These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Adaptation of left ventricle to chronic pressure overload: response to inotropic drugs.
    Author: Newman WH, Webb JG.
    Journal: Am J Physiol; 1980 Feb; 238(2):H134-43. PubMed ID: 6444783.
    Abstract:
    Left ventricular (LV) force-generating capacity was determined in eight anesthetized dogs with pressure-overload hypertrophy. Length-contractile force (CF) curves recorded from the LV with a modified Walton-Brodie arch were displaced upward from control. However, when CF was normalized for LV wall thickness changes accompanying hypertrophy and expressed as g/cm2, the length-CF curve was depressed compared to normal. The CF response to isoproterenol and calcium was depressed in dogs with hypertrophy; however, the CF response to ouabain was not different from control. Taken collectively these findings suggest that pressure-overload hypertrophy is associated with a depressed force-generating capacity per unit cross section of myocardium at any given muscle length, i.e., a depressed inotropic state, but that the hypertrophied LV has a greater than normal force-generating capacity due to an increased number of weaker cross-sectional units. Further, the depressed inotropic state is not associated with augmented plasma norepinephrine levels. Therefore, adaptation of the LV to pressure overload is by cardiac hypertrophy alone.
    [Abstract] [Full Text] [Related] [New Search]