Biomedical subjects

G A Abrams

Publications and source records attributed to G A Abrams.

25 records · Page 2Linked to original sources

PubMed1997

The role of endothelial nitric oxide synthase in the pathogenesis of a rat model of hepatopulmonary syndrome.

BACKGROUND & AIMS: The hepatopulmonary syndrome occurs when intrapulmonary vasodilatation causes impaired arterial gas exchange in liver disease. The pathogenesis is poorly understood, although nitric oxide may be involved. Common bile duct ligation in the rat is a model of the hepatopulmonary syndrome, but no studies have evaluated NO in pulmonary vasodilatation in this model. The aim of this study was to determine whether NO contributes to intrapulmonary vasodilatation after bile duct ligation. METHODS: Endothelial and inducible NO synthase (NOS) levels and localization and NO activity in pulmonary artery rings were assessed after bile duct ligation. RESULTS: Pulmonary endothelial NOS levels increased and alveolar vascular staining was enhanced after bile duct ligation. No change in pulmonary inducible NOS levels or localization was detected. Increased endothelial NOS levels correlated with alterations in gas exchange and were accompanied by enhanced NO activity and a blunted response to phenylephrine, reversible by NOS inhibition, in pulmonary artery rings. Portal-vein-ligated animals, which do not develop intrapulmonary vasodilatation, had no changes in pulmonary NOS production or in NO activity in pulmonary artery rings. CONCLUSIONS: NO, derived from pulmonary vascular endothelial NOS, contributes to intrapulmonary vasodilation in animal hepatopulmonary syndrome.

Acetylcholine↗

PubMed1997

Common bile duct ligation in the rat: a model of intrapulmonary vasodilatation and hepatopulmonary syndrome.

Hepatopulmonary syndrome (HPS) causes impaired oxygenation due to intrapulmonary vasodilatation in patients with cirrhosis. Chronic common bile duct ligation (CBDL) in the rat results in gas-exchange abnormalities similar to HPS, but intrapulmonary vasodilatation has not been evaluated. We assess intrapulmonary vasodilatation, measured in vivo, after CBDL. Sham, 2- and 5-wk CBDL, and 3-wk partial portal vein ligated (PVL) rats had hepatic and lung injury, portal pressure, and arterial blood gases assessed. The pulmonary microcirculation was evaluated by injecting microspheres (size range 5.5-10 microm) intravenously and measuring the size and number of microspheres bypassing the lungs in arterial blood. CBDL animals developed progressive hepatic injury and portal hypertension accompanied by gas-exchange abnormalities and intrapulmonary vasodilatation. PVL animals, with a similar degree of portal hypertension, did not develop intrapulmonary vasodilatation or abnormal gas exchange. No lung injury was observed. CBDL, but not PVL, causes progressive intrapulmonary vasodilatation, which accompanies worsening arterial gas exchange. These findings validate CBDL as a model to study HPS.

Animals↗

PubMed1996

Scenario number one: hepatopulmonary syndrome.

HPS is an increasingly recognized clinical entity resulting from intrapulmonary vasodilatation in patients with liver disease and/or portal hypertension. The pathogenesis of alterations in the pulmonary vascular bed in affected patients is poorly understood and the subject of ongoing investigation. The differential diagnosis of pulmonary symptoms and gas-exchange abnormalities in patients with liver disease being evaluated for transplantation is broad and should be focused on differentiating pulmonary causes that significantly increase the risk for transplantation from HPS where transplantation has emerged as a useful treatment. Specific contraindications to transplantation in patients with HPS have not been identified, though unique postoperative complications have been observed and may be treatable during the frequently prolonged resolution of intrapulmonary vasodilatation. The development of a database of information on patients with HPS undergoing transplantation will provide insight into potential contraindications, prognostic features, and postoperative complications unique to these patients.

Adult↗

PubMed1996

Muscle cramps in patients with cirrhosis.

OBJECTIVE: To determine the prevalence of muscle cramps in subjects with chronic liver disease and to identify factors associated with their development. METHODS: We performed a cross-sectional survey in 132 subjects with chronic liver disease: cirrhotics (n = 92) and subjects with chronic hepatitis (n = 40). In addition, to control for diuretic use, patients with congestive heart failure (n = 40) were included as a comparison group. RESULTS: The prevalence of chronic muscle cramps was significantly greater in cirrhotics compared with patients with chronic hepatitis [48/92 (52%) vs 3/40 (7.5%), respectively, p < 0.0001] and compared with subjects with congestive heart failure [8/40 (20%), p < 0.001]. Factors, including age, gender, alcoholic liver disease, electrolytes, and diuretic use were similar among cirrhotics with and without cramps. Significantly higher total bilirubin and lower albumin levels were noted in cirrhotics with and without cramps, respectively; however, there was no significant difference in Child's A or B classification. CONCLUSIONS: There is an increased prevalence of chronic muscle cramps in subjects with cirrhosis that appears to be independent of the etiology of cirrhosis, diuretic consumption, serum electrolyte alterations, or differences in Child's classification. These results suggest that cramps in these patients are related specifically to the development of cirrhosis, and worsening liver function may be a risk factor for the development of cramps.

