Background Ginkgo biloba extract 761 (EGb761) was studied for its nephroprotective effects in experimentally induced hypertension. Hypertension is increasingly a cause of end‑stage renal diseases. Increased cytokine release and oxidative stress are mechanisms that appear to be involved in the pathogenesis of hypertensive renal damage. EGb has antioxidant and anti‑inflammatory effects and can attenuate hypertensive renal damage. Methods and results Male adult Wistar rats were used in this study. Hypertension was induced in these rats by administering l‑NG‑nitroarginine methyl ester (l‑NAME) (10 mg/kg/day, intraperitoneal) for 12 weeks. Another group of rats received l‑NAME and EGb761 (100 mg/kg/day, orally) starting from the ninth week to the end of treatment. It was found that the blood pressure was reduced at the end of 12th week in rats treated with EGb761 compared with l‑NAME‑treated (hypertensive) rats. EGb761‑treated rats showed lower renal tissue malondialdehyde level and renal tissue tumor necrosis factor‑ level when compared with l‑NAME‑treated rats (hypertensive). Conclusion EGb761 has antihypertensive effect; it can protect the kidney from hypertension through the reduction of renal inflammation and oxidative stress.

Background Ginkgo biloba extract 761 (EGb761) was studied for its nephroprotective effects in experimentally induced hypertension. Hypertension is increasingly a cause of end‑stage renal diseases. Increased cytokine release and oxidative stress are mechanisms that appear to be involved in the pathogenesis of hypertensive renal damage. EGb has antioxidant and anti‑inflammatory effects and can attenuate hypertensive renal damage. Methods and results Male adult Wistar rats were used in this study. Hypertension was induced in these rats by administering l‑NG‑nitroarginine methyl ester (l‑NAME) (10 mg/kg/day, intraperitoneal) for 12 weeks. Another group of rats received l‑NAME and EGb761 (100 mg/kg/day, orally) starting from the ninth week to the end of treatment. It was found that the blood pressure was reduced at the end of 12th week in rats treated with EGb761 compared with l‑NAME‑treated (hypertensive) rats. EGb761‑treated rats showed lower renal tissue malondialdehyde level and renal tissue tumor necrosis factor‑ level when compared with l‑NAME‑treated rats (hypertensive). Conclusion EGb761 has antihypertensive effect; it can protect the kidney from hypertension through the reduction of renal inflammation and oxidative stress.

Objectives: ‎ The aim of this study is to evaluate the possible effects of selective cyclooxygenase 2 ‎inhibitor drug (celecoxib) on renal glutathione levels and interleukin 6 (IL6) ‎expressions in a gentamicin-induced nephrotoxicity model in mice. ‎ Methods:‎ ‎4 groups of adult male mice (5 animals each) received saline, gentamicin (100 mg/kg/ day, i.p), celecoxib ‎‎(‎30 mg/kg/day, orally‎) and gentamycin plus celecoxib for 8 days.‎ Results:‎ It was noticed that gentamicin administration to mice led to ‎significant depletion of ‎renal glutathione, this indicates the ‎deficiency of renal antioxidant capacity by ‎gentamicin and widespread tubular damage (loss of microvilli, tubular dilatation and ‎vacuolation) in histopathological examination indicating nephrotoxicity. An ‎overexpression of IL6 was noted in renal tubular epithelium by ‎immunohistochemistry.‎ In animals received celecoxib daily, there were ‎no changes in renal glutathione levels ‎compared to control animals, no histopathological changes in renal tissues and reduced ‎expression of IL6.‎ ‎In animals received celecoxib ‎plus gentamicin there is significantly reversed ‎gentamicin induced nephrotoxicity evidenced by increasing levels of glutathione, ‎reduced IL 6 expression and reduction of the degree of tubular injury by ‎histopathological examination. ‎ Conclusion: administration of celecoxib can protect the kidneys from gentamicin ‎related toxicity.

Objectives: ‎ The aim of this study is to evaluate the possible effects of selective cyclooxygenase 2 ‎inhibitor drug (celecoxib) on renal glutathione levels and interleukin 6 (IL6) ‎expressions in a gentamicin-induced nephrotoxicity model in mice. ‎ Methods:‎ ‎4 groups of adult male mice (5 animals each) received saline, gentamicin (100 mg/kg/ day, i.p), celecoxib ‎‎(‎30 mg/kg/day, orally‎) and gentamycin plus celecoxib for 8 days.‎ Results:‎ It was noticed that gentamicin administration to mice led to ‎significant depletion of ‎renal glutathione, this indicates the ‎deficiency of renal antioxidant capacity by ‎gentamicin and widespread tubular damage (loss of microvilli, tubular dilatation and ‎vacuolation) in histopathological examination indicating nephrotoxicity. An ‎overexpression of IL6 was noted in renal tubular epithelium by ‎immunohistochemistry.‎ In animals received celecoxib daily, there were ‎no changes in renal glutathione levels ‎compared to control animals, no histopathological changes in renal tissues and reduced ‎expression of IL6.‎ ‎In animals received celecoxib ‎plus gentamicin there is significantly reversed ‎gentamicin induced nephrotoxicity evidenced by increasing levels of glutathione, ‎reduced IL 6 expression and reduction of the degree of tubular injury by ‎histopathological examination. ‎ Conclusion: administration of celecoxib can protect the kidneys from gentamicin ‎related toxicity.

