Metabolic Changes after Urinary Diversion

Urinary diversion is performed on a regular basis in urological practice. Surgeons tend to underestimate the metabolic effects of any type of diversion. From the patient's perspective, diarrhea is the most bothersome complaint after urinary diversion. This might be accompanied by malabsorption syndromes, such as vitamin B12 deficiency. Electrolyte abnormalities can occur frequently such as hyperchloremic metabolic acidosis, or less frequently such as hypokalemia, hypocalcaemia, and hypomagnesaemia. Bone health is at risk in patients with urinary diversion. Some patients might benefit from vitamin D and calcium supplementation. Many patients are also subject to urinary calculus formation, both at the level of the upper urinary tract as in intestinal reservoirs. Urinary diversion can affect hepatic metabolism, certainly in the presence of urea-splitting bacteria. The kidney function has to be monitored prior to and lifelong after urinary diversion. Screening for reversible causes of renal deterioration is an integral part of the followup

A randomized placebo-controlled study on the effect of nifedipine on coronary endothelial function and plaque formation in patients with coronary artery disease: the ENCORE II study

Aims Endothelial dysfunction and plaque formation are features of atherosclerosis. Inhibition of L-type calcium channels or HMG-CoA pathway improves endothelial function and reduces plaque size. Thus, we investigated in stable coronary artery disease (CAD) the effects of a calcium antagonist on coronary endothelial function and plaque size. Methods and results In 454 patients undergoing PCI, acetylcholine (10−6 to 10−4 M) was infused in a coronary segment without significant CAD. Changes in coronary diameter were measured and an intravascular ultrasound examination (IVUS) was performed. On top of statin therapy, patients were randomized in a double-blind fashion to placebo or nifedipine GITS 30-60 mg/day and followed for 18-24 months. Blood pressure was lower on nifedipine than on placebo by 5.8/2.1 mmHg (P < 0.001) as was total and LDL cholesterol (4.8 mg/dL; P = 0.495), while HDL was higher (3.6 mg/dL; P = 0.026). In the most constricting segment, nifedipine reduced vasoconstriction to acetylcholine (14.0% vs. placebo 7.7%; P < 0.0088). The percentage change in plaque volume with nifedipine and placebo, respectively, was 1.0 and 1.9%, ns. Conclusion The ENCORE II trial demonstrates in a multi-centre setting that calcium channel blockade with nifedipine for up to 2 years improves coronary endothelial function on top of statin treatment, but did not show an effect of nifedipine on plaque volum

Demonstration of H2O2 production in vivo during aminopyrine metabolism and phenobarbital induction

It has been shown previously that, by using methanol and a catalase inhibitor, 3-amino-1, 2, 4,-triazole, changes in hepatic H2O2 production in vivo can be detected. Using this method in guinea pigs and rats we could demonstrate increased H2O2 production during metabolism in vivo of aminopyrine, especially in phenobarbital-pretreated animals. In contrast, administration of antipyrine does not lead to H2O2 production. In the guinea pigs, phenobarbital induction also stimulates the H2O2 production in vivo without administration of exogenous substrates. The rate and extent of this additional H2O2 production depend on the induction state, drug metabolism and species; the major findings are in agreement with and extend previous research in vitro on microsomes, isolated hepatocytes and perfused liver

Cytochrome P-450-dependent H₂O₂ production demonstrated in vivo: influence of phenobarbital and allylisopropylacetamide

AbstractBy administration of allylisopropylacetamide, an inhibitor of cytochrome P-450, we demonstrated that cytochrome P-450 is involved in the production of H2O2 during aminopyrine metabolism and phenobarbital induction in both the unanaesthetized guinea pig and rat. In the guinea pig we also found evidence for the existence of a basal cytochrome P-450-dependent H2O2 production, i.e. in the absence of exogenous substrate. Catalase participates in the decomposition of H2O2 produced in the endoplasmic reticulum where cytochrome P-450 is localized

Peroxisomal ß-oxidation from endogenous subtrates: demonstration through H₂O₂ production in the unanaesthetized mouse

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Exercise myocardial perfusion and wall motion imaging to predict recurrence of angina pectoris after successful angioplasty

Objectives. This study investigates the predictive value of concurrent exercise radionuclide ventriculography and myocardial perfusion scintigraphy obtained six weeks after successful percutaneous transluminal coronary angioplasty for the recurrence of angina. Methods. Both studies were obtained simulataneously with a single injection of technetium-99m sestamibi using the first-pass technique and the computerized tomographic technique, respectively. Ninety-five patients were investigated at rest and at maximal exercise 6 weeks after technically successful coronary angioplasty. Results. Exercise-induced left ventricular dysfunction was present in 44 patients (46%). Exercise-induced myocardial perfusion defects were noted in 29 patients (30%). All patients underwent a six months follow-up. Seventeen patients (18%) had recurrent angina pectoris. Exercise-induced left ventricular dysfunction at six weeks after angioplasty was significantly associated with the recurrence of angina (p = 0.002), but exercise-induced perfusion defects were not. An abnormal left ventricular response to exercise was more sensitive than exercise-induced perfusion defects (82% versus 47%) to identify those patients with recurrent angina. The combination of both test allows to select patients at very high (40%) and very low (7%) risk of recurrent angina. Conclusion. Exercise-induced left ventricular dysfunction is more strongly associated with the recurrence of angina pectoris during a 6 month follow-up than are exercise-induced myocardial perfusion defects.SCOPUS: ar.jinfo:eu-repo/semantics/publishe