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Biomedical subjects

B Deb

Publications and source records attributed to B Deb.

12 recordsLinked to original sources
PubMed1999

Inhaled nitric oxide potentiates actions of adenosine but not of sodium nitroprusside in experimental pulmonary hypertension.

Inhaled nitric oxide (NO), a selective pulmonary vasodilator, increases intracellular cyclic guanosine monophosphate. In contrast, adenosine, another selective pulmonary vasodilator, increases intracellular cyclic adenosine monophosphate. There has been only limited study on effects of inhaled NO combined with other pulmonary vasodilators. The current study examined the hypothesis that inhaled NO would potentiate in vivo pulmonary vasodilator effects of adenosine, but not those of sodium nitroprusside (SNP). Like inhaled NO, SNP acts via cyclic guanosine monophosphate. Rabbits were anesthetized and mechanically ventilated. The NO synthesis inhibitor NG-nitro-L-arginine methyl ester was administered. U46619, a thromboxane A2 mimetic, was infused to produce pulmonary hypertension. Rabbits then received either SNP at doses of 0.5, 1, 2, 4, 8, 16, and 32 microg/kg/min or adenosine at doses of 12.5, 25, 50, 100, 150, and 300 microg/kg/min. Hemodynamic measurements were obtained with or without inhaled NO (40 ppm) at each dose of SNP or adenosine. During U46619-induced pulmonary hypertension, inhaled NO decreased pulmonary artery pressure and pulmonary vascular resistance. Adenosine and SNP produced dose-related decreases in pulmonary artery pressure and pulmonary vascular resistance and increases in cardiac output. Inhaled NO decreased pulmonary artery pressure and pulmonary vascular resistance at all doses of adenosine, but had no significant pulmonary vasodilator effects at doses of SNP >0.5 microg/kg/min. We conclude that inhaled NO does not produce additional pulmonary vasodilation over that achieved at higher doses of SNP, but does produce additional vasodilation when combined with a vasodilator having different mechanisms of action. Since both inhaled NO and adenosine produce selective pulmonary vasodilation, such combination therapy may be effective in patients with pulmonary hypertension.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

Mechanical ventilation and adjuncts in acute respiratory distress syndrome.

Acute respiratory distress syndrome is a response of the lung to both direct and indirect insults. Although much knowledge has been gained in understanding the pathophysiology of the syndrome, overall mortality in the past 25 years remains unchanged. Application of scientific knowledge to present-day technology has yielded advances in ventilator and pharmacological support for the patient with ARDS. Emphasis is now made on the prevention of iatrogenic lung injury with the use of pressure-limited mechanical ventilation, permissive hypercapnia, and artificial means of gas exchange (discussed in the chapter by Dr Furukawa). The role of INO and surfactant, as well as antimediator therapy, in the armamentarium against ARDS appears promising but awaits definitive clinical trials. Only with progress and newer therapies will we be able to improve the outlook for patients and families in the future.

Administration, Inhalation↗
PubMed1993

Percutaneous balloon pericardiotomy in the treatment of malignant pericardial effusion.

Recurrent pericardial effusion can be a manifestation of metastatic malignant disease. Repeated catheter drainage or surgical pericardial window are two common treatment modalities. We report a case of recurrent malignant pericardial effusion treated successfully with percutaneous balloon pericardiotomy, a relatively new technique avoiding the need for surgery.

Catheterization↗
PubMed1992

Delayed rupture of an internal iliac artery aneurysm following proximal ligation for abdominal aortic aneurysm repair.

This is a report of a patient presenting with a contained rupture of an internal iliac aneurysm following proximal ligation after abdominal aortic aneurysm repair three years earlier. The patient presented with a large pelvic mass with symptoms of urgency, frequency, dysuria, tenesmus and fevers associated with anemia. Following evacuation of the aneurysm and direct suture ligation of the distal branches of the internal iliac artery, the patient's aortic graft was covered with omentum which also filled the pelvic cavity. The importance of proximal and distal control of aneurysms and/or the importance of complete luminal control of internal iliac artery aneurysms is emphasized by this case.

