TY - JOUR
T1 - Interactions between nitric oxide and prostacyclin in myocardial ischemia and endothelial cell cultures.
AU - Schrör, K.
AU - Woditsch, I.
AU - Strobach, H.
AU - Schröder, H.
PY - 1991
Y1 - 1991
N2 - This study investigates biochemical and functional interactions between NO and PGI2 that generate pathways in two different in vitro assays: porcine aortic endothelial cells (PAEC) and reperfused ischemic Langendorff hearts of rabbits. Using cGMP as an index of NO generation and 6-oxo-PGF1 alpha as an index for PGI2 production in endothelial cells, it is demonstrated that the two metabolic pathways for NO and prostacyclin formation act independent of each other. Moreover, NO appears to have an autocrine function in endothelial cells which does not exist with PGI2, probably because of a lack of PGI2 receptors. Endothelial damage in the course of myocardial ischemia is associated with a marked increase in mediator release whose inhibition has consequences for both myocardial and coronary function: inhibition of NO formation also inhibits PGI2 release and the recovery of coronary vessel tone with only minor if any effect on myocardial contractility. In contrast, inhibition of PGI2-generation results in marked deterioration of myocardial recovery with only minor changes in coronary perfusion. It is concluded from these data that PGI2 in endothelial injury is important for preservation of myocardial function while NO might mainly be involved in control of local vessel tone.
AB - This study investigates biochemical and functional interactions between NO and PGI2 that generate pathways in two different in vitro assays: porcine aortic endothelial cells (PAEC) and reperfused ischemic Langendorff hearts of rabbits. Using cGMP as an index of NO generation and 6-oxo-PGF1 alpha as an index for PGI2 production in endothelial cells, it is demonstrated that the two metabolic pathways for NO and prostacyclin formation act independent of each other. Moreover, NO appears to have an autocrine function in endothelial cells which does not exist with PGI2, probably because of a lack of PGI2 receptors. Endothelial damage in the course of myocardial ischemia is associated with a marked increase in mediator release whose inhibition has consequences for both myocardial and coronary function: inhibition of NO formation also inhibits PGI2 release and the recovery of coronary vessel tone with only minor if any effect on myocardial contractility. In contrast, inhibition of PGI2-generation results in marked deterioration of myocardial recovery with only minor changes in coronary perfusion. It is concluded from these data that PGI2 in endothelial injury is important for preservation of myocardial function while NO might mainly be involved in control of local vessel tone.
UR - http://www.scopus.com/inward/record.url?scp=0025987627&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025987627&partnerID=8YFLogxK
U2 - 10.1007/978-3-642-72461-9_13
DO - 10.1007/978-3-642-72461-9_13
M3 - Article
C2 - 1659372
AN - SCOPUS:0025987627
SN - 0300-8428
VL - 86 Suppl 2
SP - 117
EP - 125
JO - Basic research in cardiology
JF - Basic research in cardiology
ER -