Purpose: To evaluate the diuretic effect and acute toxicity of the crude aqueous extract of Trianthema portulacastrum in a rat model. Method: Albino rats were divided into five groups. Control group received normal saline (10 mg/kg), reference group received furosemide (10 mg/kg) and test groups were given different doses of crude extract (10, 30 and 50 mg/kg) by intraperitoneal route. Urine was collected and the total volume of urine excreted was expressed as ml/6 hr/100 g body weight. Diuretic index and Lipschitz values were also calculated to make comparison with normal saline and furosemide treated groups, respectively. Results: Significant diuretic (p < 0.001), kaliuretic (p < 0.001) and natriuretic (p < 0.001) effects were observed in treated groups in a dose-dependent manner. Urinary pH remained mostly unchanged during the course of the study. Diuretic index showed good diuretic activity of the crude extract. Lipschitz values indicated that the crude extract at the dose of 50 mg/kg exhibited 79 % diuretic activity compared with that of the reference, furosemide. No lethal effects were observed among albino mice even at the high dose of 3000 mg/kg. Conclusion: The extract of Trianthema portulacastrum, particularly, at the dose of 50 mg/kg significantly increased the urinary volume and concentration of urinary electrolytes with no signs of toxicity and therefore, is a potential diuretic. Further studies, however, are required to isolate the active constituents.

Background: A novel, fully automated right ventricular (RV) software for three-dimensional quantification of RV volumes and function was developed. The direct comparison of the software performance with cardiac magnetic resonance (CMR) was limited. Therefore, the aim of this study was to test the feasibility, accuracy, and reproducibility of a fully automated RV quantification software against CMR imaging as a reference.Methods: A total of 170 patients who underwent both CMR and three-dimensional echocardiography were enrolled. RV end-diastolic volume (RVEDV), RV end-systolic volume (RVESV), and RV ejection fraction (RVEF) were obtained using fully automated three-dimensional RV quantification software and compared with a CMR reference. For inter-technical agreement, Spearman correlation and Bland–Altman analysis were used.Results: The fully automated RV quantification software was feasible in 149 patients. RVEDV and RVESV were underestimated, and RVEF was overestimated compared with CMR values. RV measurements obtained from the manual editing method correlated better with CMR values than that without manual editing (RVEDV, 0.924 vs. 0.794: RVESV, 0.955 vs. 0.854; RVEF, 0.941 vs. 0.781 respectively, all p &lt; 0.0001) with less bias and narrower limit of agreement (LOA). The bias and LOA for RV volumes and EF using the automated software without and with manual editing were greater in patients with severely impaired RV function or low frame rate than those with normal and mild impaired RV function, or high frame rate. The fully automated RV three-dimensional measurements were highly reproducible.Conclusion: The novel fully automated RV software shows good feasibility and reproducibility, and the measurements had a high correlation with CMR values. These findings support the routine application of the novel 3D automated RV software in clinical practice.

This article explores the relationship between the renal expression of cystathionine gamma lyase (CSE) and endothelial nitric oxide synthase (eNOS) and the responsiveness of α 1A adrenergic receptors in the renal vasculature following left ventricular hypertrophy (LVH) in rats. LVH was established by administering isoprenaline (5 mg/kg, 5 injections subcutaneously, 72 h apart) with 62 mg/L caffeine in drinking water for 2 weeks. Renal vasoconstrictor responses were measured using local administration of adrenergic agonists noradrenaline (NA), phenylephrine (PE), and methoxamine (ME) and the selective α1A adrenergic antagonist 5-methylurapidil (5-MeU). Mean arterial blood pressure was higher (144 ± 9 vs. 116 ± 4 mmHg) and renal cortical blood perfusion was lower in the LVH group (102 ± 5 vs. 157 ± 19 bpu) compared to the control group (P < 0.05). There was a 68% downregulation of mRNA for renal CSE and 79% for eNOS in the LVH group compared to the control group (taken as 100%) (P < 0.05). The high dose of 5-MeU attenuated the vasoconstrictor responses to NA by 33%, PE by 44%, and ME by 43% in the LVH group compared to the same dose in the control group. The reductions in basal renal cortical perfusion and α 1A adrenergic receptor vasoconstrictor responses in LVH were associated with the downregulation of the CSE/H2S and eNOS/NO pathways.