The Change of Vascular Reactivity in Rat Thoracic Aorta 3 Days afterAcute Myocardial Infarction.
- Author:
Sub LEE
1
;
Woon Seok ROH
;
Jae Seok JANG
;
Chi Hoon BAE
;
Ki Sung PARK
;
Jong Tae LEE
Author Information
1. Department of Thoracic and Cardiovascular Surgery, Daegu Catholic University Medical Center, Korea. leesub@cu.ac.kr
- Publication Type:Original Article
- Keywords:
Ischemia/reperfusion injury;
Nitric oxide;
Endothelium;
Vascular tone and reactivity
- MeSH:
Acetylcholine;
Animals;
Aorta, Thoracic;
Blood Pressure;
Coronary Vessels;
Cyclic GMP;
Endothelium;
Heart Rate;
Indomethacin;
Myocardial Infarction;
NG-Nitroarginine Methyl Ester;
Nitric Oxide;
Nitric Oxide Synthase;
Nitric Oxide Synthase Type III;
Nitroprusside;
Phenylephrine;
Plasma;
Prostaglandin-Endoperoxide Synthases;
Radioimmunoassay;
Rats;
Real-Time Polymerase Chain Reaction;
Relaxation;
RNA, Messenger;
Salicylamides;
Up-Regulation
- From:The Korean Journal of Thoracic and Cardiovascular Surgery
2009;42(5):576-587
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The up-regulation of the nitric oxide (NO)-cGMP pathway might be involved in the change of vascular reactivity in rats 3 days after they suffer acute myocardial infarction. However, the underlying mechanism for this has not been clarified. MATERIAL AND METHOD: Acute myocardial infarction (AMI) was induced by occluding the left anterior descending coronary artery (LAD) for 30 min (Group AMI), whereas the sham-operated control rats were treated similarly without LAD occlusion (Group SHAM). The concentration-response relationships for phenylephrine (PE), KCl, acetylcholine (Ach) and sodium nitroprusside (SNP) were determined in the endothelium intact E(+) and endothelium denuded E(-) thoracic aortic rings from the rats 3 days after AMI or a SHAM operation. The concentration-response relationships of PE in the E(+) rings from the AMI rats were compared with those relationships in the rings pretreated with nitric oxide synthase (NOS) inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) or the cyclooxygenase inhibitor indomethacin. The plasma nitrite/nitrate concentrations were checked via a Griess reaction. The cyclic GMP content in the thoracic aortic rings was measured by radioimmunoassay and the endothelial nitric oxide synthase (eNOS) mRNA expression was assessed by real time PCR. RESULT: The mean infarct size (%) in the rats with AMI was 21.3+/-0.62%. The heart rate and the systolic and diastolic blood pressure were not significantly changed in the AMI rats. The sensitivity of the contractile response to PE and KCl was significantly decreased in both the E(+) and E(-) aortic rings of the AMI group (p<0.05). L-NAME completely reversed these contractile responses whereas indomethacin did not (p<0.05). Moreover, the sensitivity of the relaxation response to Ach was also significantly decreased in the AMI group (p<0.05). The plasma nitrite and nitrate content (p<0.05), the basal cGMP content (p<0.05) and the eNOS mRNA expression (p=0.056) in the AMI rats were increased as compared with the SHAM group. CONCLUSION: Our findings indicate that the increased eNOS activity and the up-regulation of the NO-cGMP pathway can be attributed to the decreased contractile or relaxation response in the rat thoracic aorta 3 days after AMI.