Aged↗
PubMed1992

Primary pulmonary hypertension and functional hyposplenism.

Primary pulmonary hypertension is a rare disease of unknown case. Functional hyposplenism is characterized by the appearance of abnormal circulating erythrocytes despite the presence of a spleen and is associated with a variety of disease states. A case of primary pulmonary hypertension associated with functional hyposplenism is described in this report.

Adult↗
PubMed1990

Adaptive cytoprotection of gastric surface epithelial cells against injury by physiologic concentrations of bile acid.

The purpose of this study was to determine whether adaptive cytoprotection of gastric mucosa could be demonstrated with concentrations of bile acid, which is normally found in the human stomach, and whether cyclooxygenase inhibition, in turn, could blunt the response. Surface epithelial cell exfoliation and ion fluxes were used as end points. A transduodenal gastric cannula was placed, and the pylorus/gastroesophageal junction was ligated in adult male Sprague-Dawley rats that had been anesthetized. In experiment 1 (N = 30), rat stomachs were exposed for 15 minutes to 5 ml of either a neutral test solution (160 mmol/L NaCl, pH 7) or 1 mmol/L acidified taurocholate (ATC) (100 mmol/L HCl, 60 mmol/L NaCl, 1 mmol/L taurocholic acid; pH 1.2). All rats were subsequently exposed for 15 minutes to 5 mmol/L ATC during which time mucosal injury was assessed by measuring net flux of H+, Na+, and K+, volume, and DNA efflux. In experiment 2 (N = 35), all stomachs were pretreated for 15 minutes with 1 mmol/L ATC before mucosal injury with 5 mmol/L ATC (15 minutes). Eighteen rats were pretreated with indomethacin (5 mg/kg) subcutaneously 75 minutes before the experiment was begun, and the same parameters were measured. Pretreatment of rat gastric mucosa with 1 mmol/L ATC significantly attenuated the mucosal injury that was seen with subsequent exposure to 5 mmol/L ATC, resulting in significantly (p less than 0.05) less luminal H+ loss (-16 +/- 4 vs -32 +/- 4 mEq/15 min) and DNA efflux (181 +/- 21 vs 270 +/- 25 micrograms/15 min) than the nonadapted group. Indomethacin pretreatment significantly attenuated the adaptive protective response, resulting in greater loss of H+ (-29 +/- 4 vs -18 +/- 3) and DNA efflux (190 +/- 35 vs 110 +/- 18, both p less than 0.05) after exposure to 5 mmol/L ATC. These studies demonstrate that adaptive cytoprotection of gastric mucosa occurs with physiologic concentrations of an irritant that is normally present in the stomach. Indomethacin blunts this effect, which suggests that adaptive cytoprotection in this setting may be mediated by production of endogenous prostaglandins.

Acids↗
PubMedDate not supplied

The effects of lisinopril on serum catecholamine concentrations both at rest and on exercise in patients with congestive cardiac failure. A double blind, placebo controlled, parallel group study.

Patients with congestive cardiac failure have elevated sympathetic activity at rest which contributes to the pathophysiology of this syndrome. In addition, the sympathetic response to exercise in these patients is abnormal. Sympathetic activity is accurately reflected by serum noradrenaline levels. In a double-blind, placebo-controlled, parallel group study, 16 patients of New York Heart Association (NYHA) functional class II, stabilised on optimum doses of diuretics were randomised into two equal groups, to receive either low-dose Lisinopril, an orally active angiotensin converting enzyme (ACE) inhibitor, or matching placebo, over a 12 week period. At the end of the 12 week treatment phase, there was no significant change in noradrenaline levels at rest (p = 0.33) mid exercise (p = 0.17), or peak exercise (p = 0.69), in the lisinopril group. Both lisinopril and placebo groups improved subjectively as assessed by change in NYHA grade, (p < 0.01 for placebo and p < 0.001 for those given lisinopril). Exercise duration improved significantly in the lisinopril group (p = 0.0296), but not in the placebo group after treatment. Low dose lisinopril is of use in congestive cardiac failure even in the absence of measurable changes in sympathetic tone.

Angiotensin-Converting Enzyme Inhibitors↗