Preservation Of Contractile Function Research Articles

Cardiac magnetic resonance spectroscopy.

The article reviews cardiac magnetic resonance spectroscopy (MRS) in Canada. 31P MRS has been used to study cardiac energetics and intracellular pH in hearts subjected to ischemia-reperfusion and to evaluate the effects of pharmacological interventions. 23Na, 87Rb, and 7Li MRS have provided unique probes to study ion balance and fluxes in intact tissue under normal and stressful physiological conditions. 1H MRS has been used to monitor the accumulation of lactate and lipids in hearts subjected to ischemia-reperfusion and follow the effects of diet on cardiac lipid levels and function. The isolated rat heart has been used most commonly to study the effects of pharmacological agents on energy balance, pH, ion fluxes, and contractile function of the heart subjected to ischemia-reperfusion. The pig heart has been developed as an alternative to the rodent heart because its metabolism is more similar to that of the human heart. Human atrial appendages have been useful in evaluating the effects of preservation strategies (temperature, composition of preservation solutions) on energy levels. The pig heart model has been useful in evaluating the effects of preservation solutions on cardiac function of hearts destined for transplantation. An isolated blood-perfused pig heart model has been developed to assess the effects of cardioplegic strategies on the preservation of contractile function of hearts following surgery on the heart. An in vivo canine model has been used to study myocardial infarction and the effects of therapies to reduce the infarct zones and areas of the heart at risk of infarction. Studies of human hearts in vivo have provided insight into the metabolic adaptations that occur in individuals living at high altitudes.

Preservation of contractile function and energy metabolites in human myocardial tissue stored in UW belzer solution

Preservation of contractile function and energy metabolites in human myocardial tissue stored in UW belzer solution

Preservation of contractile function in the post-ischemic canine myocardium with the diltiazem analog, Ro 23-6152: P. Dahlen, R. Vergona, and A.J. Higgins. Department of Pharmacology and Chemotherapy, Hoffmann-La Roche Inc., Nutley, New Jersey, USA

Preservation of contractile function in the post-ischemic canine myocardium with the diltiazem analog, Ro 23-6152: P. Dahlen, R. Vergona, and A.J. Higgins. Department of Pharmacology and Chemotherapy, Hoffmann-La Roche Inc., Nutley, New Jersey, USA

Cardiac beta-adrenergic receptors in salt-dependent genetic hypertension.

The pattern of cardiac beta-adrenergic receptor changes in different hypertrophy models varies according to the pathophysiology. In salt-sensitive Dahl rats, high dietary salt intake leads to a moderate degree of cardiac hypertrophy associated with increased numbers of cardiac beta-adrenergic receptors but unchanged affinity for agonists. Isoproterenol-stimulated cardiac adenylate cyclase is also higher in salt-loaded hypertensive rats without any change in basal or NaF-stimulated activities. In contrast, neither beta-adrenergic receptors nor adenylate cyclase activities are affected by variations in dietary salt in salt-resistant Dahl rats. The extent of isoproterenol-induced down regulation of beta-adrenergic receptors on isolated cardiac myocytes as well as the recovery from this down regulation is not significantly different in either strain of Dahl rats and is not influenced by dietary salt. The enhancement of beta-adrenergic pathways in salt-dependent genetic hypertension may be involved both in the initiation of cardiac hypertrophy and the preservation of contractile function.

Cardiac contractile and coronary flow reserves in deoxycorticosterone acetate-salt hypertensive rats.

Cardiac contractility and coronary flow were compared in conscious rats with established deoxycorticosterone acetate-salt hypertension and in those with sham treatment. The hypertensive rats showed a 32% increase in left ventricular/body weight ratio at 9 weeks of treatment and 42% at 18 weeks of treatment. Resting peak rate of change of pressure (dp/dt) was unchanged at 9 weeks and increased at 18 weeks in hypertensive rats, while isoproterenol-stimulated maximal, propranolol-induced minimal, and Ca2+-stimulated maximal peak dp/dt were greater at 18 weeks. These data indicate the preservation of contractile function. At 18 weeks, the beta-adrenergic receptor-mediated contractile reserve, estimated from isoproterenol-stimulated maximal and resting peak dp/dt, was reduced but the propranolol-induced decrease in peak dp/dt was increased in hypertensive rats compared with sham-treated rats. Thus, at this stage, a greater portion of the total contractile capacity appeared to be mobilized with prolongation of hypertension and progression of left ventricular hypertrophy. No differences were observed in left ventricular and right ventricular coronary flow (microspheres) and left ventricular inner/outer flow ratio at rest and with dipyridamole-induced maximal coronary dilatation, at 9 and 18 weeks. There were no alterations in left or right ventricular coronary flow reserves, as estimated from resting and dipyridamole-induced values. The minimal coronary vascular resistance (normalized for gram of tissue) of both the left and right ventricles was increased at either stage, which suggests the occurrence of structural coronary vascular changes. Thus, basal coronary flow and a coronary flow reserve were uncompromised despite evidence of structural coronary vascular alterations in these hypertensive rats.