Coronary vasomotor disorders during hypoxia-reoxygenation: do calcium channel blockers play a protective role?
During heart surgery, myocardial dysfunction may occasionally appear when extracorporeal circulation is discontinued, causing serious haemodynamic disorders. Many mechanisms are involved in this hypoxia-reoxygenation syndrome. The aim of this experimental study was to characterize the vasomotor disorders that take place in the isolated porcine coronary artery during in vitro hypoxia-reoxygenation and to analyse the effect of nifedipine on them. Rings of porcine coronary artery were placed in an organ chamber connected to a system that recorded isometric forces. The vascular rings were divided into two groups: control group (no nifedipine) and study group (nifedipine, 10(-6) mol/l). The vascular rings were precontracted with 30 mmol/l KCl and then hypoxia-reoxygenation was induced. Control arterial rings showed important changes in coronary vasomotor tone: severe hypoxic contraction (from 14.48+/-1.16 g of stable contraction to 17.6+/-0.44 g after the imposition of hypoxia), and transient vasodilation during reoxygenation (69.9+/-10.1% of the maximum contraction achieved). The nifedipine group experienced a slow, progressive, vasodilation throughout the whole experiment (73+/-3.5% of the maximum contraction). Neither hypoxic vasospasm nor fluctuations of the coronary vascular tone occurred. Thus, at the end of the hypoxia, the control vessels presented a degree of contraction similar to the initial level. However, in the rings treated with nifedipine, the percentage of dilation was 73+/-3.5% (P<0.05). In the isolated porcine coronary artery with intact endothelium undergoing a situation of hypoxia-reoxygenation, we have detected transient vasoconstriction during the first period of hypoxia, followed by vasodilation during reoxygenation. The intracoronary administration of nifedipine prior to the imposition of hypoxia prevents hypoxic contraction, achieving a greater and more stable degree of coronary vasorelaxation during the complete process of hypoxia-reoxygenation.
Ordoñez Fernández
A
A
Cardiac Transplant Unit, Virgen del Rocio University Hospital, Seville, Spain.
Hernandez Fernandez
A
A
Borrego Dominguez
J M
JM
Gutierrez Carretero
E
E
Muñoz García
J
J
Prieto Rodriguez
M F
MF
Viloria Peñas
M M
MM
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D003326:Coronary Circulation / Q000187:drug effects; D003329:Coronary Vasospasm / Q000188:drug therapy* / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D000860:Hypoxia / Q000188:drug therapy / Q000503:physiopathology; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D015425:Myocardial Reperfusion / Q000009:adverse effects*; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000503:physiopathology; D009543:Nifedipine / Q000494:pharmacology*; D013552:Swine; D014661:Vasoconstriction / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects
D002121:Calcium Channel Blockers; D000244:Adenosine Diphosphate; D009543:Nifedipine