title: Platelets do not modulate leukocyte-mediated coronary microvascular damage during early reperfusion.
abstract: 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.
authors.affiliation: Department of Pharmacology, Drake University College of Pharmacy, Des Moines, Iowa 50311.
authors.forename: J M
authors.initials: JM
authors.lastname: Reynolds
authors.forename: P F
authors.initials: PF
authors.lastname: McDonagh
mesh_terms: D000818:Animals; D001792:Blood Platelets / Q000502:physiology*; D001808:Blood Vessels / Q000473:pathology / Q000503:physiopathology; D002199:Capillary Permeability; D003326:Coronary Circulation / Q000502:physiology*; D006439:Hemodynamics; D066298:In Vitro Techniques; D007962:Leukocytes / Q000502:physiology*; D008297:Male; D008833:Microcirculation / Q000502:physiology; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012709:Serum Albumin / Q000378:metabolism
chemical_list: D012709:Serum Albumin