title: The effect of acute hypoxaemia on ventricular function during beta-adrenergic and cholinergic blockade in the fetal sheep.
abstract: The effect of acute hypoxaemia on right and left ventricular function was investigated in 8 fetal sheep (137-140 days gestation). Fetuses were instrumented with electromagnetic flow sensors on the ascending aorta and the main pulmonary artery. After 8 days recovery, hypoxaemia was achieved by reducing the maternal ewe's inspired O2 concentration to 13.1 +/- 1.5%. Control and hypoxaemic arterial blood values were pH 7.37 +/- 0.04 (SD) and 7.35 +/- 0.06, PCO2 48.0 +/- 2.8 and 47.6 +/- 5.1 mmHg, PO2 19.9 +/- 2.2 and 11.4 +/- 1.5 mmHg, haematocrit 37.5 +/- 1.2 and 39.5 +/- 2.2, respectively. Arterial pressure increased insignificantly with acute hypoxaemia (50.2 +/- 3.9 to 53.6 +/- 8.1 mmHg). Left and right ventricular performance was assessed by generating biventricular function curves relating stroke volume to mean atrial pressure. All function curves were composed of steep ascending and plateau limbs that intersected at a breakpoint. Comparing control and hypoxaemia function curves, the left ventricular stroke volume breakpoints were 0.79 +/- 0.20 and 0.78 +/- 0.21 ml/kg, respectively, while the right ventricular stroke volume breakpoints were 0.99 +/- 0.11 and 0.88 +/- 0.21 ml/kg (n.s.). In 4 fetuses, acute hypoxaemia was associated with significant increases in arterial blood pressure (P less than 0.05). In these fetuses, the right ventricular function curve was shifted significantly downward compared to the control right ventricular curve. When nitroprusside was given to these hypertensive fetuses to return blood pressure to control levels, the right ventricular function curve returned to baseline. We conclude that even under conditions of extreme hypoxaemia, ventricular function is well preserved in the normotensive fetal sheep. However, when increases in arterial pressure also accompany hypoxaemia, detectable changes in right ventricular function can be accounted for by changes in arterial pressure.
authors.affiliation: Department of Pediatrics, Oregon Health Sciences University, Portland 97201.
authors.forename: M D
authors.initials: MD
authors.lastname: Reller
authors.forename: M J
authors.initials: MJ
authors.lastname: Morton
authors.forename: G D
authors.initials: GD
authors.lastname: Giraud
authors.forename: D L
authors.initials: DL
authors.lastname: Reid
authors.forename: K L
authors.initials: KL
authors.lastname: Thornburg
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D005333:Fetus / Q000502:physiology*; D005865:Gestational Age; D006352:Heart Ventricles / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology; D010100:Oxygen / Q000008:administration & dosage / Q000097:blood; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology*; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000502:physiology*; D012756:Sheep; D013318:Stroke Volume / Q000502:physiology
chemical_list: D011943:Receptors, Adrenergic, beta; D011950:Receptors, Cholinergic; D009599:Nitroprusside; D010100:Oxygen