Recurrent secondary hyperparathyroidism and calciphylaxis due to a retro-oesophageal gland.
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Aged↗
Biomedical subjects
Mauro Rathaus
Publications and source records attributed to Mauro Rathaus.
Effect of tetrahydrobiopterin on blood pressure in rats after subtotal nephrectomy.
BACKGROUND: Previous studies have shown that endothelial dysfunction after 5/6 nephrectomy (5/6 Nx) in rats is associated with decreased nitric oxide (NO) bioavailability and increased vascular superoxide production. Blood pressure is significantly increased by day 10 after surgery. Tetrahydrobiopterin (BH4) is a key cofactor of NO synthase. Suboptimal levels of BH4 result in uncoupling of NO synthase, low NO synthesis and augmented production of superoxide anions. The aim of this study was to evaluate whether BH4 supplementation may improve NO production and prevent the increase of blood pressure after 5/6 Nx. METHODS: Three groups were evaluated: 5/6 Nx (untreated rats), BH4 (5/6 Nx rats treated with BH4, 10 mg/day i.p. for 10 days) and L-ARG (5/6 Nx rats treated with L-arginine, 260 mg/kg BW, p.o for 10 days). Systolic blood pressure (SBP), urinary nitrate excretion (UNO(3)) and creatinine clearance (CCR) were measured before surgery and on days 3 and 10 after surgery. Endothelial NO synthase (eNOS) protein content of mesenteric resistance vessels was measured at the end of the study. RESULTS: SBP increased from 107 +/- 2 to 127 +/- 4 mm Hg in untreated 5/6 Nx rats (p < 0.01). By contrast, rats treated with BH4 or L-ARG remained normotensive. Ten days after 5/6 Nx, creatinine clearance decreased similarly in all groups. Both BH4 and L-ARG supplementation markedly increased UNO(3) excretion. The mesenteric vascular expression of eNOs protein was significantly higher in BH4 but not in L-ARG, compared with Nx rats. CONCLUSIONS: BH4 supplementation prevents the earlier increase in blood pressure observed in rats after 5/6 Nx, possibly by upregulating eNOS in resistance vessels.
Animals↗
Lower extremity amputations in chronically dialysed patients: a 10 year study.
BACKGROUND: Lower limb critical ischemia is a major problem in dialysed patients. OBJECTIVE: To evaluate the results of revascularization procedures, amputations and prosthetic rehabilitation in dialysed amputees. METHODS: In this retrospective study we examined the charts of selected dialysis patients. Forty-eight patients had undergone major amputation (4.5% of the dialysis population), and 24 patients entered the rehabilitation program. Widespread arterial calcification was common and led to falsely elevated ankle-brachial pressure indices in 9 of 14 limbs. Eight patients underwent revascularization. Subsequent major amputation was carried out 4 +/- 4.5 months after the revascularization (above knee in 5 patients and below knee in 3). Of the 16 patients who underwent primary amputation, only 2 were above-knee amputees. Seven patients with toe or metatarsal amputation went on to a major amputation 1.8 +/- 1.2 months after the distal amputation. RESULTS: No differences were found between diabetic and non-diabetic patients regarding the number of revascularization operations performed, the level of major amputation, or overall survival. Prosthetic rehabilitation was considered successful in 12 patients, partially successful in 8, and failed in 4 patients. Patient survival time was shortest in those patients with failed rehabilitation. A younger age confirmed favorable rehabilitation results, while long-standing diabetics and bilateral amputees were poor rehabilitation candidates. Patients who underwent primary amputation had more successful rehabilitation. A comparison between 24 dialysed amputees and 138 non-uremic amputees revealed similar rehabilitation results, although hospitalization time was longer in the dialysed patients. CONCLUSIONS: Early definitive therapy is essential when dealing with critical ischemia. After diagnostic angiography, proximal revascularization should be performed where feasible. Primary amputation is indicated in patients with extensive foot infection or gangrene. Prosthetic rehabilitation is warranted in most dialysed amputees.
Adult↗
Endothelial dysfunction and hypertension in 5/6 nephrectomized rats are mediated by vascular superoxide.
BACKGROUND: Nitric oxide inactivation by superoxide impairs endothelium-dependent vasodilation and plays a role in various forms of hypertension. Almost no data exist regarding hypertension secondary to chronic renal failure. Previous studies have shown that endothelium-related relaxations, secondary to decreased nitric oxide bioactivity, are impaired in resistance vessels from rats 3 to 10 days after renal mass reduction (RMR). METHODS: The membrane-permeable superoxide dismutase (SOD)-mimetic (tempol) was administered IP (1.5 mmol/kg/day for 10 days) to RMR rats and sham-operated controls (SN). Systolic blood pressure (SBP) was measured by tail cuff manometry at days 0, 3, 6 and 10. The increase of flow induced by acetylcholine (10-6 mol/L) was measured in isolated perfused mesenteric arteries from RMR and SN rats pre-contracted with noradrenaline (1 to 5 micromol/L), with or without exogenous SOD. Plasma levels of advanced oxidative protein products (AOPPs; chloramine-T equivalents) were measured in SN and RMR rats. RESULTS: Tempol prevented the increase of SBP: 118 +/- 2.2 mm Hg at baseline and 122 +/- 1.6 mm Hg at 10 days in tempol-treated vs 118.14 +/- 1.65 mm Hg at baseline and 145 +/- 7.69 mm Hg at 10 days in untreated RMR rats (P < 0.01). Responsiveness to acetylcholine was reduced in RMR rats (peak flow increase: 139 +/- 7.8% vs. 176 +/- 11% in SN, P=0.028 at 3 days and 140 +/- 6.4% vs. 187 +/- 16.9% in SN at 10 days, P=0.007). In arteries pre-incubated with SOD (200 U/mL) the peak flows were 175 +/- 9.4% at 3 days and 157 +/- 5.8% at 10 days (P=0.007 and P=0.051, respectively, vs. control RMR vessels). AOPP values were significantly increased in plasma from RMR rats 3 days after 5/6 nephrectomy (747 +/- 107 vs. 481 +/- 77 micromol/L, P < 0.05) but returned to normal by day 10. AOPP levels were not significantly reduced by tempol. CONCLUSIONS: Increased vascular superoxide production plays a central role in the development of vascular endothelial dysfunction and hypertension early after 5/6 nephrectomy.
Acetylcholine↗
Oxygen species in the microvascular environment: regulation of vascular tone and the development of hypertension.
Derangements of the three endothelium-related vasodilator systems (prostaglandins, endothelium-derived hyperpolarizing factor(s) and nitric oxide) cause the endothelial dysfunction observed in hypertension. Free radical-induced nitric oxide degradation plays a crucial role in hypertension. An increase in superoxide producing enzymes such as NAD(P)H oxidase and xanthine oxidase has been demonstrated. Superoxide dismutase may correct endothelial dysfunction in vitro and superoxide dismutase mimetics can lower blood pressure in experimental animals. Antioxidant agents and xanthine oxidase-inhibiting compounds have been used in humans. In addition, the synthesis of vasoconstrictor peroxides derived from the activity of cyclooxygenase in the endothelium and the vascular smooth muscle is stimulated by the OH. radical. Hydrogen peroxide levels are augmented in hypertension, but its role is unclear because recent investigations have shown that this substance may act as a hyperpolarizing factor. It is thought that the therapeutic benefit of anti-hypertensive drugs, such as calcium antagonists and angiotensin-converting enzyme inhibitors, could be in part due to an inhibition of free radical production. A role of superoxide in the endothelial dysfunction and hypertension of chronic renal failure has also been suggested by recent animal experiments.
Animals↗