Intramyocardial pressure: interaction of myocardial fluid pressure and fiber stress.
Previous measurements of intramyocardial pressure (IMP) have yielded systolic pressures that range from values lower than to far exceeding systolic left ventricular pressure (LVP). This study identifies a possible mechanism underlying these divergent observations by building on established morphology of the ventricular wall. It is hypothesized here that the generation of fiber stress as a manifestation of myocardial contraction increases fluid pressure in the myocytes and the interstitial spaces. This increase in fluid pressure in turn generates the pressure in the ventricular cavity. Thus there are two quantities of interest: intramyocardial fluid pressure (IFP) and intramyocardial fiber stress (IFS). To test the hypothesis, we conducted experiments on conditioned dogs, utilizing a side-mounted catheter-tip strain gauge transducer to sense IMP as the sum of IFP and some component of IFS. In addition, a recessed end-tip fiber-optic transducer with its sensing element shielded from local myocardial fibers was employed to sense IFP. Both IFP and IMP were measured at various depths in the left ventricular free wall. The effects of inotropic interventions by administration of epinephrine and propranolol, mechanical interventions via clamping of the aorta and ligation of the left anterior descending coronary artery, and neural interventions by stimulation of the ansa subclavian of the stellate ganglion and right vagus were recorded. A transmural gradient in the wall for both IMP and IFP was observed. Systolic values of IFP recorded in the endocardium match those of LVP, with peak IMP exceeding both. The results support the hypothesis and offer an interpretation of the long-standing controversy regarding the magnitude of IMP with respect to LVP.
Cardiovascular Studies Unit, University of Pennsylvania, Philadelphia 19104.
S Y
SY
Rabbany
J Y
JY
Kresh
A
A
Noordergraaf
D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D004837:Epinephrine / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006439:Hemodynamics; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D011312:Pressure; D011433:Propranolol / Q000494:pharmacology; D013314:Stress, Mechanical
D011433:Propranolol; D004837:Epinephrine