Biomedical subjects

Leocadio Rodríguez-Mañas

Publications and source records attributed to Leocadio Rodríguez-Mañas.

5 recordsLinked to original sources

PubMed2006

Outcome of older critically ill patients: a matched cohort study.

BACKGROUND: Admission of older patients to intensive care units is a controversial issue. OBJECTIVE: To estimate age-associated mortality of critically ill patients. METHODS: A prospective matched cohort study in the Medical-Surgical Intensive Care Unit of a tertiary hospital was conducted. We included 100 consecutive patients older than 70 years admitted to the intensive care unit (cases) and 100 patients younger than 70 years (controls). The matching criterion was the severity of illness at admission to the intensive care unit as estimated by the simplified acute physiological score (SAPS II) without including age in its calculation. RESULTS: Mortality in the intensive care unit was higher, but not statistically significant, in the older group: 26% vs. 19% (p = 0.23). Patients older than 70 years had a longer duration of mechanical ventilation (median 7 vs. 3 days) and longer stay in the intensive care unit (median 8 vs. 5 days). There were no differences in organ dysfunctions, except for a higher incidence of respiratory failure in the older group (p < 0.001). The use of invasive procedures was similar in both groups. There were more orders for the withholding/withdrawal of treatment in patients older than 70 years (9 vs. 3%, p = 0.07). CONCLUSION: In our study, age was not related with a significant higher mortality. In the older patients included in our study the survival was greater than 70% with a similar resource utilization except for a longer stay in the intensive care unit.

Adult↗

PubMed2005

Amadori adducts activate nuclear factor-kappaB-related proinflammatory genes in cultured human peritoneal mesothelial cells.

Diabetes mellitus leads to a high incidence of several so-called complications, sharing similar pathophysiological features in several territories. Previous reports points at early nonenzymatic glycosylation products (Amadori adducts) as mediators of diabetic vascular complications. In the present study, we analysed a possible role for Amadori adducts as stimulators of proinflammatory pathways in human peritoneal mesothelial cells (HPMCs). Cultured HPMCs isolated from 13 different patients (mean age 38.7+/-16 years) were exposed to different Amadori adducts, that is, highly glycated haemoglobin (10 nM) and glycated bovine serum albumin (0.25 mg ml(-1)), as well as to their respective low glycosylation controls. Amadori adducts, but not their respective controls, elicited a marked increase of NF-kappaB activation, as determined by electromobility shift assays and transient transfection experiments. Additionally, Amadori adducts significantly increased the production of NF-kappaB-related proinflammatory molecules, including cytokines, such as TNF-alpha, IL-1beta or IL-6, and enzymes, such as cyclooxygenase-2 and inducible nitric oxide (NO) synthase, this latter leading to the release of NO by HPMCs. The effects of Amadori adducts were mediated by different reactive oxygen and nitrosative species (e.g. superoxide anions, hydroxyl radicals, and peroxynitrite), as they were blunted by coincubation with the appropriate scavengers. Furthermore, NO generated upon exposure to Amadori adducts further stimulated NF-kappaB activation, either directly or after combination with superoxide anions to form peroxynitrite. We conclude that Amadori adducts can favour peritoneal inflammation by exacerbating changes in NO synthesis pathway and triggering NF-kappaB-related proinflammatory signals in human mesothelial cells.

Blotting, Western↗

PubMed2005

Evidence for sodium azide as an artifact mediating the modulation of inducible nitric oxide synthase by C-reactive protein.

C-reactive protein (CRP) is an acute-phase protein identified as a cardiovascular risk marker. In recent years, an increasing number of studies have investigated the possible direct effects of CRP on the vasculature, using mainly commercial CRP. In the present work, a potential role for CRP as a modulator of inducible nitric oxide synthase (iNOS) induction was explored. Cultured human aortic vascular smooth muscle cells (HASMC) were stimulated for 18 hours with 10 ng/mL interleukin-1beta (IL-1beta), resulting in a marked increase of iNOS levels and NO production, as determined by Western blotting and nitrite measurement, respectively. Commercial CRP (1 to 100 microg/mL) concentration-dependently inhibited the effects elicited by IL-1beta. Unexpectedly, similar results were observed when the commercial CRP solution was replaced by the corresponding vehicle medium containing growing concentrations of sodium azide. The inhibitory effects of commercial CRP or vehicle medium were lost on sodium azide removal by dialysis. In conclusion, sodium azide from the commercial CRP solution, but not CRP itself, mainly accounts for the inhibitory effect on IL-1beta-evoked iNOS induction and NO release. Care should be taken before attributing any biologic role to commercial CRP containing sodium azide.

Artifacts↗

PubMed2003

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Age Factors↗

PubMed2003

Effect of glycaemic control on the vascular nitric oxide system in patients with type 1 diabetes.

OBJECTIVE: The mechanisms underlying the relationship between the vascular complications of diabetes and the glycaemic control are not well understood. We tested whether glycaemic control influences the functioning of the nitric oxide system in type 1 diabetic patients and the role for oxidative stress. METHODS: The changes in the forearm blood flow after the infusion in the brachial artery of NG-monomethyl-l-arginine, methacholine, methacholine plus superoxide dismutase, and nitroprusside were evaluated using strain gauge plethysmography in 14 healthy subjects and 24 patients with type 1 diabetes (12 with HbA(1c) < 7.5%; 12 with HbA(1c) > or = 7.5%). After adjusting insulin treatment, the vascular studies were repeated in the initially poorly controlled patients (HbA(1c) > or = 7.5%). RESULTS: Compared with healthy people, impaired vascular responses to NG-monomethyl-l-arginine (P = 0.0001), methacholine (P = 0.007) and nitroprusside (P = 0.0015) were found in the patients with type 1 diabetes and a poor glycaemic control (HbA(1c) >/= 7.5%), but not in subjects with good control (HbA(1c) < 7.5%). Superoxide dismutase improved the responses to methacholine only in those patients with poor control (P = 0.0037). After the adjustment of the insulin treatment in poorly-controlled patients, the responses improved and the effect of superoxide dismutase disappeared only in the patients that achieved good control (n = 9), but not in those who remained poorly-controlled (n = 3). CONCLUSIONS: In patients with diabetes type 1, glycaemic control determines the functioning of the NO system by a reversible mechanism involving superoxide anions. This finding provides an explanation of the relationship between glycaemic control and vascular complications in diabetes.

Adult↗