Primary non-Hodgkin's lymphoma of the common bile duct.

Primary non-Hodgkin's lymphoma of the common bile duct is rare. To date, nine cases have been recorded in the literature. We report an additional case of a 39-yr-old woman presented with obstructive jaundice. Pathological studies of the surgical specimen disclosed that the wall of the common bile duct was transmurally infiltrated by non-Hodgkin's lymphoma of diffuse large cell type of B-cell lineage intimately associated with reticular fibers. The patient received postoperative brachytherapy, followed by six cycles of chemotherapy according to the CHOP regimen. There is no evidence of lymphoma recurrence 13 months after the surgery. Our analysis of the reported cases indicates that common bile duct non-Hodgkin's lymphoma is a rapidly progressive disease, terminating in death within a year. A complete surgical resection of the lymphoma followed by chemotherapy has shown a promising result.

Laboratory implementation of a rapid three-stain technique for detection of microorganisms from lower respiratory specimens.

A rapid, cost-effective method for the evaluation of lower respiratory specimen has become increasingly important in the diagnosis of pulmonary diseases in immunocompromised patients. In the past, the technically demanding, time-consuming, and expensive Gomori-methenamine-silver (GMS) stain was the principal means for the evaluation of these specimens. In this study, we compared the GMS stain with a new rapid, three-stain protocol for the evaluation of lower respiratory specimens. Lower respiratory specimens were obtained by bronchoalveolar lavage (BAL). Conventional Wright/Giemsa and Gram stains were utilized, as well as a contemporary strain, calcofluor white (CW). A cell count was performed on the BAL specimens, and cytospins were stained by the three stains. The calcofluor white-stained slides were examined with an epi-fluorescent microscope, whereas the other stains were evaluated with a conventional light microscope. Gomorimethenamine-silver (GMS), acid-fast bacillus (AFB), and Papanicolaou (PAP) stains were performed as controls. Thirty-two BAL procedures were performed in 20 (63%) male patients and 12 (37%) female patients. The clinical diagnosis was pneumonia in 31% of the patients, malignant hematologic disease in 28%, acute respiratory distress syndrome (ARDS) in 9%, and acquired immunodeficiency syndrome (AIDS) in 28%. Of these specimens, 78% were adequate for interpretation and 22% were inadequate. Bacteria were found in 50% (16/32) of all BALs, fungi were found in 9% (3/32), and Pneumocystis carinii was found in 9% (3/32). Gram-positive bacteria were most frequently found in patients with pneumonia (80%, 4/5), whereas P. carinii was identified in patients with AIDS. There were no false-positive results. One CW stain was equivocal for P. carinii due to high fluorescent background. Laboratory implementation of the rapid, three-staining technique was accomplished without difficulty in microbiology and hematology laboratory sections. Specimen evaluation with the rapid staining protocol was technically easy to perform; however, experience in ultraviolet fluorescent microscopy was crucial for interpretation of CW stain. All results were available in 2 hr, cost was reduced by 30%, and the assays were available 7 days/week. Further studies are ongoing to substantiate the sensitivity, specificity, and predictive value of this technique, as well as clinical guidelines for its optimal utilization.

NG-methyl-L-arginine and somatostatin decrease glucose and insulin and block endothelin-1 (ET-1)-induced insulin release but not ET-1-induced hypoglycemia.

We have previously demonstrated that endothelin-1 (ET-1) increases plasma insulin and decreases blood glucose. The present study was designed to determine if ET-1-induced hypoglycemia occurs in the presence of the insulin secretion inhibitor, somatostatin, and whether ET-1-induced insulin secretion is affected by the nitric oxide synthase I inhibitor, NG-methyl-L-arginine (NMLA), in the anesthetized rat. ET-1 increased plasma insulin and decreased blood glucose in all protocols. Somatostatin alone decreased blood glucose and plasma insulin. Somatostatin blocked ET-1-induced plasma insulin release but did not completely block ET-1-induced hypoglycemia. NMLA alone decreased blood glucose and plasma insulin. NMLA also blocked ET-1-induced insulin release but not ET-1-induced hypoglycemia. The present study confirms our previous finding that ET-1 decreases blood glucose and increases plasma insulin. Because hypoglycemia occurs during insulin inhibition with somatostatin, the present study suggests that ET-1-induced hypoglycemia is partially caused by non-insulin-mediated mechanisms. Because insulin secretion is blocked by nitric oxide synthase I inhibitor, NMLA, the present study suggests that ET-1-induced insulin release may be mediated by production of nitric oxide.

Endothelin-1 decreases glucose, inhibits glucagon, and stimulates insulin release in the rat.

