Volume 54, Issue 3 pp. 319-332
ORIGINAL ARTICLE: PULMONARY HYPERTENSION

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

Reem Amer

Reem Amer

Section of Neonatology, Department of Pediatrics, University of Manitoba, Winnipeg, Canada

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Yasser N. Elsayed

Yasser N. Elsayed

Section of Neonatology, Department of Pediatrics, University of Manitoba, Winnipeg, Canada

Biology of Breathing Group, Children's Hospital Research Institute of Manitoba, Winnipeg, Canada

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Marjory Ruth Graham

Marjory Ruth Graham

Biology of Breathing Group, Children's Hospital Research Institute of Manitoba, Winnipeg, Canada

Departments of Anesthesia, University of Manitoba, Winnipeg, Canada

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Anurag S. Sikarwar

Anurag S. Sikarwar

Departments of Oral Biology, University of Manitoba, Winnipeg, Canada

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Martha Hinton

Martha Hinton

Biology of Breathing Group, Children's Hospital Research Institute of Manitoba, Winnipeg, Canada

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Shyamala Dakshinamurti

Corresponding Author

Shyamala Dakshinamurti

Section of Neonatology, Department of Pediatrics, University of Manitoba, Winnipeg, Canada

Biology of Breathing Group, Children's Hospital Research Institute of Manitoba, Winnipeg, Canada

Departments of Physiology, University of Manitoba, Winnipeg, Canada

Correspondence

Shyamala Dakshinamurti, MD MSc, Pediatrics and Physiology, University of Manitoba, Section of Neonatology, WS012 Women's Hospital, 735 Notre Dame Ave, Winnipeg, Canada R3E 0L8

Email: [email protected]

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First published: 15 January 2019
Citations: 8

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.

CONFLICTS OF INTEREST

No financial ties or conflicts of interest to disclose.

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