Non-specific Inhibitors Of Nitric Oxide Synthase Cause Myocardial Necrosis In The Rat.

dc.creatorMoreno Júnior, H
dc.creatorNathan, L P
dc.creatorMetze, K
dc.creatorCosta, S K
dc.creatorAntunes, E
dc.creatorHyslop, S
dc.creatorZatz, R
dc.creatorde Nucci, G
dc.date1997-May
dc.date2015-11-27T12:18:56Z
dc.date2015-11-27T12:18:56Z
dc.date.accessioned2018-03-29T00:52:11Z
dc.date.available2018-03-29T00:52:11Z
dc.identifierClinical And Experimental Pharmacology & Physiology. v. 24, n. 5, p. 349-52, 1997-May.
dc.identifier0305-1870
dc.identifier
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/9143786
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/194021
dc.identifier9143786
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1294254
dc.description1. To study the effect of acute nitric oxide (NO) inhibition on the rat heart both in vitro and in vivo, male Wistar rats received a single bolus injection of saline, N omega-nitro-L-arginine methyl ester (L-NAME; 0.5, 1.5, 5.0, 15.0 and 45.0 mg/kg) and D-NAME (45.0 mg/kg). 2. Animals were killed 72 h after the bolus injection of L-NAME and the hearts were removed and studied under light microscopy. In other groups of animals; saline, L-NAME and D-NAME were administered as above and the mean arterial blood pressure (MABP/carotid) was recorded. Furthermore, L-NAME was also administered in the drinking water (20 mg/kg per day) for 72 h and animals were then killed and their hearts evaluated as described above. Hearts of control animals were perfused in vitro and coronary flow was measured following saline, L-NAME (45 micrograms/heart) and D-NAME (45 micrograms/heart). 3. Areas of necrosis were observed in the left ventricle of animals that had received L-NAME at 5.0, 15.0 and 45.0 mg/kg. Also, only doses higher than 1.5 mg/kg caused an important increase in MABP. The frequency and extent of the lesions paralleled the dose of L-NAME administered and no lesions were observed in D-NAME- and saline-treated animals. 4. The oral administration of L-NAME also caused myocardial lesions similar to those described above, but the frequency and extent of these lesions were more discrete compared with those observed following 5.0 mg/kg, i.v., L-NAME. 5. Bolus injection of L-NAME into control rat hearts in vitro resulted in a small and transient fall in coronary flow (17.2 +/- 1.4 and 12.2 +/- 1.2 mL/min before and after L-NAME administration, respectively) within 30 s and this was followed 4.5 min later by a further (11.5 +/- 1.6 mL/min) decrease. The administration of D-NAME to control hearts caused no change in coronary flow. 6. In conclusion, the acute inhibition of NO biosynthesis by L-NAME causes myocardial necrosis. Both high levels of MABP and a small but significant reduction in coronary flow (associated or not) can be responsible for the lesions we found.
dc.description24
dc.description349-52
dc.languageeng
dc.relationClinical And Experimental Pharmacology & Physiology
dc.relationClin. Exp. Pharmacol. Physiol.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAnimals
dc.subjectBlood Pressure
dc.subjectCoronary Circulation
dc.subjectEnzyme Inhibitors
dc.subjectMale
dc.subjectMyocardial Infarction
dc.subjectMyocardium
dc.subjectNg-nitroarginine Methyl Ester
dc.subjectNecrosis
dc.subjectNitric Oxide Synthase
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectStereoisomerism
dc.titleNon-specific Inhibitors Of Nitric Oxide Synthase Cause Myocardial Necrosis In The Rat.
dc.typeArtículos de revistas


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