Coronary artery endothelial cell and smooth muscle dysfunction after global myocardial ischemia

The role of the endothelium in the regulation of vascular smooth muscle cell contractions induced by angiotensin II after ischemia and reperfusion

“…The increase in tonic smooth muscle tension after ischemia/reperfusion leads to an uncontrolled increase in [Ca 2+ ] i , damage to both endothelium and smooth muscle, and, as a consequence, disturbances in the balance between vasoconstricting and vasorelaxating factors (Corr et al, 1981;Dignan et al, 1992;. It has been shown that ischemia/reperfusion causes endothelial dysfunction, which leads to reduction of synthesis of endothelial vasorelaxing agents such as NO and prostaglandins (Corr et al, 1981;Dignan et al, 1992;Fullerton et al, 1993aFullerton et al, , 1993b. Under these conditions, vasorelaxation in reaction to acetylcholine, bradykinin, ADP, serotonin and thrombin is impaired, while the effects of NO, sodium nitroprusside and nitrates remain unchanged (Corr et al, 1981;Dauber et al, 1990;Lombard et al, 1999).…”

“…Ischemia and subsequent reperfusion cause an increase in blood vessel resistance and reduced perfusion of transplanted organs (Dauber et al, 1990;Dignan et al, 1992;. The increase in tonic smooth muscle tension after ischemia/reperfusion leads to an uncontrolled increase in [Ca 2+ ] i , damage to both endothelium and smooth muscle, and, as a consequence, disturbances in the balance between vasoconstricting and vasorelaxating factors (Corr et al, 1981;Dignan et al, 1992;.…”

“…Ischemia and subsequent reperfusion cause an increase in blood vessel resistance and reduced perfusion of transplanted organs (Dauber et al, 1990;Dignan et al, 1992;. The increase in tonic smooth muscle tension after ischemia/reperfusion leads to an uncontrolled increase in [Ca 2+ ] i , damage to both endothelium and smooth muscle, and, as a consequence, disturbances in the balance between vasoconstricting and vasorelaxating factors (Corr et al, 1981;Dignan et al, 1992;. It has been shown that ischemia/reperfusion causes endothelial dysfunction, which leads to reduction of synthesis of endothelial vasorelaxing agents such as NO and prostaglandins (Corr et al, 1981;Dignan et al, 1992;Fullerton et al, 1993aFullerton et al, , 1993b.…”

Endothelial Function Related to Vascular Tone in Cardiac Surgery

“…Studies from other laboratories and our own, in contrast, have shown that crystalloid hyperkalemic cardioplegia does not significantly affect the NO-related, endothelium-dependent relaxation for up to 4 h. 17,18, 28 We have good reasons, therefore, to believe that widely used hyperkalemic cardioplegia containing moderate hyperkalemia has little effect on the NO-related function during the usual cardiac arrest time (1-2 h). The major cause of injury to the NO-related function is due to the ischemia-reperfusion injury to the coronary endothelial function 16 but not due to the cardioplegia, per se. Therefore, in order to protect the NO-related endothelial function, prevention of ischemia-reperfusion injury should be the primary concern.…”

“…There are numerous studies on endothelial function during cardioplegic arrest in cardiac surgery. [13][14][15][16][17][18][19][20][21][22][23][24][25][26] Some of these studies suggest that the endothelial function related to NO is damaged during this period. 13 However, in most of these studies, the effect of ischemia-reperfusion and the effect of cardioplegia are combined and the measurement is often the coronary flow in the perfused heart.…”