Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From March 1988 to March 1990, 11 children with cystic fibrosis (age 5-15 years) underwent combined heart-lung transplantation at our institutes. Maintenance immunosuppression consisted of cyclosporin and azathioprine with corticosteroids and antithymocyte globulin used perioperatively and during rejection episodes. Six patients (55%) survive from 1.5-23 months all of whom have improved life quality. Actuarial survival to 1 year was 55%. At six months after transplant, mean forced expiratory volume at one second was 73.5% of predicted normal, compared with 25% before transplant. There was one perioperative death, three later deaths associated with obliterative bronchiolitis at two, eight, and nine months, and one from mediastinitis at four months. Of the 15 children accepted for transplantation but not receiving grafts, 10 have died (eight within four months of being placed onto the transplant list). Early postoperative problems included acute reversible rejection (n = 10), meconium ileus equivalent (n = 3), and pancreatitis (n = 1). There was a high incidence of later pulmonary rejection with a mean of 5.7 episodes per patient in the first six months. Pulmonary infection occurred relatively infrequently, with Pseudomonas aeruginosa being the most common pathogen. Persistent diabetes mellitus requiring insulin occurred in four and systemic hypertension developed in one.
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PMID:Heart-lung transplantation for cystic fibrosis. 2: Outcome. 192 6

Tumor necrosis factor (TNF) may be involved in the pathogenesis of acute lung injury (ALI) associated with septicemia. Therefore, we measured plasma TNF activity during sepsis and development of lung injury in a porcine model of ALI. Plasma samples were obtained from anesthetized saline-infused control pigs (n = 10) and those infused for 1 h with live Pseudomonas aeruginosa (10(8) organisms/ml, 0.3 ml/20 kg/min) (n = 16). TNF activity was measured in plasma using the L929 fibroblast cytolytic assay. L929 cytotoxicity caused by TNF-alpha or TNF-beta was determined in plasma by measuring the cytotoxicity neutralized by TNF antisera. No significant TNF activity was detected in control pig plasma. In septic pigs, TNF activity appeared in plasma 15 min after onset of septicemia and remained elevated throughout the experiment (6.1 +/- 10.2% to 80.0 +/- 5.0%, 15 and 300 min, respectively). The appearance of pulmonary arterial hypertension, increased lung water, decreased lung compliance, and deteriorating gas exchange was correlated with the rise in plasma TNF activity, which reached a peak at 90 to 120 min in septic pigs. Our results provide evidence that both TNF subtypes are present in plasma during septicemia. Anti-TNF-alpha and anti-TNF-beta neutralized TNF activity in whole septic plasma at 15, 30, and 45 min after onset of septicemia, and the antibodies blocked TNF activity in serially diluted septic plasma at all time points up to 210 min of sepsis. TNF activity in septic plasma at 210 to 300 min was not neutralized entirely by TNF antisera.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tumor necrosis factor. Alpha and beta subtypes appear in circulation during onset of sepsis-induced lung injury. 202 17

In this study we investigated the effects of right atrial infusion of PGE1 (RAIPGE1) in doses from 40 to 500 ng/kg/min on sepsis-induced pulmonary artery hypertension (SIPAH). Thirteen pigs were randomized into a time-course group (n = 6) and a PGE1-treated group (n = 7). Pulmonary hypertension (PAH) was induced with the infusion of Pseudomonas Aeruginosa (PsAr) at a concentration of 2 X 10(8) CFU/20 kg/min in both groups. The infusion of PsAr caused a significant and persistent rise in mean pulmonary artery pressure (MPA), pulmonary vascular resistance (PVRI), right ventricular compliance (RVC), RV dp/dt, and right ventricular stroke work index (RVSWI), 30 min after the onset of infusion (P less than 0.05 vs baseline). Systemic hemodynamics and gas exchange were not affected throughout the 3-hr period of infusion (P = NS); however, left ventricular compliance (LVC) was depressed at a MPA greater than 35 mm Hg. The RAIPGE1 following SIPAH caused a concentration-dependent reduction above 40 ng/kg/min of MPA, PVRI, RVSWI, and RV dp/dt (P less than 0.05, 120 and 500 ng/kg/min vs PAH). RVC returned to baseline values during the infusion of PGE1. Systemic hemodynamics, including oxygen delivery and extraction, were unaffected by the infusion of PGE1, but LVC was improved (P less than 0.05, PGE1 500 vs PAH). The infusion of PGE1 caused a concentration-dependent rise in shunt fraction (Qs/Qt) and alveolararterial oxygen gradients which reached statistical significance during the infusion of 500 ng/kg/min. Our data show that RAIPGE1 is effective in ameliorating RV and pulmonary hemodynamics, but at the largest dose it negatively affects gas exchange.
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PMID:Efficacy of right atrial infusion of PGE1 in sepsis-induced pulmonary hypertension. 212 41