The effects of endothelin-1 (ET-1) infusion at 0, 25, 50, and 75 ng/kg/min on blood glucose, insulin, and ET-1 levels were determined in anesthetized rats. In a separate group of rats, ET-1 was infused at 75 ng/kg/min and glucagon and glucose levels were determined. In another group of rats, the effect on blood glucose of glucagon infusion at 0.2 ng/kg/min with ET-1 infusion at 75 ng/kg/min for 30 minutes was determined. Glucose decreased 10 minutes after initiation of ET-1 infusion at 75 ng/kg/min and at 15 minutes during ET-1 infusion at 25 and 50 ng/kg/min. After 45 minutes, glucose decreased by 1.05 +/- 0.1, 1.44 +/- 0.11, and 1.39 +/- 0.22 mmol/L and ET-1 increased by 4.4 +/- 0.8, 5.2 +/- 1.2, and 11.2 +/- 0.8 pmol/L during ET-1 infusion at 25, 50, and 75 ng/kg/min, respectively. Insulin levels increased during ET-1 infusion of 50 ng/kg/min at 30 and 45 minutes by 300 +/- 75 and 405 +/- 120 pmol/L, respectively. During ET-1 infusion of 75 ng/kg/min, insulin increased at 45 minutes by 570 +/- 180 pmol/L. Glucagon decreased during ET-1 infusion at 15 minutes associated with a decrease in glucose. Glucagon levels subsequently returned to baseline values despite a continued decline in glucose levels. Glucagon infusion at 0.2 microgram/kg/min prevented the early ET-1-induced hypoglycemia. These findings demonstrate that ET-1 decreased blood glucose initially associated with a decrease in glucagon and subsequently associated with enhanced insulin release.

Effect of verapamil and captopril on endothelial injury in the diabetic hypertensive rat.

Microvascular and macrovascular complications are a major cause of increased morbidity and mortality in patients with diabetes mellitus and hypertension. Atherosclerosis is the major cause of these complications. Recently, Hebden and colleagues demonstrated endothelial injury in a rat model with streptozotocin-induced diabetes mellitus and deoxycorticosterone acetate-induced hypertension. To determine if captopril and verapamil reduce endothelial injury in this model of diabetic hypertensive (DH) rats, we evaluated mean medial thickness and intimal cell changes in four groups of rats: control, untreated DH rats, captopril-treated DH rats, and verapamil-treated DH rats. Mean medial thickness increased from 63.5 +/- 4.8 microns in control rats (n = 7) to 107.2 +/- 7.5 microns in untreated DH rats (n = 8), (P < .05). Verapamil and captopril blunted DH-induced medial thickening to 90.1 +/- 4.9 and 93.7 +/- 8.3 microns, respectively (P < .05 compared with control and untreated rats). An endothelial injury index (EI), consisting of white blood cells adhered to the intimal surface and rounded endothelial cells per 25-microns arc in aortic vessels, was determined for each group. The EI increased from 0.2 +/- 0.1 cells/25-microns arc in control rats to 6.3 +/- 4.0 cells/25-microns arc in untreated DH rats. Both verapamil and captopril diminished the EI in DH rats to 0.8 +/- 0.2 and 2.7 +/- 0.3 cells/25-microns arc, respectively (P < .05 compared with untreated DH rats). In addition, verapamil decreased the EI in DH rats to a greater degree than captopril (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Endothelin blockade lowers total peripheral resistance in hemorrhagic shock recovery.

To determine whether endothelin (ET) has a role in maintaining circulatory support during hypotensive hemorrhage, we (1) examined cardiac and systemic hemodynamics after a 6-mL hemorrhage in the presence and absence of the ETA receptor blocker BQ-123, (2) examined cardiac and systemic hemodynamics during BQ-123 infusion in nonhemorrhaged rats, (3) measured changes in circulating immunoreactive endothelin (IR-ET) after a 6-mL hemorrhage, and (4) infused pathophysiological doses of ET-1 into rats anesthetized with thiobutabarbital. Twenty minutes after hemorrhage, cardiac output and mean arterial pressure had stabilized in part because of an increase in systemic vascular resistance from 0.86 +/- 0.04 (baseline) to 1.04 +/- 0.05 (20 minutes) mm Hg/mL per minute. The rise in systemic vascular resistance was temporally associated with a significant (24%) increase in circulating IR-ET from 29 +/- 2 to 36 +/- 3 pg/mL 20 minutes after hemorrhage. During BQ-123 infusion mean arterial pressure at 5, 10, and 20 minutes after hemorrhage was 9 +/- 2, 23 +/- 4, and 23 +/- 3 mm Hg lower than values obtained after hemorrhage alone (P < .05). Mean arterial pressure was unaffected by BQ-123 infusion at baseline and 30 minutes after hemorrhage. Systemic vascular resistance was not affected at baseline by BQ-123 infusion. However, systemic vascular resistance was significantly lower 5, 10, 20, and 30 minutes after hemorrhage during BQ-123 infusion compared with hemorrhage alone at each time point. Infusion of BQ-123 into nonhemorrhaged rats had no effect on mean arterial pressure, systemic vascular resistance, or cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of endothelin on plasma volume and albumin escape.

Previous studies have demonstrated that endothelin-1 (ET-1) is a potent vasoconstrictor that decreases cardiac output and increases hematocrit. The present study was designed to determine if the rise in hematocrit and decrease in cardiac output are in part due to shifts of plasma from the vascular space to the interstitial space. Red blood cell volume and plasma volume were determined by using chromium-51-labeled erythrocytes and iodine-125-labeled albumin, respectively, in anesthetized, nephrectomized, splenectomized rats. The present study demonstrates that ET-1 increases mean arterial pressure and hematocrit. This effect is associated with an increase in total-body albumin escape, which is reflected by a marked reduction in whole-body plasma volume. ET-1 enhanced albumin escape primarily in the liver, lung, and heart at low doses. At high doses, albumin escape increased primarily in the liver, heart, and gastrointestinal tract but not the lung. The present study demonstrates that ET-1 increases hematocrit independent of splenic contraction or renal losses by enhancing loss of plasma volume to the interstitial space without affecting red blood cell volume. Because of the profound pressor effects of ET-1, it is likely that the plasma loss results from increased capillary hydrostatic pressure.