumin-red blood cell solution [K(2)RBC], whole rat blood diluted with Krebs buffer (DWB), leukocyte-free, platelet-rich DWB (LFB), or leukocyte-rich, platelet-free DWB (LRB) before and after a 30-min period of global, no-flow ischemia. We found that in isolated hearts perfused with K(2)RBC before 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 with LFB. These effects were exacerbated in hearts perfused with DWB or LRB. O/I values were increased 90% (P < 0.01), and Caps values were decreased 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)/Caps values were significantly increased in the hearts perfused with DWB (+93%, P < 0.01) and LRB (+84%, P < 0.01) compared with the hearts perfused with K(2)RBC or LFB. These results suggest that interactions between leukocytes and platelets are not requisite for the development of coronary microvascular damage early during reperfusion after ischemia.
多项研究表明,白细胞和血小板会加剧缺血再灌注(I/R)后发生的心肌功能损害。然而,尚不清楚在缺血后再灌注早期,白细胞和血小板是否都必须存在才能介导冠状动脉微血管损伤。为了研究白细胞和血小板对I/R后微血管损伤的影响,我们测量了在灌注Krebs-白蛋白-红细胞溶液[K(2)RBC]、用Krebs缓冲液稀释的全血(DWB)、无白细胞富含血小板的DWB(LFB)或富含白细胞无血小板的DWB(LRB)的离体大鼠心脏中,经冠状动脉的白蛋白外渗(O/I)、灌注的冠状动脉毛细血管密度(Caps)以及每根灌注毛细血管的经冠状动脉白蛋白外渗[(O/I)/Caps],在30分钟的全心无血流缺血前后进行测量。我们发现,在缺血前用K(2)RBC灌注的离体心脏中,再灌注25分钟后O/I值显著增加(+68%,P<0.01),Caps值显著降低(-25%,P<0.05)。在用LFB灌注的心脏中观察到类似的O/I值(+72%,P<0.01)和Caps值(-40%,P<0.05)变化模式。在用DWB或LRB灌注的心脏中,这些影响加剧。在DWB灌注的心脏中,O/I值增加90%(P<0.01),Caps值降低62%(P<0.01)。在LRB灌注的心脏中测量到类似的O/I值增加(+82%,P<0.01)和Caps值降低(-65%,P<0.01)。此外,与用K(2)RBC或LFB灌注的心脏相比,用DWB(+93%,P<0.01)和LRB(+84%,P<0.01)灌注的心脏中,(O/I)/Caps值显著增加。这些结果表明,白细胞和血小板之间的相互作用并非缺血后再灌注早期冠状动脉微血管损伤发生所必需的。