Endothelial dysfunction in rat mesenteric artery after regional cardiac ischaemia–reperfusion

Abstract

In most previous studies, ischaemia-reperfusion (I/R)-induced vascular injury referred to injury in the tissue or blood vessel that was directly subjected to I/R. However, less attention has been focused on remote vascular injury that might be caused by cardiac I/R. In the present study, we aimed to assess whether cardiac I/R could affect vasoconstriction and vasodilatation in mesenteric arteries from Sprague-Dawley rats. Left anterior descending coronary arteries from adult male Sprague-Dawley rats were occluded (60 min) and then reperfused (120 min). Changes in haemodynamic parameters indicated that this procedure caused evident cardiac dysfunction. In mesenteric arteries isolated from the animals, cardiac I/R significantly increased the maximal contractions in response to KCl, 5-hydroxytryptamine, phenylephrine and U46619 and decreased the maximal relaxation in response to acetylcholine, but not to sodium nitroprusside, compared with sham-operated animals. The nitric oxide synthase inhibitor l-NAME abolished differences of contractile responses to phenylephrine between sham-operated and I/R rats. The antioxidant N -acetyl-l-cysteine reversed the impairment of acetylcholinestimulated vasodilatation induced by regional cardiac I/R. However, l-NAME caused a similar degree of inhibition of acetylcholine-stimulated relaxation in mesenteric arteries from shamoperated and I/R rats. Electron microscopy revealed that mesenteric arterial endothelial structure was degraded in the I/R group and that N -acetyl-l-cysteine treatment prevented this structural damage. In conclusion, regional cardiac I/R caused by transient occlusion and reperfusion of the left anterior descending coronary artery results in peripheral vascular endothelial dysfunction.

Soy Isoflavone Protects Myocardial Ischemia/Reperfusion Injury through Increasing Endothelial Nitric Oxide Synthase and Decreasing Oxidative Stress in Ovariectomized Rats

“…More intriguingly, cardiac I/R causes not only myocardial but also vascular injury [ 56 ]. It has also been proposed that reperfusion induced endothelial dysfunction, characterized by decreased endothelium-dependent vasodilatation [ 57 ]. Studies have displayed a potential role of ROS in endothelial dysfunction [ 58 , 59 ].…”

Delayed preconditioning prevents ischemia/reperfusion-induced endothelial injury in rats: role of ROS and eNOS

“…At the end of the equilibration period, the contractile capacity of each ring was tested by exposure to a high-K þ Krebs' solution (obtained by equimolar replacement of NaCl by KCl in the Krebs' solution), and the ring was considered viable and used for experiments only if two reproducible high-K þ contractions were obtained. 20,22 Vascular Reactivity Studies Endothelium-dependent and -independent relaxations were assessed by measuring the dilatory responses of mesenteric arteries to cumulative concentrations of acetylcholine (ACh; 10 À 10 -10 À 5 mol/l) and sodium nitroprusside (SNP; 10 À 10 -10 À 5 mol/l), respectively. All experiments were performed in vessels pre-contracted with phenylephrine (PE; 10 mmol/l).…”

“…19,20 Organ chambers (2-ml volume) were filled with the Krebs' solution (37 1C and gassed with 95% air and 5% CO 2 ; pH 7.4). Each ring was mounted on two L-shape stainless-steel holders, one of which was fix to the organ bath and the other connected to a force displacement transducer (Beijing Aeromedicine Engineering Research Institute, Beijing, China) attached to a Taimeng BL-420 biotic signal collection and analysis system (Taimeng Instruments, Chengdu, China) for continuous recording of isometric tension.…”

“…In addition, disturbance in peripheral vascular resistance are basic contributors to different cardiovascular pathologies and mesenteric arteries are an essential constituent of peripheral resistance vessels. [18][19][20] Therefore, the aim of this study was to investigate the effects of delayed IPC on endothelial function and morphology, as well as the involvement of ROS in mesenteric resistance arteries. The activation of phosphatidylinositol 3-kinase (PI3K)/Akt/eNOS signaling pathway as possible mechanism recruited by IPC in the peripheral arteries was also assessed.…”

Normobaric, intermittent hypoxia conditioning is cardio- and vasoprotective in rats

“…63 Recently, we reported that myocardial infarction caused endothelial dysfunction in rat aorta, 64 and Zhao et al showed that myocardial IR produced endothelial dysfunction in mesentery vessels. 51 Accordingly, endothelial dysfunction was studied in the coronary circulation and the aorta of rat hearts with IR. At both sites, there was marked endothelial dysfunction, as reflected by the attenuated vasodilatory response to acetylcholine after IR.…”