Growth of the tambaqui Colossoma macropomum (Cuvier) (Characiformes: Characidae): which is the best model?

Para determinar qual o modelo de crescimento que melhor se ajusta ao tambaqui Colossoma macropomum Cuvier, 1818, foram utilizados 249 e 256 observações de comprimento-idade obtidos por meio de leituras de anéis em otólitos e em escamas, respectivamente, para os mesmos indivíduos. Para tanto, foi utilizado o modelo de Schnute, modelo genérico em que vários modelos tradicionais de crescimento estão incluídos. Com esse procedimento constatou-se que o modelo de von Bertalanffy realmente é o mais adequado, pois se mostrou altamente estável para o conjunto de dados, sendo pouco sensível aos valores iniciais adotados para as estimativas dos parâmetros. Os valores de F' estimados a partir de cinco conjuntos diferentes de dados apresentaram CV = 4.78%, o que não é preocupante, pois as discrepâncias numéricas entre esses valores são conseqüência da alta correlação negativa entre k e L¥ , visto que quando um aumenta o outro diminui e o resultado final expresso por F' permanece praticamente inalterado

Relative participation of adenosine and endothelium derived mediators in coronary reactive hyperemia in the dog

The metabolites that mediate coronary reactive hyperemia have not been definitely identified. Although adenosine and endothelium derived substances seem to be involved, their relative contributions have not been defined yet. In the canine coronary circulation, we studied the relative participation of adenosine, nitric oxide and prostacyclin in reactive hyperemia, by measuring the changes produced by interfering with the synthesis or action of these metabolites. The dose-response curve for flow changes vs intracoronary administration of adenosine was displaced to the right after the inhibition of nitric oxide synthesis with N-omega-nitro-L-arginine, revealing that nitric oxide release partly mediates the vasodilator action of adenosine. The inhibition of PGI-2 synthesis with indomethacin did not modify reactive hyperemia. Interference with adenosine action, by administration of adenosine deaminase plus theophylline, decreased reactive hyperemia by 31.0 +/- 4.0 percent (p < 0.001). Inhibition of nitric oxide synthesis decreased reactive hyperemia by a larger (p < 0.005) magnitude, 41.0 +/- 3.9 percent (p < 0.001), revealing the existence of other stimuli for nitric oxide release in reactive hyperemia besides adenosine. Simultaneous inhibition of nitric oxide and PGI-2 syntheses and of adenosine action reduced reactive hyperemia, but the effect was not additive, reaching 49.5 +/- 4.5 percent of control. Since nitric oxide and adenosine are the most important mediators in reactive hyperemia so far described, our results suggest that other metabolites, acting directly or through mediators other than adenosine or nitric oxide, are responsible for about 50 percent of coronary reactive hyperemia