dc.creator | Moreno, H | |
dc.creator | Nathan, LP | |
dc.creator | Metze, K | |
dc.creator | Costa, SKP | |
dc.creator | Antunes, E | |
dc.creator | Hyslop, S | |
dc.creator | Zatz, R | |
dc.creator | deNucci, G | |
dc.date | 1997 | |
dc.date | MAY | |
dc.date | 2014-12-16T11:36:25Z | |
dc.date | 2015-11-26T16:22:38Z | |
dc.date | 2014-12-16T11:36:25Z | |
dc.date | 2015-11-26T16:22:38Z | |
dc.date.accessioned | 2018-03-28T23:04:07Z | |
dc.date.available | 2018-03-28T23:04:07Z | |
dc.identifier | Clinical And Experimental Pharmacology And Physiology. Blackwell Science, v. 24, n. 5, n. 349, n. 352, 1997. | |
dc.identifier | 0305-1870 | |
dc.identifier | WOS:A1997WX25800010 | |
dc.identifier | 10.1111/j.1440-1681.1997.tb01200.x | |
dc.identifier | http://www.repositorio.unicamp.br/jspui/handle/REPOSIP/62080 | |
dc.identifier | http://www.repositorio.unicamp.br/handle/REPOSIP/62080 | |
dc.identifier | http://repositorio.unicamp.br/jspui/handle/REPOSIP/62080 | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1268124 | |
dc.description | 1. 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 mu g/heart) and D-NAME (45 mu g/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.description | 24 | |
dc.description | 5 | |
dc.description | 349 | |
dc.description | 352 | |
dc.language | en | |
dc.publisher | Blackwell Science | |
dc.publisher | Carlton | |
dc.publisher | Australia | |
dc.relation | Clinical And Experimental Pharmacology And Physiology | |
dc.relation | Clin. Exp. Pharmacol. Physiol. | |
dc.rights | fechado | |
dc.source | Web of Science | |
dc.subject | arterial hypertension | |
dc.subject | coronary flow | |
dc.subject | ischaemic cardiopathy | |
dc.subject | myocardial infarctions | |
dc.subject | N-omega-nitro-L-arginine methyl ester | |
dc.subject | syndrome X | |
dc.subject | Angina | |
dc.subject | Model | |
dc.title | Non-specific inhibitors of nitric oxide synthase cause myocardial necrosis in the rat | |
dc.type | Artículos de revistas | |