Biomedical subjects

Maria Marques

Publications and source records attributed to Maria Marques.

4 recordsLinked to original sources

PubMed2006

Victims of cardiac arrest occurring outside the hospital: a source of transplantable kidneys.

BACKGROUND: The use of non-heart-beating donors could help shorten the list of patients who are waiting for a kidney transplant. Several reports describe acceptable results of transplantations from non-heart-beating donors who had in-hospital cardiac arrest, but few reports describe results of transplantations from non-heart-beating donors who had cardiac arrest that occurred outside of the hospital (Maastricht type I and type II donors). OBJECTIVE: To compare graft survival rates among patients receiving kidneys from heart-beating donors versus type I or type II non-heart-beating donors. DESIGN: Retrospective cohort study of transplantations performed from January 1989 to December 2004. SETTING: Kidney transplant program of a teaching hospital in Madrid, Spain. PATIENTS: 320 patients who received a kidney transplant from non-heart-beating donors (273 type I donors and 47 type II donors) and 584 patients who received a kidney transplant from heart-beating donors divided into 2 groups according to donor age (age <60 years [n = 458] and age > or =60 years [n = 126]). MEASUREMENTS: The primary outcome measure was graft survival. The median follow-up time was 68 months (range, 9 to 198 months). RESULTS: One- and 5-year graft survival rates were 90.7% and 85.5%, respectively, for transplants from heart-beating donors younger than 60 years of age; 79.8% and 73.3%, respectively, for transplants from heart-beating donors 60 years of age or older (P < 0.001); and 87.4% and 82.1%, respectively, for transplants from non-heart-beating donors (P = 0.22 [vs. those from heart-beating donors < 60 years of age] and P = 0.014 [vs. those from heart-beating donors >or = 60 years of age]). Graft survival did not differ between patients who received kidneys from heart-beating donors younger than 60 years of age and patients who received kidneys from non-heart-beating donors. LIMITATIONS: This single-site, observational study was retrospective, and immunosuppressive therapy regimens given to transplant recipients varied over time. CONCLUSIONS: Outcomes of transplants from non-heart-beating donors and younger heart-beating donors are similar, and results for transplants from non-heart-beating donors improved compared with those from older heart-beating donors. On the basis of these results, the authors encourage other transplant units to adopt the use of type I and type II non-heart-beating donors.

Adult↗

PubMed2005

Endothelial hypoxic preconditioning in rat hypoxic isolated aortic segments.

Our aim was to analyse endothelial hypoxic preconditioning after hypoxia-reperfusion (HR). Endothelial functionality was analysed through the vasorelaxation responses to acetylcholine (Ach) and the level of serine1177 phosphorylated endothelial nitric oxide synthase (eNOS) (ser1177-eNOS) measured by Western blot in in vitro hypoxic preconditioned (P + HR) isolated rat aortic segments. Relaxation in response to Ach was reduced in phenylephrine-precontracted aortic segments after HR (control: IC50, 5 +/- 2.5 x 10(-8) mol l(-1); HR: IC50, 3 +/- 1.2 x 10(-7) mol l(-1); P < 0.05). Ach-dependent vasodilatation was improved by P + HR. The content of ser1177-eNOS in the HR segments was 1.5-fold lower than in P + HR. Confocal microscopy showed an increased content of both superoxide anion and peroxynitrite in the vascular wall of HR aortic segments, which it was reduced by P + HR. Geldanamycin (10 microg ml(-1)), an agent known to inhibit heat shock protein 90 (hsp90), reduced the level of ser1177-eNOS in P + HR aortic segments. However in the presence of geldanamycin, endothelial hypoxic preconditioning persisted. We conclude that short periods of hypoxia induced endothelial hypoxic preconditioning that was accompanied by enhanced levels of ser1177-eNOS in the vascular wall. The fact that endothelial hypoxic preconditioning persisted in the presence of geldanamycin suggests that other molecular mechanisms are involved in the endothelial adaptation to HR injury.

Acetylcholine↗

PubMed2003

Treatment of calcium channel blocker intoxication with insulin infusion: case report and literature review.

We present a case report of successful treatment of shock induced by the calcium channel blocker (CCB) diltiazem. A 75-year-old woman took a combination of tablets, including diltiazem. Soon after arrival, she developed haemodynamic shock which persisted despite treatment with fluids, dopamine, dobutamine, norepinephrine (noradrenaline), calcium gluconate and glucagon. Haemodynamic stability was not achieved until an insulin infusion and glucose administration was started. We review the literature and the updated guidelines for the treatment of CCB intoxication, with particular emphasis on situations where insulin and glucose infusions can be live saving.

Aged↗

PubMed2003

Lead-induced downregulation of soluble guanylate cyclase in isolated rat aortic segments mediated by reactive oxygen species and cyclooxygenase-2.

Lead exposure is a known cause of hypertension. Although most studies have focused on lead-induced endothelial dysfunction and on the involvement of reactive oxygen species (ROS), it has been recently demonstrated that the vascular wall of lead-exposed rats has both an altered the endothelium-independent relaxing response and a reduced expression of soluble guanylate cyclase (sGC). The aim of the present study was to determine in in vitro incubated rat isolated aortic segments if lead downregulates sGC expression, analyzing the involvement of ROS and cyclooxygenase-2 (COX-2). The experiments were performed in isolated aortic segments from Wistar rats that were incubated with lead for 24 h. Lead significantly reduced sGC-beta(1) subunit expression in a concentration-dependent manner. The maximal reduction in sGC-beta(1) subunit expression was achieved with 1 ppm lead. Vitamin C (30 micromol/L) partially restored sGC-beta( 1) subunit expression in lead (1 ppm)-exposed aortic segments. A similar protection of sGC-beta(1) subunit expression was obtained with both a protein kinase A inhibitor, H89 (1 micromol/L) and with rofecoxib (1 micromol/L), an inhibitor of COX-2 activity. Moreover, lead exposure increased COX-2 expression in the arterial wall. While vitamin C reduced both COX-2 expression and superoxide anion production related to lead exposure, rofecoxib failed to modify superoxide anion generation in lead-incubated aortic segments. In conclusion, the present results suggest the involvement of ROS and COX-2 in the downexpression of sGC-beta(1) subunit induced by lead in the rat vascular wall.

Animals↗