Chronic exposure to cocaine binging predisposes to an accelerated course of dilated cardiomyopathy in conscious dogs following rapid ventricular pacing.

Despite extensive study, the extent to which cocaine use predisposes to cardiac injury remains unknown. We hypothesized that chronic cocaine binging would increase susceptibility to a subsequent cardiac insult, even in the absence of demonstrable effects on baseline hemodynamics. We studied progression of dilated cardiomyopathy (DCM) induced by rapid ventricular pacing (240 beats per minute) in five conscious, chronically instrumented dogs, after exposure to repetitive cocaine binging (COC) in the form of four consecutive 1 mg/kg i.

Coronary blood flow responses are impaired independent of NO and endothelial function in conscious dogs with dilated cardiomyopathy.

Background: Dilated cardiomyopathy (DCM) is characterized by nitric oxide (NO) deficiency and endothelial dysfunction. Whether endothelium-independent vasodilation is preserved, particularly in the coronary circulation, remains controversial.

Methods And Results: We studied systemic and coronary flow responses to the endothelium-dependent agonist, acetylcholine, the cGMP-dependent NO-donor, nitroglycerin, the predominantly endothelium-independent agonist, adenosine, the beta-adrenergic cAMP-dependent agonist, isoproterenol, and the calcium channel antagonist, nicardipine, in conscious dogs with pacing-induced DCM.

Recombinant glucagon-like peptide-1 increases myocardial glucose uptake and improves left ventricular performance in conscious dogs with pacing-induced dilated cardiomyopathy.

Background: The failing heart demonstrates a preference for glucose as its metabolic substrate. Whether enhancing myocardial glucose uptake favorably influences left ventricular (LV) contractile performance in heart failure remains uncertain. Glucagon-like peptide-1 (GLP-1) is a naturally occurring incretin with potent insulinotropic effects the action of which is attenuated when glucose levels fall below 4 mmol.

The development of myocardial insulin resistance in conscious dogs with advanced dilated cardiomyopathy.

Background: The failing heart demonstrates a preference for glucose as its metabolic substrate. Advanced, severe DCM is characterized by depletion of adenosine triphosphate (ATP) stores, which may be a consequence of impaired insulin mediated glucose uptake and oxidation at a time when the myocardium prefers glucose as its substrate. We examined the time course and magnitude of myocardial insulin resistance during the evolution of dilated cardiomyopathy.

Quantitative reverse transcription-polymerase chain reaction of GABA(A) alpha1, beta1 and gamma2S subunits in epileptic rats following photothrombotic infarction of neocortex.

Photothrombotic brain infarction can result in altered expression of cortical GABA(A) receptors and in epileptic seizures. We sought to determine whether infarct size and/or epileptic seizures resulted in a differential expression of cortical GABA(A) receptor subunit mRNA in adult rats. A reverse transcription-polymerase chain reaction (RT-PCR) was used with internal standards for GABA(A) receptor subunits to quantify alpha(1), beta(1), and gamma(2S) subunit mRNA expression in cortex ipsilateral and contralateral to left cerebral infarcts in small or large infarct/nonepileptic cohorts, a large infarct/epileptic cohort, and a young adult control cohort.

Catecholamine stimulation is associated with impaired myocardial O(2) utilization in heart failure.

Objectives: To investigate the effect of alpha,beta(1) and beta(2) adrenergic receptor (AR) stimulation on coronary hemodynamics, myocardial oxygen consumption (M(v)O(2)) and metabolic substrate preference in advanced dilated cardiomyopathy (DCM).

Methods: We studied 19 conscious, instrumented dogs with pacing-induced DCM. We evaluated systemic, coronary hemodynamics and M(v)O(2) in response to norepinephrine (NOR, 0.