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M Sainz

Publications and source records attributed to M Sainz.

24 records · Page 2Linked to original sources
PubMedDate not supplied

Human hepatocyte transplantation for acute liver failure: state of the art and analysis of cell sources.

Liver transplantation is the only treatment available for acute liver failure. However, mortality rates remain high because of the shortage of donor organs. Indeed up to 20% of patients with acute liver failure may survive without transplantation. In the last two decades, research has focused on the development of alternative or supportive measures to deal with acute liver failure; one of the most studied is hepatocyte transplantation, because it is thought that the function of the liver can only be replaced with a biological substrate characterized by functioning liver cells. Hepatocyte transplantation has been successful in many animal models of acute liver failure, although only several clinical attempts have been made in humans with encouraging but not yet convincing results, mainly because of the lack of a reliable source of live liver cells. Allogenic and xenogenic fresh or cryopreserved hepatocytes have been tested. Recent research has focused on fetal hepatocytes and progenitor liver cells of both hepatic and bone marrow origin. The ability to preserve and bank human hepatocytes would allow pooling of cells from multiple donors to increase the numbers for transplantation. The development of a reliable and large-scale available source of live liver cells would probably have a major impact on the introduction of hepatocyte transplantation in clinical practice.

Hepatocytes↗
PubMedDate not supplied

[Cardiovascular disease after renal transplantation].

Cardiovascular disease is the leading cause of morbidity and mortality following renal transplantation. Because many renal transplant recipients die with functioning grafts, deaths resulting from cardiovascular disease have became an increasingly important cause of graft loss, particularly after the first post-transplantation year. Moreover, a contribution of some cardiovascular risk factors to renal allograft dysfunction has been demonstrated. A number of observational studies suggest that cardiovascular disease is more common in renal transplant patients than in the general population. The excessive risk for cardiovascular disease is related to a high prevalence and accumulation of atherogenic risk factors before and after transplantation. Hypertension, post-transplantation diabetes and hyperlipidemia are well-recognized risk factors for the development of cardiovascular events after renal transplantation and are strongly associated with immunosuppressive therapy. Progressive renal dysfunction may also influence the risk of cardiovascular complications after renal transplantation. The elevated risk may also be caused by non- traditional risk factors such as anaemia, adhesion molecules, hyperhomocysteinemia, microinflammatory state, abnormal coagulation and oxidative stress. To prevent post-transplantation cardiovascular disease it is crucial to define the etiological risk factors. Some risk factors can be modified, and for some of these, there is strong evidence from studies in the general population that intervention improves survival. Given the significant morbidity and mortality of cardiovascular disease in renal transplant recipients, aggressive treatment intervention for potentially modifiable factors are strongly advocated after transplantation. In addition to treatment intervention, risk management should also involve tailoring the immunosuppressive regimen to minimize both direct and indirect cardiovascular risks. In this article we attempted to review and quantify the post-transplant risk factors for cardiovascular disease as well as offer suggestions on optimizing the therapy or treatment strategies to minimize the risk of cardiovascular complications in renal transplant patients. Reduction of cardiovascular morbidity and mortality can improve not only the life expectancy and quality of life of the transplant recipients but also their graft function and survival.

Anemia↗
PubMedDate not supplied

Brainstem and middle latency auditory evoked responses in rabbits with halothane anaesthesia.

The effects of different concentrations of halothane (0.5, 1 and 1.5%) in brainstem and middle latency auditory evoked responses were studied in 14 adult rabbits. The animals were firstly curarized, tracheostomized and ventilated mechanically. Various recording were made under these conditions for control purposes. During the experiment, arterial pressure, temperature, arterial concentrations of O2, CO2 and pH were monitored. Halothane produce an increase in latency a decrease in amplitude and at higher concentrations even abolished the later waves of middle latency auditory evoked responses. Brainstem potentials are stable, but slight changes in latency were observed at high concentrations (1.5%). Modifications of these potentials as a result of the different concentrations of this anaesthetic in relation with the recordings obtained in the animals curarized without anaesthesia are discussed and the results compared with previous reports in humans.

Animals↗