title: Coronary hypertension and diastolic compliance in isolated rabbit hearts.
abstract: Acute pulmonary edema during hypertensive crisis has been attributed to acute left ventricular systolic failure secondary to increased afterload. We tested the hypothesis that the increase in coronary artery perfusion pressure associated with systemic hypertension could also contribute to increased left ventricular filling pressures by acutely increasing coronary intravascular volume and decreasing left ventricular diastolic compliance. Isolated isovolumic (balloon in left ventricle) normal rabbit hearts (n = 13) with pericardium removed and right ventricle vented were blood perfused at an initial coronary artery perfusion pressure of 100 mm Hg; left ventricular balloon volume was adjusted to produce an initial left ventricular end-diastolic pressure of 15 +/- 1 mm Hg; left ventricular systolic pressure was 102 +/- 3 mm Hg. When coronary perfusion pressure was increased to 130 +/- 1 mm Hg to simulate a hypertensive crisis, coronary flow increased from 2.0 +/- 0.2 to 3.0 +/- 0.2 ml/min/g left ventricle (p less than 0.001), left ventricular systolic pressure increased to 116 +/- 4 mm Hg, and isovolumic left ventricular end-diastolic pressure increased to 21 +/- 1 mm Hg (p less than 0.001), which indicated a decrease in left ventricular diastolic compliance. When coronary perfusion pressure was decreased to a physiological level of 70 mm Hg, coronary flow rate decreased to 1.4 +/- 0.1 ml/min/g left ventricle (p less than 0.001), left ventricular systolic pressure fell to 82 +/- 4 mm Hg, and left ventricular end-diastolic pressure fell to 14 +/- 1 mm Hg (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Cardiovascular Institute, Boston University School of Medicine, Massachusetts.
authors.forename: L F
authors.initials: LF
authors.lastname: Wexler
authors.forename: W N
authors.initials: WN
authors.lastname: Grice
authors.forename: M
authors.initials: M
authors.lastname: Huntington
authors.forename: J F
authors.initials: JF
authors.lastname: Plehn
authors.forename: C S
authors.initials: CS
authors.lastname: Apstein
mesh_terms: D000818:Animals; D001011:Aorta / Q000502:physiology; D001794:Blood Pressure; D003971:Diastole; D006321:Heart; D006352:Heart Ventricles / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction; D010477:Perfusion; D011817:Rabbits