Determinants of self-efficacy in patients with Parkinson's disease.

BACKGROUND: Self-efficacy is the individual's assessment of his or hers ability to complete a specific task successfully and has been closely related to self-management and quality of life in several diseases. OBJECTIVE: To investigate self-efficacy in a population of Parkinson's disease (PD) patients in Mexico and study the factors that are associated with this measure. METHODS: We carried out a cross-sectional observational study involving patients with PD in an outpatient neurology clinic in Mexico, using the following instruments: Spanish version of the Chronic Disease Self-Efficacy Scale (CDSES), Quality of Life Questionnaire PDQ-8, Movement Disorders Society-Unified Parkinson's disease Rating Scale (MDS-UPDRS), Montreal Cognitive Assessment (MoCA), and Non-Motor Symptom Scale (NMSS). Clinical and demographic variables were also recorded. RESULTS: We included 73 patients with a mean age of 65 years and most patients were male. Patients with lower CDSES scores (<7.75) had worse scores in MDS-UPDRS, NMSS, and PDQ-8 scales. CDSES scores were significantly correlated with MDS-UPDRS Part I (r=-0.497, p=<0.001), Part II (r= -0.271, p=0.020), Part III (r=-0.304, p=<0.001), PDQ-8 (r=-0.472, p=<0.001), and NMSS (r=-0.504, p=<0.001). Furthermore, when assessing the simultaneous effect of covariates associated with CDSES score, only Mood/Apathy domain of NMSS was significant (beta= -0.446, t= -3.807, p= 0.012). CONCLUSIONS: PD patients with lower self-efficacy scores had worse motor and non-motor symptomatology and quality of life. Mood/Apathy disorders were negatively associated with self-efficacy and contributed significantly to this measure.

Determinants of self-efficacy in patients with Parkinson's disease / Determinantes de autoeficacia en pacientes con enfermedad de Parkinson

ABSTRACT Background: Self-efficacy is the individual's assessment of his or hers ability to complete a specific task successfully and has been closely related to self-management and quality of life in several diseases. Objective: To investigate self-efficacy in a population of Parkinson's disease (PD) patients in Mexico and study the factors that are associated with this measure. Methods: We carried out a cross-sectional observational study involving patients with PD in an outpatient neurology clinic in Mexico, using the following instruments: Spanish version of the Chronic Disease Self-Efficacy Scale (CDSES), Quality of Life Questionnaire PDQ-8, Movement Disorders Society-Unified Parkinson's disease Rating Scale (MDS-UPDRS), Montreal Cognitive Assessment (MoCA), and Non-Motor Symptom Scale (NMSS). Clinical and demographic variables were also recorded. Results: We included 73 patients with a mean age of 65 years and most patients were male. Patients with lower CDSES scores (<7.75) had worse scores in MDS-UPDRS, NMSS, and PDQ-8 scales. CDSES scores were significantly correlated with MDS-UPDRS Part I (r=-0.497, p=<0.001), Part II (r= -0.271, p=0.020), Part III (r=-0.304, p=<0.001), PDQ-8 (r=-0.472, p=<0.001), and NMSS (r=-0.504, p=<0.001). Furthermore, when assessing the simultaneous effect of covariates associated with CDSES score, only Mood/Apathy domain of NMSS was significant (beta= -0.446, t= -3.807, p= 0.012). Conclusions: PD patients with lower self-efficacy scores had worse motor and non-motor symptomatology and quality of life. Mood/Apathy disorders were negatively associated with self-efficacy and contributed significantly to this measure.