Objectives: ‎ The aim of this study is to evaluate the possible effects of selective cyclooxygenase 2 ‎inhibitor drug (celecoxib) on renal glutathione levels and interleukin 6 (IL6) ‎expressions in a gentamicin-induced nephrotoxicity model in mice. ‎ Methods:‎ ‎4 groups of adult male mice (5 animals each) received saline, gentamicin (100 mg/kg/ day, i.p), celecoxib ‎‎(‎30 mg/kg/day, orally‎) and gentamycin plus celecoxib for 8 days.‎ Results:‎ It was noticed that gentamicin administration to mice led to ‎significant depletion of ‎renal glutathione, this indicates the ‎deficiency of renal antioxidant capacity by ‎gentamicin and widespread tubular damage (loss of microvilli, tubular dilatation and ‎vacuolation) in histopathological examination indicating nephrotoxicity. An ‎overexpression of IL6 was noted in renal tubular epithelium by ‎immunohistochemistry.‎ In animals received celecoxib daily, there were ‎no changes in renal glutathione levels ‎compared to control animals, no histopathological changes in renal tissues and reduced ‎expression of IL6.‎ ‎In animals received celecoxib ‎plus gentamicin there is significantly reversed ‎gentamicin induced nephrotoxicity evidenced by increasing levels of glutathione, ‎reduced IL 6 expression and reduction of the degree of tubular injury by ‎histopathological examination. ‎ Conclusion: administration of celecoxib can protect the kidneys from gentamicin ‎related toxicity.

Background Objective To investigate the impact of right ventricular (RV) internal work (IW), Ea/Emax (VVC), and RV-late gadolinium enhancement (LGE) on outcome in pulmonary hypertension (PH). LGE is known to be present within the RV insertion point (IP) and interventricular septum (IVS) in PH, but its prognostic role in such patients remains complex and potentially overestimated via 2D qualitative relative to 3D quantitative measures now available. However, RV-Ea/Emax, a measure of ventriculo-arterial coupling (VVC) and RV Internal Work (IW) when added to external cardiac work i.e. the P-V loop area denoting the RV's energetic demands, might fundamentally improve measures of PH prognosis as these metrics interrogate complex pulmonary physiology beyond the RV. Methods CMR exams of 124 advanced PH patients (>50% WHO I; age=60 ± 13; 85 F, NYHA II-IV) referred to a large tertiary PH center were examined for RV volumetric and functional indices along with visual and quantitiative 2D and 3D RV-LGE. RHC were performed within 1 ± 2 months of the CMR. Ea/Emax (VVC) was derived as RV end-systolic volume (ESV)/RVSV. IW was estimated as RVESV × (RV end-systolic pressure-RV diastolic pressure). Patients were followed from date of CMR for up to 5 years for MACE (death, hospitalized RV failure, initiation of parenteral prostacyclin, sustained ventricular arrhythmia or referral for lung transplantation). Results Over one-third (48/124; 39%) of the patients had MACE by 18 months (1.6 ± 0.3 years). However, neither RVIP nor IVS LGE using visual assessment, 2D or 3D quantitation predicted MACE. The strongest predictor of MACE was RV IW versus multiparametric RV-LGE, VVC, mPAP, RV mass and RVEF. Conclusions Neither a single time point visual, 2D or 3D RV-LGE metric can predict outcome in PH patients when compared with conventional or contemporary metrics of disease progression. In this largest 3D LGE assessment to date, physiologic, not anatomic parameters best represented MACE in patients with PH.

Objectives: External cardiac work performed is represented by the area within the ejection loop (P-V) and correlates poorly with the heart’s total energy demands until the internal work component is added. Further, the ratio of the arterial elastance (Ea) to the ventricular end-systolic elastance (Emax) is a measure of ventriculo-arterial coupling. We investigated the impact of both indices of right ventricular (RV) performance on outcome in patients with pulmonary hypertension (PH). Methods: Cardiac magnetic resonance (CMR) studies of a retrospective consecutive cohort of 115 PH pts (61±14 yrs) were examined for RV volumetrics, functional indices and the presence of RV late gadolinium enhancement (LGE) from 2008-2014. Right heart cath (RHC) parameters were included in the analysis (performed within 1±1.5 mo of CMR) as was 3D RV mass and RVEF. The Ea/Emax ratio was derived in part as RV end-systolic volume (ESV)/RV stroke volume. Internal mechanical work was estimated as RVESV*(RV-ES pressure- RV-ED pressure). Patients were followed up to 5 yrs. Results: During follow-up, 42/115 (37%) pts had a MACE. On a multivariable logistic regression analysis, the strongest predictor of MACE was the internal RV mechanical work followed in order by Ea/Emax versus mean pulmonary artery pressure, RV mass, RV EF, and RV LGE. The strongest predictors of time to MACE were the RV internal mechanical work (χ2=10.8) and Ea/Emax ratio (χ2=9.2). Kaplan-Meier analysis of time to MACE for quartiles of RV internal mechanical work and Ea/Emax are shown in Figure 1A & B. Conclusions: Higher RV internal mechanical work and Ea/Emax are both markers for worsening prognosis in PH patients; Ea/Emax having the added advantage of being an entirely non-invasive CMR derivation and statistically equivalent. Both metrics were superior to standard clinical metrics including RV LGE, RVEF, PA pressure and RV mass and for the first time address integrated cardio-pulmonary physiology as early markers for MACE.

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