PubMed · 2872246
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P J Barnes. 1986. Endogenous catecholamines and asthma.. https://doi.org/10.1016/0091-6749(86)90375-1
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Fumonisins are mycotoxins produced primarily by Fusarium verticillioides, a fungus that commonly contaminates corn. Fumonisin ingestion increases plasma and tissue sphingosine and sphinganine concentrations and causes porcine pulmonary edema, which has been attributed to acute left-sided heart failure or increased vascular permeability. We investigated the effect of short-term ingestion of fumonisin B1-containing culture material on cardiac function in pigs. Treated male pigs (n = 7) received fumonisin-containing culture material which was mixed into the grower diet at 20 mg fumonisin B1/kg body weight each day, while control pigs (n = 7) were fed only the grower diet on the same schedule as the treated pigs. Pigs were anesthetized after 3 days of receiving either diet and instrumented to accurately characterize the cardiovascular effects of fumonisin ingestion. Fumonisin-treated pigs had lower cardiac outputs and heart rates than control pigs. Fumonisin-treated pigs also had a marked reduction in cardiac contractility, as indicated by decreased values for end-systolic elastance (the gold standard in vivo measure of cardiac contractility), V(0) (the intercept value for the end-systolic pressure-volume relationship), and mechanical efficiency. These data indicate that in pigs, short-term ingestion of fumonisin B1-containing culture material produces negative inotropic and chronotropic effects and decreases mechanical efficiency of the left ventricle. Theses cardiovascular effects are consistent with fumonisin-induced, sphingosine-mediated l-type Ca(2+) channel blockade and suggest that pulmonary edema in pigs fed fumonisin is primarily due to acute left-sided heart failure instead of increased vascular permeability.
BACKGROUND: Metoprolol provides clinical benefits in patients with congestive heart failure (CHF). In this study, we investigated the effects of controlled-release metoprolol (metoprolol CR) on clinical status, on left ventricular (LV) volumes and function, and on neurohumoral activation in a large number of patients with CHF of mixed causes. METHODS AND RESULTS: Four hundred twenty-six patients with symptomatic CHF were randomized to receive metoprolol CR or placebo for 24 weeks. Metoprolol CR did not affect 6-minute walk distance, New York Heart Association functional class, or quality of life. However, there was a significant improvement in measures of LV function with an attenuation in the increase in LV end-diastolic (+23+/-65 mL [placebo] versus +6+/-61 mL, P=0.01) and LV end-systolic (+19+/-55 mL [placebo] versus -2+/-51 mL, P<0.001) volumes after 24 weeks of therapy. LV ejection fraction was unchanged (-0.05% or -0.005) in the placebo group but increased by 2. 4% in the metoprolol CR-treated patients (P=0.001). Patients receiving metoprolol CR had a greater decrease in angiotensin II (P=0.036) and renin (P=0.032) levels but an increase in N-terminal atrial natriuretic peptide and brain natriuretic peptide levels (P<0. 01). There were fewer deaths in the group receiving beta-blockers (3. 4% versus 8.1%), and there was a similar number of patients experiencing the composite outcomes of death or any hospitalization. CONCLUSIONS: When added to ACE inhibitors, angiotensin II receptor antagonists, or both, the use of metoprolol CR improves ventricular function, reduces activation of the renin-angiotensin systems, and results in fewer deaths.