Biomedical subjects

Durval Rosa Borges

Publications and source records attributed to Durval Rosa Borges.

7 recordsLinked to original sources

PubMed2005

Kallikrein-kinin system in hepatic experimental models.

The purpose of this brief review is to describe some characteristics of the kallikrein-kinin system (KKS) in the liver. The liver synthesizes kininogens and prekallikrein and the synthesis of both proteins is increased in rats during the acute phase reaction. It is also the main organ to clear tissue as well as plasma kallikrein from the circulation in normal and pathological conditions. Bradykinin (BK), yielded by the kallikrein-kinin system, is a potent arterial hypotensive peptide, but in the liver it induces a portal hypertensive response. The portal hypertensive action of bradykinin is mediated by B2 receptors located on sinusoidal cells of the periportal region and is followed by its hydrolysis by angiotensin-converting enzyme, which is primarily present in the perivenous (centrolobular) region.

Animals↗

PubMed2005

Hemodynamic and metabolic effects of angiotensin II on the liver.

To ascertain the mechanism of interaction between angiotensins (AI and AII) and the liver, an angiotensin-converting enzyme inhibitor (captopril) and a receptor antagonist (losartan) were used. Monovascular or bivascular liver perfusion was used to assess both hemodynamic (portal and arterial hypertensive responses) and metabolic (glucose production and oxygen consumption) effects. Microphysiometry was used for isolated liver cell assays to assess AII or losartan membrane receptor-mediated interaction. Captopril abolishes portal hypertensive response (PHR) to AI but not the AII effect. AII infused via the portal pathway promotes calcium-dependent PHR but not a hypertensive response in the arterial pathway (AHR); when infused into the arterial pathway AII promotes calcium-dependent PHR and AHR. Losartan infused into the portal vein abolishes PHR to AII but not the metabolic response; when infused via both pathways it abolishes the hypertensive responses and inhibits the metabolic effects. Isolated liver cells specifically respond to AII. Sinusoidal cells, but not hepatocytes, respond to 10 nM losartan. We conclude that AI has to be converted to AII to produce PHR. Quiescent stellate cells interacts in vitro with AII and losartan. Hemodynamic responses to AII are losartan-dependent but metabolic responses are partially losartan-independent. AII hemodynamic actions are mainly presinusoidal.

Angiotensin II↗

PubMed2005

Fate of bradykinin on the rat liver when administered by the venous or arterial route.

BACKGROUND AND AIM: Bradykinin (BK) infused into the portal vein elicits a hypertensive response via the B2 receptor (B2R) and is efficiently hydrolyzed by the liver. Our purpose was to characterize the mechanism of interaction between BK and the liver. METHOD: BK, HOE-140 (a B2R antagonist), des-R(9)-BK (a B1R agonist) and enzyme inhibitors were used in monovascular or bivascular perfusions and in isolated liver cell assays. RESULTS: Des-R(9)-BK did not elicit a portal hypertensive response (PHR); BK infused into the hepatic artery elicited a calcium-dependent PHR and a calcium-independent arterial hypertensive response (HAHR), with the latter being almost abolished by naproxen. BK has a predominant distribution in the extracellular space and an average hepatic extraction of 8% in the steady state. Hydrolysis products of infused BK (R(1)-F(5) and R(1)-P(7)) did not elicit PHR. Angiotensin converting enzyme (ACE) is concentrated in the perivenous region and B2R in the periportal region. Microphysiometry showed that BK (and not a B1 agonist) interacts with stellate cells and the endothelial sinusoidal/Kupffer cell fraction. This effect was inhibited by the B2R antagonist. CONCLUSIONS: Events can be summarized as: the hypertensive action of BK on sinusoidal cells of the periportal region is followed by its hydrolysis by ACE which is primarily present in the perivenous region; there is no functional B1R in the normal liver; BK induces HAHR via eicosanoid release and PHR by a distinct pathway on the B2R. Our data suggest that BK may participate in the modulation of sinusoidal microvasculature tonus both in the portal and the arterial routes.

Adrenergic beta-Antagonists↗

PubMed2004

[Educational program in schistosomiasis: a model for a methodological approach].

