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Pulmonary arterial pressure and electrocardiograms in broiler chickens infused intravenously with L-NAME, an inhibitor of nitric oxide synthase, or sodium nitroprusside (SNP), a nitric oxide donor

1. Broilers were divided at 42 to 44 d of age into a Control group ( n =30) and a Treatment group ( n =30). The mean pulmonary arterial pressure (mPAP) and electrocardiogram (ECG) leads II and aV F were measured 1, 2 and 4 h after an intravenous injection of 0.9% saline (Control group) or Nω -nitro-L-arginine methyl esther (L-NAME), an inhibitor of nitric oxide synthase and thus an inhibitor of endothelial nitric oxide (NO) production (Treatment group). 2. At 1 and 2 h but not 4 h post-injection, L-NAME significantly increased the mPAP and the amplitudes of the ECG S-wave and RS-wave leads II and aV F when compared with Control values. 3. The correlation coefficients between the mPAP and the ECG S-wave and RS-wave amplitudes for lead II within the Treatment group were-0.848 and-0.553 at 1 h and-0.798 and-0.512 at 2 h, respectively. The corresponding coefficients for lead aV F were-0.735, -0.596, -0.663 and-0.724, respectively. 4. After suitable mPAP and ECG values had been recorded at each time interval, sodium nitroprusside (SNP), which acts as a short-lived NO donor molecule, was injected intravenously via a right-cardiac catheter. Within 5 min after the SNP injection, the mPAP and the ECG lead II S-wave and RSwave amplitudes were transiently reduced to levels that, at 1 and 2 h after L-NAME injection, did not differ from Control values. Within 10 min after the SNP injection, all values returned to the levels previously induced by L-NAME. 5. These results demonstrate that L-NAME increased the myocardial contractility and PAP, whereas SNP transiently reversed the effects of L-NAME on myocardial contractility and PAP. It appears likely from these results that the pulmonary vascular endothelium releases NO that in turn reduces the pulmonary vascular resistance or attenuates myocardial contractility in broiler chickens.