Different effect of inhaled nitric oxide on yucatan micropig with and without congenital ventricular septal defect.

A strain of Yucatan micropigs is known to have heritable ventricular septal defects (VSDs) and thus may develop overflow pulmonary hypertension. Since inhaled nitric oxide (NO) selectively dilates pulmonary vessels, we determined its hemodynamic and co-agulatory effects in this new animal model. Eight Yucatan micropigs were anesthetized with midazolam, piritramide (a synthetic opioid) and vecuronium bromide. The presence and the size of the VSD were determined by using transesophageal color flow Doppler echocardiography. Four animals showed VSDs of 1-2 mm size. Inhaled NO was then administered with increasing inspired concentrations of 0, 5, 10, 20, 40, 80 and again 0 ppm NO for 10-min periods. NO inhalation did not affect heart rate, right cardiac output, mean arterial pressure, pulmonary arterial wedge pressure, or central venous pressure. Inhaled NO in animals with proven VSDs decreased pulmonary artery pressure (PAP) in a dose dependent manner; 5 ppm NO reduced mean PAP from 25 +/- 2.3 mm Hg to 18 +/- 0.8 mm Hg (p < 0.05), while pulmonary vascular resistance (PVR) decreased from 954 +/- 143 dyn.cm. s-5 to 661 +/- 88 dyn.cm.s-5 (p < 0.01) at the same dose. The maximum reduction in mean PAP and PVR occurred when 80 ppm NO was inhaled. Yucatan micropigs without VSDs did not respond hemodynamically to NO inhalation. Methemoglobin levels remained unchanged during the entire study. Platelet function was assessed according to the method of BREDDIN and BORN (BORN 1962). Initial aggregation and slope were affected when NO inhalation commenced. Yucatan micropigs with VSDs may represent a suitable model for further research of the in vivo effects of inhaled NO.