RESUMEN Antecedentes: La autoeficacia es la autoevaluación de un individuo sobre su capacidad para completar una tarea con éxito y se ha relacionado con automanejo y calidad de vida en otras enfermedades. Objetivo: Investigar la autoeficacia en una población de pacientes con enfermedad de Parkinson (EP) en México y estudiar factores asociados con esta medida. Métodos: Realizamos un estudio observacional transversal con pacientes con EP en una clínica de neurología en México. Se registraron datos demográficos y escalas que evalúan la función motora (MDS-UPDRS), no motora (NMSS) y cognitiva (MoCA), así como la calidad de vida (PDQ-8). Para valorar autoeficacia se utilizó la versión en español de la Escala de autoeficacia de enfermedades crónicas (CDSES). Resultados: Se incluyeron 73 pacientes, con una edad media de 65 años y la mayoría eran hombres. Pacientes con puntajes CDSES más bajos (<7.75) tuvieron peores puntajes en las escalas MDS-UPDRS, NMSS y PDQ-8. Las puntuaciones de CDSES se correlacionaron significativamente con la escala MDS-UPDRS Parte I (r=-0.497, p=<0.001), Parte II (r= -0.271, p=0.020), Parte III (r=-0.304, p=<0.001), PDQ-8 (r= -0.472, p=<0.001), y NMSS (r=-0.504, p=<0.001). Al evaluar el efecto simultáneo de covariables asociadas con la escala CDSES, solo el dominio estado de ánimo/apatía del NMSS resultó significativo (Beta = -0.449, t = -3.783, p = <0.001). Conclusiones: Los pacientes con menores puntajes de autoeficacia tienen peor calidad de vida y sintomatología motora y no motora. Los trastornos del estado de ánimo contribuyen negativamente a la autoeficacia.

[Impacto en el desenlace funcional en pacientes con ictus: experiencia de una unidad de cuidados neurovasculares].

Background and objective: Neurovascular care units (NCU) have a positive impact on the functional prognosis of stroke patients. The effectiveness of NCUs in Mexico has not been evaluated. Our objective was to determine the impact of an NCU in a third-level academic hospital in northeastern of Mexico. Method: We performed a prospective observational, analytic cohort study. The population was divided into two periods: the first one consisted of those patients admitted before the implementation of the NCU (2008-2010), and the second period consisted of patients admitted after the implementation of the UCN (2010-2014). Functional status was assessed with the modified Rankin scale at discharge and 3 months. Results and conclusions: 598 patients were included (period 1: 246; period 2: 352). Patients in period 2 had a higher deep venous thrombosis prophylaxis (odds ratio [OR]: 3.235; 95 % confidence interval [95 % CI]: 2.18-4.80; p = 0.01), a shorter hospital stay (OR: 0.42; 95 % CI: 0.29-0.62; p = 0.01) and less severe disability (Rankin ≥ 3) at 3 months of follow-up (OR: 0.42; 95 % CI: 0.29-0.62; p = 0.01). The implementation of an NCU in a third-level academic hospital improved the functional outcome at 3 months and decreased the days of in-hospital stay of patients with stroke.

Antecedentes y objetivo: Las unidades de cuidados neurovasculares (UCN) impactan favorablemente en el pronóstico funcional del paciente con ictus en comparación con las salas de internamiento general. La efectividad de las UCN en México no ha sido evaluada. Nuestro objetivo fue determinar el impacto que tiene una UCN en un hospital académico de tercer nivel del noreste de México. Método: Estudio de cohorte prospectivo, observacional y analítico. La población fue dividida en dos periodos: el primero consistió en aquellos pacientes ingresados antes de la implementación de la UCN (2008-2010), y el segundo consistió en pacientes ingresados posterior a la implementación de la UCN (2010-2014). Se evaluó el estado funcional al egreso y a los 3 meses. Resultados y conclusiones: Se incluyeron 598 pacientes (periodo 1: 246; periodo 2: 352). En el periodo 2 se incrementó la profilaxis de trombosis venosa profunda (razón de momios [RM]: 3.235; intervalo de confianza del 95 % [IC 95 %]: 2.18-4.80; p = 0.01) y se redujeron la estancia hospitalaria (RM: 0.42; IC 95 %: 0.29-0.62; p = 0.01) y la discapacidad funcional grave (Rankin ≥ 3) a los 3 meses de seguimiento (RM: 0.42; IC 95 %: 0.29-0.62; p = 0.01). La implementación de una UCN mejoró el desenlace funcional a 3 meses y disminuyó los días de estancia intrahospitalaria de pacientes con ictus.

Mean platelet volume in the differential diagnosis of tuberculous and bacterial meningitis.

