Acute warming in fish increases heart rate (f H) and cardiac output to peak values, after which performance plateaus or declines and arrhythmia may occur. This cardiac response can place a convective limitation on systemic oxygen delivery at high temperatures. To test the hypothesis that autonomic cardiac regulation protects cardiac performance in rainbow trout during acute warming, we investigated adrenergic and cholinergic regulation during the onset and progression of cardiac limitations. We explored the direct effects of adrenergic stimulation by acutely warming an in situ working perfused heart until arrhythmia occurred, cooling the heart to restore rhythmicity and rewarming with increasing adrenergic stimulation. Adrenergic stimulation produced a clear, dose-dependent increase in the temperature and peak f H achieved prior to the onset of arrhythmia. To examine how this adrenergic protection functions in conjunction with cholinergic vagal inhibition in vivo, rainbow trout fitted with ECG electrodes were acutely warmed in a respirometer until they lost equilibrium (CT max) with and without muscarinic (atropine) and β-adrenergic (sotalol) antagonists. Trout exhibited roughly equal and opposing cholinergic and adrenergic tone on f H that persisted up to critical temperatures. β-Adrenergic blockade significantly lowered peak f H by 14-17%, while muscarinic blockade significantly lowered the temperature for peak f H by 2.0°C. Moreover, muscarinic and β-adrenergic blockers injected individually or together significantly reduced CT max by up to 3°C, indicating for the first time that cardiac adrenergic stimulation and cholinergic inhibition can enhance acute heat tolerance in rainbow trout at the level of the heart and the whole animal.
The aim of the present investigation was to evaluate the protective effect of a 70% methanolic leaf extract of Cyclea peltata Lam on cisplatin-induced renal toxicity. The concentration of creatinine, urea, sodium, and potassium in serum and levels of malonyldyaldehyde (MDA), glutathione (GSH), as well as gluathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities were determined in kidney tissue. The marked cisplatin-induced renal damage, characterized by a significant increase in creatinine and urea levels, decreased in extract-treated group, whereas sodium and potassium levels did not change significantly. C. peltata Lam extract significantly changed the increased MDA level and decreased GSH levels found in rats treated with cisplatin alone. The reduced activities of GSH-Px, SOD, and CAT in groups treated with cisplatin alone were significantly increased by the extract. The protective effect was greater in the post-treated than in the pre-treated group of animals. The results indicate that the post-treatment of C. peltata Lam extract might effectively ameliorate the oxidative stress parameters observed in cisplatin induced renal toxicity and could be used as a natural antioxidant against cisplatin-induced oxidative stress.
A large body of evidence indicates that chronic obstructive pulmonary disorder (COPD) is accompanied by oxidative stress and inflammatory and genetic pathways. Epidemiological studies indicate that COPD is a major cause of mortality and morbidity in the world. Recent research development in COPD focuses on accelerated aging and various oxidative stress biomarkers. It involves the clinical manifestation of the disease process and may also contain biochemical, immunological, physiological, morphological, and genetic aspects that add to the progressiveness of the disease. Herein, we summarize findings that highlight the role of dimensions of COPD in the investigation of oxidative stress, inflammatory responses, genetic and epigenetic studies, and pharmacological and dietary antioxidant intervention.
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