Adult↗

PubMed1995

Diagnostic utility of contrast echocardiography and lung perfusion scan in patients with hepatopulmonary syndrome.

BACKGROUND & AIMS: Two modalities, contrast echocardiography and lung perfusion scan, are used to identify intrapulmonary vascular dilatation and diagnose hepatopulmonary syndrome (HPS), but a comparison of these two procedures has not been performed. The aim of this study was to compare the use of these diagnostic modalities in detecting intrapulmonary vascular dilatation and diagnosing HPS. METHODS: Forty consecutive outpatients with biopsy-proven cirrhosis had contrast echocardiography, a lung perfusion scan, and arterial blood gases analyzed. RESULTS: Fifteen of 40 cirrhotics (38%) had positive contrast echocardiogram results. Seven patients with positive echocardiogram results had gas exchange abnormalities and could be considered to have HPS (7 of 40 [17.5%]). Three of these patients were hypoxemic and had no concurrent cardiopulmonary disease, and each had positive contrast echocardiogram and lung perfusion scan results and were readily diagnosed as having HPS. The other 4 patients (3 hypoxemic and 1 normoxemic with an elevated alveolar-arterial gradient) had coexisting intrinsic lung disease and/or chest radiograph abnormalities complicating the diagnosis of HPS, and each had positive echocardiogram and negative lung scan results. The remaining 8 patients with positive echocardiogram results had normal lung scan and normal gas exchange results. No patient had positive lung scan and negative contrast echocardiogram results. CONCLUSIONS: Contrast echocardiography is the most useful screening test for intrapulmonary vasodilatation and may be positive more frequently than lung perfusion scans in patients with HPS.

Adult↗

PubMed1995

Nitric oxide and liver disease.

Nitric oxide is a highly reactive, diffusible gas that is produced by many tissues, and it exerts a range of physiological and pathophysiological effects. The liver is one organ clearly influenced by nitric oxide, and acute versus chronic exposure to this substance has been associated with distinct patterns of liver disease. Bacterial infections, including the sepsis syndrome, acutely increase nitric oxide systemically and may lead to acute hepatic dysfunction. We review etiology, diagnosis, and treatment of cholestasis associated with these infections, because this condition in particular has been linked to nitric oxide. Chronic increases in nitric oxide may cause the hyperdynamic circulation seen in cirrhosis and portal hypertension. Therefore, we also review etiology, diagnosis, and treatment of the hepatorenal and hepatopulmonary syndromes, because both these syndromes occur in end-stage liver disease, and they may be linked to nitric oxide as well. An appreciation of nitric oxide and its evolving role in hepatology may be important to understand the pathogenesis of and treatment strategies for these different types of liver disease.

Humans↗

PubMed1989

Experimental autoimmune encephalomyelitis: isolation and characterization of inflammatory cells from the central nervous system.

Lymphocytes from the central nervous system (CNS) of animals with acute experimental autoimmune encephalomyelitis (EAE) have been isolated and characterized. The lymphocytes were separated from Lewis rats which were injected either with an emulsion of myelin basic protein (BP) emulsified in complete Freund's adjuvant (CFA) to cause EAE or with CFA alone as a control. Using density gradient centrifugation, from 9 days post-inoculation (d.p.i.) (before clinical signs appear), to 19 d.p.i. (after signs abate), lymphocytes were recovered from the spinal cords and popliteal lymph nodes of BP-injected animals. Lymphocyte cell number, phenotype, and antigen specificity were determined. Results show that the onset of clinical signs correlated with lymphocyte influx into the CNS. A clinical index of 1 was associated with less than 10(6) cells per gram of CNS wet weight (cells/g CNS) while animals with a clinical index of 4 had more than 15 X 10(6) cells/g CNS. During remission, when only minor residual neurologic signs were evident, significant numbers of lymphocytes (greater than 10(7) cells/g CNS) could still be isolated. In contrast, no lymphocytes were obtained from control CNS tissue. The phenotype of the recovered cells was predominantly of the helper/inducer T cell subset (greater than 40%). Although the percentages of these cells in the CNS were increased when compared to the lymph nodes, I-A expression on CNS-isolated lymphocytes showed the most significant increase with disease progression. Recovered lymphocytes responded to both BP and CFA-related antigens indicating that both CNS-specific and CNS-non-specific inflammatory cells were present in the exudate.

Animals↗