INTRODUCTION: Mean platelet volume (MPV) has been shown to reflect the inflammatory burden in different inflammatory and autoimmune diseases. Our objective was to analyze the MPV in patients with tuberculous (TBM) and bacterial meningitis (BM). METHODOLOGY: The demographic and clinical data of 73 consecutive patients that presented with either BM (n = 35) or TBM (n = 38) were retrospectively analyzed, as well as that of 28 age- and sex-matched controls. RESULTS: MPV was 8.78±1.58 fL in patients with BM and 6.42±1.39 fL in the TBM group (p < 0.05). In the control group, MPV was 7.4±0.66 fL, significantly higher and lower when compared with TBM and BM, respectively. MPV was significantly associated with diagnosis (adjusted OR: 5.15, 95% CI: 1.090-23.7; p = 0.03). With the optimal cut-off value of 7.62 fL, MPV had 82% sensibility and 78% specificity for the differential diagnosis of TBM versus BM. Lower platelet counts, higher serum creatinine, higher white blood cell counts, and higher blood-cerebrospinal fluid glucose ratio were also predictive of BM. CONCLUSIONS: Platelet counts were lower and MPV was higher in patients with BM compared to patients with TBM.  Platelet indices, available in routine bloodwork, could be useful in the early differential diagnosis of these entities.

Acute toluene intoxication--clinical presentation, management and prognosis: a prospective observational study.

BACKGROUND: Toluene is one of the most widely abused inhaled drugs due to its acute neurologic effects including euphoria and subsequent depression. However, dangerous metabolic abnormalities are associated to acute toluene intoxication. It has been previously reported that rhabdomyolysis and acute hepatorenal injury could be hallmarks of the condition, and could constitute risk factors for poor outcomes. The objective was to describe the clinical presentation, to characterize the renal and liver abnormalities, the management and prognosis associated to acute toluene intoxication. METHODS: We prospectively assessed 20 patients that were admitted to a single center's emergency department from September 2012 to June 2014 with clinical and metabolic alterations due to acute toluene intoxication. RESULTS: The main clinical presentation consisted of weakness associated to severe hypokalemia and acidosis. Renal glomerular injury (proteinuria) is ubiquitous. Biliary tract injury (alkaline phosphatase and gamma-glutamyl transpeptidase elevations) disproportional to hepatocellular injury is common. Rhabdomyolysis occurred in 80% of patients, probably due to hypokalemia and hypophosphatemia. There were three deaths, all female, and all associated with altered mental status, severe acidosis, hypokalemia and acute oliguric renal failure. The cause of death was in all cases due to cardiac rhythm abnormalities. CONCLUSION: The hallmarks of acute toluene intoxication are hypokalemic paralysis and metabolic acidosis. Liver injury and rhabdomyolysis are common. On admission, altered mental status, renal failure, severe acidemia and female gender (not significant in our study, but present in all three deaths) could be associated with a poor outcome, and patients with these characteristics should be considered to be treated in an intensive care unit.

Clinical features and outcome of mucormycosis.

Mucormycosis (MCM) is a life-threatening infection that carries high mortality rates despite recent advances in its diagnosis and treatment. The objective was to report 14 cases of mucormycosis infection and review the relevant literature. We retrospectively analyzed the demographic and clinical data of 14 consecutive patients that presented with MCM in a tertiary-care teaching hospital in northern Mexico. The mean age of the patients was 39.9 (range 5-65). Nine of the patients were male. Ten patients had diabetes mellitus as the underlying disease, and 6 patients had a hematological malignancy (acute leukemia). Of the diabetic patients, 3 had chronic renal failure and 4 presented with diabetic ketoacidosis. All patients had rhinocerebral involvement. In-hospital mortality was 50%. All patients received medical therapy with polyene antifungals and 11 patients underwent surgical therapy. Survivors were significantly younger and less likely to have diabetes than nonsurvivors, and had higher levels of serum albumin on admission. The clinical outcome of patients with MCM is poor. Uncontrolled diabetes and age are negative prognostic factors.

1,25-dihydroxyvitamin D and PTHrP mediated malignant hypercalcemia in a seminoma.

