BackgroundThe customary puerperal practice of Natron consumption has been identified as one of the predisposing factors in the etiology of peripartum cardiomyopathy (PPCM). This study was designed to investigate the effect of Natron in postpartum Wistar albino rats.MethodsA total of 30 postpartum Wistar rats were exposed to different doses (50 mg/kg, 100 mg/kg, 200 mg/kg and 300 mg/kg) of Natron for 28 days. After the treatment, we carried out biochemical analyses and histological evaluations of kidney, liver and heart.ResultsThe study revealed that the exposure of postpartum rats to 100 mg/kg of Natron and above significantly (p < 0.05) increase the cardiac markers; myoglobin, creatine kinase-MB, troponin I and T as compared with control. The result of liver function indicated no significant difference in alanine aminotransferase, aspartate aminotransferase, gamma-glutamyltransferase, albumin and total protein of the Natron treated groups as compared with control. However, at higher doses, the levels of total protein, globulin and alkaline phosphatase activity were significantly increased in comparison to the control. There was no significant difference in the kidney function markers of the treatment groups as compared with control. Histological examinations revealed no changes in the kidney of the treated groups. Mild portal triaditis was observed in the liver of the treated rats. The heart of the rats administered ≥100 mg/kg of Natron showed myocyte hypertrophy.ConclusionThe study demonstrated that the administration of Natron for 28 days caused changes in the heart of postpartum rats and thus may contribute to the pathogenesis of PPCM.

The alkaloid cycleanine ([12aR-(12aR,24aR)]-2,3,12a,13,14,15,24,24a-octa hydro-5,6,17,18- tetramethoxy-1,13-dimethyl-8, 11:20,23-dietheno-1H,12H [1,10]dioxacyclooctadecino[2,3,4-ij:11,12,13-i'j']diisoquinolin e) was extracted from the bulbs of Stephania glabra (Roxb) Miers and its effects on cardiac and smooth muscle preparations were studied and compared to those of nifedipine (1,4-dihydro-2, 6-dimethyl-4-(2-nitrophenyl)-3,5-pyridine dicarboxylic acid dimethylesther). Cycleanine inhibited the KCl-induced contraction of rabbit aortic rings with higher potency than nifedipine. IC50s for cycleanine and nifedipine were 0.8 and 7.10(-9) M respectively. Cycleanine had minor effects on the norepinephrine-induced contraction of rabbit aortic rings. Cycleanine and nifedipine also depressed the contraction of rat ventricular preparations but with lower potency (IC50 = 3 and 0.03.10(-6) M respectively). Action potential duration of rat right ventricular strips was decreased by both compounds. L-type Ca-current (ICaL) of single rat ventricular cardiomyocytes was inhibited by cycleanine in a voltage- and frequency-dependent manner. With a higher potency nifedipine inhibited ICaL in a tonic and almost frequency-independent manner. The results suggest that cycleanine can act as a potent vascular selective Ca-antagonist.

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Diarrhea has a very high morbidity and mortality, especially in children and in developing countries. Chrozophora senegalensis is used in its management among North-Western Nigeria traditional healers. This claim was scientifically investigated using some diarrhea models. The leaves were also subjected to both phytochemical and proximate analyses, for possible explanations. Phytochemical studies of the leaves revealed the presence of alkaloid (1.20%), tannins (0.92%) and flavonoids (0.029%) while proximate composition showed carbohydrates (73.3%), crude fibre (8.5%), crude protein (6.48%), ash (10.0%), moisture (4.0%) and crude fat (2.0%). The acute oral toxicity studies showed no mortality at 5000 mg/kg body weight. The anti-diarrheal activity of the plant using Activated Charcoal Model showed increase in average latent period and decrease in purging index with increase in dose of the extract using castor oil model. In conclusion, Chrozophora senegalensis could be a potential source of anti-diarrheal drug.