DIFFERENT EFFECT OF INHALED NITRIC-OXIDE ON YUCATAN MICROPIG WITH ANDWITHOUT CONGENITAL VENTRICULAR SEPTAL-DEFECT

A strain of Yucatan micropigs is known to have heritable ventricular s eptal defects (VSDs) and thus may develop overflow pulmonary hypertens ion. Since inhaled nitric oxide (NO) selectively dilates pulmonary ves sels, we determined its hemodynamic and coagulatory effects in this ne w animal model. Eight Yucatan micropigs were anesthetized with midazol am, piritramide (a synthetic opioid) and vecuronium bromide. The prese nce and the size of the VSD were determined by using transesophageal c olor flow Doppler echocardiography. Four animals showed VSDs of 1-2 mm size. Inhaled NO was then administered with increasing inspired conce ntrations of 0, 5, 10, 20, 40, 80 and again 0 ppm NO for 10-min period s. NO inhalation did not affect heart rate, right cardiac output, mean arterial pressure, pulmonary arterial wedge pressure, or central veno us pressure. Inhaled NO in animals with proven VSDs decreased pulmonar y artery pressure (PAP) in a dose dependent manner; 5 ppm NO reduced m ean PAP from 25 +/- 2.3 mm Hg to 18 +/- 0.8 mm Hg (p < 0.05), while pu lmonary 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. Th e maximum reduction in mean PAP and PVR occurred when 80 ppm NO was in haled. Yucatan micropigs without VSDs did not respond hemodynamically to NO inhalation. Methemoglobin levels remained unchanged during the e ntire study. Platelet function was assessed according to the method of BREDDIN and BORN (BORN 1962). Initial aggregation and slope were affe cted when NO inhalation commenced. Yucatan micropigs with VSDs may rep resent a suitable model for further research of the in vivo effects of inhaled NO.