BACKGROUND: Seminomas have been rarely associated with malignant hypercalcemia. The responsible mechanism of hypercalcemia in this setting has been described to be secondary to 1,25-dihydroxyvitamin D secretion. The relationship with PTHrP has not been determined or studied.The aim of this study is to describe and discuss the case and the pathophysiological mechanisms involved in a malignant hypercalcemia mediated by 1,25-dihydroxyvitamin D and PTHrP cosecretion in a patient with seminoma. CASE PRESENTATION: A 35-year-old man was consulted for assessment and management of severe hypercalcemia related to an abdominal mass. Nausea, polyuria, polydipsia, lethargy and confusion led him to the emergency department. An abdominal and pelvic enhanced CT confirmed a calcified pelvic mass, along with multiple retroperitoneal lymphadenopathy. Chest x-ray revealed "cannon ball" pulmonary metastases. The histopathology result was consistent with a seminoma. Serum calcium was 14.7 mg/dl, PTH was undetectable, 25-dihydroxyvitamin D was within normal values and PTHrP and 1,25-dihydroxyvitamin were elevated (35.0 pg/ml, and 212 pg/ml, respectively). After the first cycle of chemotherapy with bleomycin, etoposide and cisplatin, normocalcemia was restored. Both PTHrP and 1,25-dihydroxyvitamin D, dropped dramatically to 9.0 pg/ml and 8.0 pg/ml, respectively. CONCLUSION: The association of seminoma and malignant hypercalcemia is extremely rare. We describe a case of a patient with a seminoma and malignant hypercalcemia related to paraneoplastic cosecretion of 1,25-dihydroxyvitamin D and PTHrP. After successful chemotherapy, calcium, PTHrP and 1,25-Dihydroxyvitamin D returned to normal values.

Temporal relationship of serum markers and tissue damage during acute intestinal ischemia/reperfusion.

OBJECTIVE: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chiús classification to grade the histopathological damage. METHODS: We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ± standard deviation and compared the baseline and maximum values for each marker using Student's t-test. RESULTS: The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group. CONCLUSION: For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis factor alpha as indicators of acute inflammation three hours after reperfusion.

Temporal relationship of serum markers and tissue damage during acute intestinal ischemia/reperfusion

OBJECTIVE: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chiús classification to grade the histopathological damage. METHODS: We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ± standard deviation and compared the baseline and maximum values for each marker using Student's t-test. RESULTS: The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group. CONCLUSION: For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis ...

Isolated rheumatoid arthritis-associated cerebral vasculitis: a diagnostic challenge.

Central nervous system involvement in rheumatoid arthritis is uncommon. In order of frequency, published cases have reported rheumatoid nodules, meningeal vasculitis, and cerebral vasculitis (CV). The frequency of vasculitic cerebral involvement in rheumatoid arthritis is unknown. However, it is known that it is more common in patients with seropositive, long-standing rheumatoid arthritis, and in those with concomitant systemic vasculitis. We report the case of a 47-year-old woman with an 11-year history of seropositive rheumatoid arthritis without any extra-articular manifestations, with the exception of secondary Sjogren's syndrome, presenting with mental status changes and tonic-clonic seizures as symptoms of isolated CV. Magnetic resonance imaging (T2) showed hyperintense white-matter lesions in the frontal and temporal lobes, as well as in the hippocampus and cerebellum. Transcranial Doppler ultrasound findings were consistent with CV. Other differential diagnoses were ruled out. The patient responded favorably to methylprednisolone and intravenous gammaglobulin therapy.

Arachidonic acid derivatives and their role in peripheral nerve degeneration and regeneration.

After peripheral nerve injury, a process of axonal degradation, debris clearance, and subsequent regeneration is initiated by complex local signaling, called Wallerian degeneration (WD). This process is in part mediated by neuroglia as well as infiltrating inflammatory cells and regulated by inflammatory mediators such as cytokines, chemokines, and the activation of transcription factors also related to the inflammatory response. Part of this neuroimmune signaling is mediated by the innate immune system, including arachidonic acid (AA) derivatives such as prostaglandins and leukotrienes. The enzymes responsible for their production, cyclooxygenases and lipooxygenases, also participate in nerve degeneration and regeneration. The interactions between signals for nerve regeneration and neuroinflammation go all the way down to the molecular level. In this paper, we discuss the role that AA derivatives might play during WD and nerve regeneration, and the therapeutic possibilities that arise.

