Significance of right ventricular filling for left ventricular enddiastolic pressure-volume relationship under acute hypoxia in the dog.
In 14 closed-chest dogs, the significance of right ventricular filling for left ventricular enddiastolic pressure-volume relationship was investigated under acute hypoxia by means of single plane cineventriculography and simultaneous intraventricular pressure recording. Both after 5 min asphyxia (respirator switched off) (n = 5) and after 3 min hypoxia (ventilation with pure N2) (n = 9), there was a significant leftward shift (p less than 0.005) of the left ventricular enddiastolic pressure-volume curve as compared to the control curves under normoxia. To simulate the elevated filling of the right ventricle under acute hypoxia, rapid intraventricular infusion was applied under normoxic conditions to raise right ventricular enddiastolic pressure to the same values as that measured under hypoxia. The extent of the ensuing leftward shift of the left ventricular enddiastolic pressure-volume curve was on average 60% of the shift under hypoxia in both sets of experiments. Neither the slope of the relationship between volume stiffness and enddiastolic pressure, nor the relationship between tangent elastic modulus and left ventricular wall stress, was affected by hypoxia or asphyxia. Thus, the shift of the left ventricular enddiastolic pressure-volume curve in the early stage of hypoxia is predominantly due to the influence of increased right ventricular filling. Since the increased volume of the atria under acute hypoxia limits left ventricular distensibility additionally, the changes in left ventricular enddiastolic pressure-volume relationships observed in the early stage of hypoxia are mainly, or even entirely, the result of interaction of the various heart compartments, and not a reflection of alterations in myocardial tissue elasticity.
D000818:Animals; D001794:Blood Pressure; D002306:Cardiac Volume; D003971:Diastole; D004285:Dogs; D005069:Evaluation Studies as Topic; D006352:Heart Ventricles / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D009200:Myocardial Contraction; D010100:Oxygen / Q000097:blood
D010100:Oxygen