Improvement in oxygen tensions and pulmonary blood flow with intermittent distal aortic compression during normoxia, hypoxic hypoxia, and hyperoxia in neonatal piglets.
METHODS
We investigated the hypothesis that, in a newborn piglet during normoxia, hypoxia, and hyperoxia, increasing aortic pressure transiently by intermittent short-duration aortic compression would affect left-to-right shunting of blood and thus increase pulmonary artery blood flow, pulmonary arterial PO2, and aortic PO2 proximal to the point of compression. We also investigated whether a balloon atrial septostomy, by providing an open channel for communication between the right- and left-sided circulations, would further improve pulmonary blood flow and aortic PO2. Studies were performed in eight 7- to 10-day-old newborn piglets in three phases (FIO2 of 0.21, 0.12, and 1.0) before and after balloon arterial septostomy in each piglet. Blood gas measurements and hemodynamic variables were recorded before and at the end of a 30-sec period of aortic compression.


RESULTS
During aortic compression, all the animals demonstrated a 50 to 70 mm Hg increase in aortic pressure proximal to the compression. Before balloon septostomy, there were 21%, 41%, and 8% increases in aortic PO2 in the room air, hypoxic, and hyperoxic phases of the experiment, respectively. There were also statistically significant increments in pulmonary blood flow and arterial pressures. After balloon septostomy, there were 35%, 25%, and 21% increments in aortic PO2 during the room air, hypoxic, and hyperoxic phases of the experiment, respectively. However, there was no statistically significant further improvement in the effects of aortic compression on PO2 with septostomy compared with those effects before septostomy.


CONCLUSIONS
Our results suggest that increasing systemic arterial pressures in order to forcibly affect left-to-right shunting of blood may be potentially beneficial in the management of hypoxia in situations where low pulmonary artery blood flow may be contributing to hypoxia, e.g., in persistent pulmonary hypertension of the newborn.
Ghai
V
V
Department of Pediatrics, University of Illinois College of Medicine, Chicago.
Del Nido
P
P
Nakamura
H
H
Fujii
Y
Y
Vidyasagar
D
D
Wilson
G
G
D000818:Animals; D000831:Animals, Newborn / Q000097:blood / Q000502:physiology*; D001013:Aorta, Thoracic / Q000503:physiopathology*; D002404:Catheterization; D003250:Constriction; D005260:Female; D006325:Heart Atria; D006439:Hemodynamics; D006801:Humans; D000860:Hypoxia / Q000097:blood; D007231:Infant, Newborn; D008297:Male; D010100:Oxygen / Q000097:blood / Q000502:physiology*; D010547:Persistent Fetal Circulation Syndrome / Q000097:blood / Q000503:physiopathology*; D011652:Pulmonary Circulation; D013552:Swine
D010100:Oxygen