Solitary Apical Lung Mass in a Patient With Cervical Cancer.

We present the case of a 40 years old female presenting with a solitary apical lung mass, associated Horner syndrome and evidence of medullary compression. Although she had a history of cervical cancer, a primary lung tumor was suspected. Tissue biopsy confirmed cervical cancer metastasis, highlighting the fact that although metastasis usually presents as multiple lung nodules, solitary lesions can be the presenting sign.

Ketamine reduces intestinal injury and inflammatory cell infiltration after ischemia/reperfusion in rats.

PURPOSE: Intestinal ischemia reperfusion (I/R) induces severe injury and significant mortality. New therapeutic interventions are needed; ketamine is an anesthetic with anti-inflammatory properties, which has shown protective effects on I/R in various organs. This study investigated effects of ketamine on intestinal I/R injury. METHODS: Male Wistar rats underwent either sham surgery or 30 min of intestinal ischemia followed by 60 min reperfusion. Ketamine pretreatment was administered by intraperitoneal injections at doses of 100, 50, 12.5, or 6.25 mg/kg. The intestinal morphology, mucosal damage, leukocyte infiltration, serum P-selectin, serum intracellular adhesion molecule-1 (ICAM-1), serum antithrombin-III (ATIII), and myenteric ganglion cell structure were evaluated. RESULTS: Intestinal I/R led to severe mucosal damage, leukocyte (especially neutrophil) infiltration, P-selectin and ICAM-1 elevations, ATIII depletion, and myenteric ganglion cell morphological alterations. The ketamine dose dependently diminished these alterations (except for ICAM-1 serum levels), reaching statistical significance at 100, 50, and 12.5 mg/kg. CONCLUSIONS: Ketamine protects the intestine against I/R injury. Ketamine anesthesia has been recommended for clinical situations of sepsis and hemodynamic instability, both frequent during intestinal I/R. The clinical application of ketamine in situations of intestinal I/R warrants consideration.

Dengue hemorrágico en un lactante después de primoinfección / Dengue hemorrhagic fever in an infant after primoinfection

Introducción. El dengue es una enfermedad infecciosa causada por un flavivirus y transmitida por un vector. Puede originar cuadros febriles inespecíficos, fiebre hemorrágica por dengue (FHD) o, incluso, síndrome de choque. El tratamiento se basa en el control hemodinámico y control del balance hídrico. Caso clínico. Paciente femenino de 4 meses, inicia con fiebre y desarrolla síntomas y signos, primero de FHD y posteriormente síndrome de choque. Se corroboró el diagnóstico serológico de primoinfección por dengue. No existió evidencia de infección previa en la madre. Con tratamiento de soporte mejora y posteriormente se egresa asintomática. Conclusiones. Según algunas teorías, la FHD en lactantes se asocia a anticuerpos no neutralizantes, transmitidos de manera pasiva por una madre previamente infectada, que ocasionan en el lactante una reacción severa ante una primoinfección. En este caso, otros factores independientes del huésped, como virulencia del virus infectante, pudieran ser los responsables.

Background. Dengue fever is an infectious disease caused by a flavivirus and transmitted by a vector. It causes dengue fever, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). When one of these last two appears, treatment consists of intensive fluid balance control. Case report. A 4-month-old female infant presented fever. She was admitted and later showed signs and symptoms of DHF followed by DSS. Serological diagnosis was confirmed, and appropriate treatment offered. The mother does not have evidence of prior infection. Discussion. One theory proposes that DHF occurs in infants when passively transferred maternal antibodies from a previous infection cause an enhanced immune response when the infant is infected by a different type of dengue virus. This theory does not explain the occurrence of DHF in our report. Factors not dependent on the host, such as virological factors, may be responsible.

Molecular inflammatory mediators in peripheral nerve degeneration and regeneration.

