Korean J Thorac Cardiovasc Surg.  2009 Oct;42(5):576-587.

The Change of Vascular Reactivity in Rat Thoracic Aorta 3 Days afterAcute Myocardial Infarction

Affiliations
  • 1Department of Thoracic and Cardiovascular Surgery, Daegu Catholic University Medical Center, Korea. leesub@cu.ac.kr
  • 2Department of Anesthesiology and Pain Medicine, School of Medicine, Catholic University of Daegu, Korea.
  • 3Department of Thoracic and Cardiovascular Surgery, Kyungpook University Hospital, Korea.

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.

Keyword

Ischemia/reperfusion injury; Nitric oxide; Endothelium; Vascular tone and reactivity

MeSH Terms

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
Acetylcholine
Cyclic GMP
Indomethacin
NG-Nitroarginine Methyl Ester
Nitric Oxide
Nitric Oxide Synthase
Nitric Oxide Synthase Type III
Nitroprusside
Phenylephrine
Prostaglandin-Endoperoxide Synthases
RNA, Messenger
Salicylamides
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