OBJECTIVE: Lack of knowledge is one of the factors responsible for the persistence of infectious diseases in Brazil. This study had the objective of developing, implementing and evaluating a low-cost educational program using schistosomiasis patients as a model. METHODS: This was a descriptive study developed using a population of healthy people (group 1) and schistosomiasis patients (groups 2 and 3), with 20 individuals in each group. Teaching material (illustrated manual and album of leaflets) and a questionnaire consisting of 17 questions to evaluate the groups' knowledge were devised. The questionnaire was applied to groups 1 and 2 before and to group 3 after the educational program. The variables studied were the educational program, level of schooling, age, clinical form of schistosomiasis, symptoms, and the subject's performance when answering the questionnaire. For the statistical analysis, Fisher's exact test and variance analysis with one fixed factor were utilized. RESULTS: The educational program was evaluated in the form of four topics: cycle, clinical presentation, treatment and prevention of the disease. The median number of correct responses to the questionnaire was higher for group 3 than for groups 1 and 2, for all the topics dealt with. This median was also higher for group 2 than for group 1, for all topics except for the item "prevention". CONCLUSIONS: The educational process applied was efficient and improved the knowledge of the disease. It may provide an effective low-cost methodological model that can also be applied to combating other endemic diseases.

Adult↗

PubMed2004

[Construction and implementation of nursing actions in the gastroenterology outclinic].

UNLABELLED: The reorganization of the Schistosomiasis Sector of Gastroenterology at UNIFESP started in 1998, when the Nursing Service was implanted. OBJECTIVE: to develop administrative nursing actions, systematization of care and orientation program for the schistosomic patient. METHOD: a descriptive study carried out at the Gastroenterology Outclinic, which attends schistosomic patients of different clinical types. RESULTS AND DISCUSSION: the reorganization of activities in this Sector resulted in the creation of an organizational structure and the implantation of the nursing visit; creation and distribution of explanatory leaflets and development of the Schistosomiasis Education Program; beginning of the database pilot project with all outpatients and an electronic register of the collection of biologic material. CONCLUSION: this initiative opens up a new opportunity for nursing actions and contributes to quality improvement in ambulatory care.

Ambulatory Care↗

PubMed2002

Enzyme release from injured, preserved, and ex vivo reperfused liver does not indicate malfunction.

OBJECTIVE: We compared the enzyme release from preserved and ex vivo reperfused livers after acute injury or inflammatory stimulus with organ function. METHODS: Acute injury was induced by carbon tetrachloride and inflammation was induced by turpentine oil treatments. Livers were exsanguinated and preserved for 8 or 24 hr. Enzymes were measured in preservation and reperfusion solutions, and reperfused liver function was evaluated by O(2) consumption and bromsulphalein clearance. RESULTS: The release of lysosomal enzymes was negligible in the preservation solution, and that of alanine aminotransferase and lactate dehydrogenase was similar in all groups. Release of aspartate aminotransferase and of EC 3.4.24.15 was more than that of the controls. During reperfusion liver function was normal in the injured group. CONCLUSION: Release of enzymes, mainly aspartate aminotransferase and EC 3.4.24.15, into the preservation solution is a sensitive and early indicator of either inflammatory or acute injury alterations of the preserved liver, but does not reflect organ malfunction.

Acute Disease↗

PubMedDate not supplied

[Serum gamma-glutamyltransferase alteration in hepatic schistosomiasis doesn't correlate with parasitic load and precedes ultrasound alterations].

BACKGROUND: Liver disorders are the major manifestations of schistosomiasis mansoni. Factors that account for increased concentrations of cholestasis-indicating enzymes in the hepatosplenic form of the disease are unknown. OBJECTIVE: To assess the correlation between increased gamma-glutamyltransferase serum levels and both the parasitic load and ultrasound alterations in patients with schistosomiasis. PATIENTS AND METHODS: Twenty-five patients with the chronic form of schistosomiasis were assessed for the presence or absence of increased enzymatic levels, for the parasitic load (low x medium/high) and for ultrasound parameters. Furthermore, analysis of prothrombin time and a platelet count were performed. RESULTS: Of the 25 patients, 13 showed increased gamma-glutamyltransferase plasma levels. No significant correlation was found between increased gamma-glutamyltransferase levels and the parasitic load, or between increased enzyme levels and ultrasound alterations. Nor did the prothrombin index or the platelet count differ between the two groups (normal gamma-glutamyltransferase levels and increased gamma-glutamyltransferase levels). CONCLUSION: The parasitic load explains no rise in gamma-glutamyltransferase plasma levels in patients with the chronic form of schistosomiasis, and conventional ultrasound is not a sensitive method to detect the alteration suggested by the increased enzyme level in those patients.

Adult↗