Wallerian degeneration, the self-destructive set of cellular and molecular processes by which degenerating axons and myelin are cleared after injury, is initiated by macrophages and Schwann cells. Molecular inflammatory mediators such as cytokines (IL-1, IL-6, IL-10, and TNF-alpha, among others), transcription factors (NF-kappaB, c-Jun), the complement system and arachidonic acid metabolites have been shown to modulate these processes in various studies. However, the exact role that each of these mediators plays during axonal degeneration and regeneration has not been fully established. Understanding the molecular basis of these interactions between the immune system and peripheral nerve injury would open the possibility of targeting these inflammatory mediators as therapeutic interventions. In this review we attempt to integrate the current evidence generated around this issue, and to explore the therapeutic possibilities that arise.

Ketamine and the myenteric plexus in intestinal ischemia/reperfusion injury.

BACKGROUND AND AIMS: Intestinal ischemia/reperfusion (I/R) is a common clinical entity with severe consequences. We studied the effects of ketamine and the participation of the myenteric plexus in I/R injury. METHODS: Rats were divided into six groups: sham, IR (30 min ischemia/60 min reperfusion), KET+IR (50 mg/kg i.p. ketamine injection before I/R), DEN (myenteric plexus ablated with benzalkonium chloride (BAC) and sham operation performed), DEN+IR (BAC treated and I/R induced), and DEN+KET+IR (BAC treated, ketamine administered, and I/R induced). Serum concentrations of p-selectin, intracellular adhesion molecule-1 (ICAM-1), and antithrombin III (ATIII) were measured, and tissue samples were obtained for histological analysis. RESULTS: IR group had higher intestinal mucosa injury and elevated serum concentrations of ICAM-1 and p-selectin, as well as ATIII depletion, compared with sham group (P < 0.05). In KET+IR group these alterations were significantly reduced (P < 0.05). DEN group showed ICAM-1 elevations when compared with sham group (P < 0.05), and DEN+IR group showed no difference in any parameter compared with IR group. However, ketamine administration in group DEN+KET+IR had no effect on any parameter when compared with DEN+IR group. CONCLUSIONS: Ketamine was able to diminish alterations induced by I/R. Myenteric plexus ablation with BAC treatment alone had no effects on intestinal I/R injury. However, this procedure abolished ketamine's protective effects. Ketamine seems to require an intact enteric nervous system to exert its protective action.

The effects of NMDA receptor antagonists over intestinal ischemia/reperfusion injury in rats.

Intestinal ischemia/reperfusion causes severe injury and alters motility. N-methyl-D-aspartate (NMDA) receptor antagonists have been shown to reduce ischemia/reperfusion injury in the nervous system, and in other organs. In this study, we set out to investigate the effects of NMDA receptor antagonists over intestinal ischemia/reperfusion injury. Male Wistar rats were randomly divided into four groups: (1) a control, sham-operated group; (2) an intestinal ischemia/reperfusion group subjected to 45 min ischemia and 1h reperfusion; (3) a group treated with 10 mg/kg ketamine before ischemia/reperfusion; and (4) a group treated with 10 mg/kg memantine before ischemia/reperfusion. Intestinal samples were taken for histological evaluation. Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), malondialdehyde (MDA), total antioxidant capacity, tumor necrosis factor alpha (TNF-alpha), P-selectin and antithrombin III (ATIII) were measured. Intestinal transit time was determined to evaluate intestinal motility. Fecal pellet output and animal weight were also registered daily for 7 days post-ischemia. After reperfusion, AST, LDH, TNF-alpha and P-selectin levels were elevated, ATIII levels were depleted, and ALT levels were unchanged in serum. Additionally, levels of MDA were increased and total antioxidant capacity was reduced in serum, indicating oxidative stress. Intestinal mucosa showed severe injury. Ketamine, but not memantine, diminished these alterations. Intestinal motility and fecal pellet output were also altered after ischemia/reperfusion. Both drugs abolished the alterations in motility. In conclusion, ketamine's protective effects over ischemia/reperfusion do not appear to be NMDA mediated, but they could be playing a role in protecting the intestine against ischemia-induced functional changes.