Physical training limits the fall of blood pressure and the endothelium overactivation in acute myocardial infarction
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
9085347
Knihovny.cz E-zdroje
- MeSH
- akutní nemoc MeSH
- aorta fyziologie MeSH
- cévní endotel metabolismus fyziologie MeSH
- hypotenze patofyziologie MeSH
- infarkt myokardu patofyziologie prevence a kontrola MeSH
- kondiční příprava zvířat fyziologie MeSH
- koronární cirkulace fyziologie MeSH
- krysa rodu Rattus MeSH
- oxid dusnatý metabolismus MeSH
- potkani Wistar MeSH
- vazodilatace fyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- oxid dusnatý MeSH
Physical training (PT) is beneficial in cardiovascular diseases associated with NO deficiency such as coronary disease, hypertension, etc. However, it is not known whether PT can also prevent pathological conditions associated with excess NO and fall of blood pressure (BP) such as acute myocardial infarction (AMI). The aim was to compare the effect of AMI on BP and functional state of the endothelium in rats trained by swimming and in untrained animals. After AMI, BP fell from 110 +/- 2 to 74 +/- 4 mm Hg (p < 0.05), the endothelium-dependent relaxation increased from 37 +/- 4 to 66 +/- 6% (p < 0.05) and the extent of contraction suppression by the endothelium was significantly greater than in the controls. PT itself increased the endothelium-dependent relaxation of rat aorta but left BP unaffected. PT limited the AMI-induced fall of BP to 87 +/- 3 mm Hg, the endothelium- dependent relaxation to 53 +/- 4% and prevented the hyporesponsiveness of the aorta to norepinephrine. We suggest that the protective effect of PT is related to inhibition of inducible NO synthase by a negative feedback mechanism.