Effect of vasopressin on a porcine model of persistent pulmonary hypertension of the newborn

Abstract

Background Persistent pulmonary hypertension of the newborn (PPHN) is due to a failure of pulmonary vascular relaxation. Vasopressin, a systemic vasoconstrictor acting on smooth muscle AVPR1a receptors, is used in treatment of PPHN. We sought to determine acute effects of vasopressin infusion on pulmonary hemodynamics in a large animal model of hypoxic PPHN. Methods PPHN was induced in 6 newborn piglets by 72 h normobaric hypoxia (FiO2 = 0.10); controls were 7 age‐matched 3‐day‐old piglets. Animals were anesthetized and ventilated with central venous and arterial lines, and after stabilization, randomized using a crossover design to normoxic or hypoxic ventilation, then 30 min infusion of 0.0012 U/kg/min vasopressin, followed by 45 min vasopressin washout period. Echocardiographic parameters and oxygen consumption were measured before and after vasopressin. Relaxation to vasopressin was tested in isolated PPHN and control pulmonary arteries by isometric myography. Expression of AVPR1a receptor mRNA was quantified in arterial and myocardial tissues. Results Vasopressin did not alleviate hypoxia‐responsiveness of PPHN pulmonary circuit. There were no significant differences in pulmonary hypertension, cardiac function indices, or oxygenation indices after vasopressin infusion. Vasopressin did not dilate control or PPHN pulmonary arteries, and AVPR1 was minimally expressed. Conclusions Vasopressin does not have a direct pulmonary vasodilator effect in PPHN, within the timeframe studied.

Lung ultrasound predicts histological lung injury in a neonatal model of acute respiratory distress syndrome

“…Baseline cardiovascular hemodynamics included heart rate (HR), mean arterial (mBP), and central venous blood pressures (CVP). Functional echocardiography 14 and POCUS scores were obtained at baseline, immediately following lung injury induction, and after 1 hour equilibration of lung injury, using GE Vivid e9 machine with 12 MHz high frequency probe. Pulmonary aeration was imaged in the supine position as three anterior regions and one posterior US region for each lung 15 .…”

Sildenafil protects against pulmonary hypertension induced by hypoxia in neonatal rats via activation of PPARγ‑mediated downregulation of TRPC

“…clinical studies have shown that sildenafil significantly reduces mortality and that it is more effective than placebo in improving oxygenation (1,9). In previous animal studies, large experimental animals, such as newborn sheep and newborn pigs, have been used (31)(32)(33)(34). Sildenafil has rarely been used in neonatal rat models of pulmonary hypertension to the best of our knowledge, but the use of such small animals can reduce the cost and increase the repeatability of the experiments.…”

A New Physiologic Based Integrated Algorithm in the Management of Neonatal Hemodynamic Instability

“…Right ventricle output should be used in cases of a hemodynamically signi cant patent ductus arteriosus (HSPDA) for a more accurate representation of systemic blood ow as LVO, in this case, is more representative of the pulmonary over-circulation (4). Many diseases and factors may decrease SVR and cause vasodilator circulatory shock.…”

“…DO2= LVO× oxygen content = LVO (ml kg/ min) × 1.39×Hb (g/ml) × SpO2 (expressed as a fraction) Right ventricle output should be used in cases of a hemodynamically signi cant patent ductus arteriosus (HSPDA) for a more accurate representation of systemic blood ow as LVO, in this case, is more representative of the pulmonary over-circulation (4).…”