The effects of two pharmacologically distinct histamine H2 receptor antagonists were studied in combination with ibuprofen (I) and diphenhydramine (D) in a porcine model of septic ARDS. Cimetidine (C) is reported as having direct oxygen radical scavenging abilities and is an inhibitor of cytochrome P-450, whereas ranitidine (R) acts solely by H2 receptor blockade. Four groups were studied: Group Ps (n = 8) received a continuous infusion of live Pseudomonas aeruginosa 5 x 10(8) CFU/ml at 0.3 ml/20kg/min, Group C (n = 6) received a control saline infusion, and the treatment groups received I (12.5 mg/kg) and D (10 mg/kg) in combination with either C (150 mg, CID, n = 6) or R (25 mg, RID, n = 5) given at 20 and 120 minutes after the onset of Ps. Pulmonary (PAP) and systemic (SAP) arterial pressures, cardiac index (CI), PaO2, thermal cardiogreen extravascular lung water (EVLW) and scintigraphically determined pulmonary albumin flux (slope index, SI) were measured. Ps infusion produced significant (p less than 0.05) cardiovascular collapse, hypoxemia and increased EVLW and SI. Both CID and RID temporarily reversed pulmonary arterial hypertension and maintained PaO2, EVLW, SAP and CI at control levels throughout the study, and significantly improved SI at 180 min. These results suggest that cimetidine and ranitidine act in this combination therapy primarily as H2 receptor antagonists.
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PMID:Ranitidine compared to cimetidine in multiagent pharmacological treatment of porcine Pseudomonas ARDS. 231 Dec 2

Twenty-six episodes of Pseudomonas aeruginosa bacteremia treated with intravenous ceftazidime, 4-6 g/day were evaluated. Treatment was begun within the first 24 hours after the isolation of the microorganism and was maintained for 10-12 days. In two patients with neutropenia amikacin was added during the initial 48-72 hours until the susceptibility to ceftazidime was known. All isolates were sensitive to ceftazidime. The most common underlying diseases were neoplasia (12), diabetes with stroke (4), neurosurgical and vascular procedures (4), rheumatoid arthritis (2), burns (2), cor pulmonale (1), and hypertension (1). The origins of bacteremia were urinary (12), pulmonary (9), and unknown (5). The infection was hospital-acquired in 77% and community-acquired in 23%. A critical clinical status and the presence of complications were significantly (p less than 0.01) associated with an increased mortality rate. Clinical outcome was good in 18/26 (70%), with a 30% mortality rate. The microbiological evolution showed 14 eradications, 6 persistences, 3 relapses and 3 colonizations. Resistance did not develop during therapy. Ceftazidime may be a good alternative therapy for these severe infections, although wider comparative studies are required for a better evaluation.
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PMID:[Evaluation of ceftazidime monotherapy in Pseudomonas aeruginosa bacteremias. Prospective study]. 268 60

The characteristics of chronic pyelonephritis are studied in 37 patients out of a total of 53 patients with proved renal polycystosis. A group of 71 patients with chronic pyelonephritis selected at random are used as a control group. The frequency of chronic pyelonephritis among the patients with renal polycystosis is 69.8%. The difference between the mean age of the patients with renal polycystosis and chronic pyelonephritis and the patients with renal polycystosis without chronic pyelonephritis is 8.6 years. A significant difference is established between these two groups of patients concerning the frequency of symptomatic hypertension--89.2% for the patients with renal polycystosis and chronic pyelonephritis and 45% for the patients with uncomplicated renal polycystosis. A similar difference is established also for the renal failure--respectively 64.9% and 37.5%. The frequency of hypertension and chronic renal failure is lower in the control group of patients. 59% of the patients with renal polycystosis and chronic pyelonephritis have significant bacteriuria, E. coli and Proteus being the most frequently isolated bacteria but Pseudomonas shows the highest drug resistance. The isolated bacteria are most sensitive to nitroxoline and aminoglycoside antibiotics.
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PMID:[Chronic pyelonephritis in polycystic kidney]. 277 65

Porcine Pseudomonas adult respiratory distress syndrome (ARDS) has been shown to respond to combination therapy of 150 mg of cimetidine, 12.5 mg/kg of ibuprofen, 10 mg/kg of diphenhydramine, 0.2 mg/kg of ketanserin, and 30 mg/kg of methylprednisolone (CIDKM or Poly-5) given at 20 and 120 minutes after the onset of a continuous infusion of liver Pseudomonas aeruginosa, 5 X 10(8) colony-forming units (CFU) ml at 0.3 ml/20 kg/min. The present study was designed to determine the minimal, effective therapy by selective deletion of individual agents from CIDKM. Eight groups were studied: saline control (S, n = 9), Pseudomonas control (P, n = 8), and the following Pseudomonas plus treatment groups (each n = 5): CIDKM (cimetidine, ibuprofen, diphenhydramine, and ketanserin), CID (cimetidine, ibuprofen, and diphenhydramine), IC (ibuprofen and cimetidine), ID (ibuprofen and diphenhydramine), and CD (cimetidine and diphenhydramine). Pseudomonas alone produced severe ARDS with significant (p less than .05) decreases in PAO2 cardiac index, and systemic arterial pressure and significant increases in pulmonary artery pressure, extravascular lung water (EVLW) and scintigraphically determined pulmonary albumin flux measured as slope index (SI). Full therapy, CIDKM or Poly-5, showed significant improvement in all parameters. Deletion of methylprednisolone did not significantly effect any parameter measured. The deletion of ketanserin, leaving CID, did not alter treatment efficacy, except for a significant decline in cardiac index at 3 hours. Deletion of ibuprofen from CID resulted in a failure to reverse pulmonary arterial hypertension, hypoxemia, elevated EVLW, and increased SI. Removal of either cimetidine or diphenhydramine from CID resulted in significant increases in EVLW compared with control levels and SI compared with both control levels and CID. These results indicate that a combination of both histamine H1 and H2 receptor blockers and the cyclooxygenase inhibitor, ibuprofen, is effective and essential in the treatment of hypoxemia, early pulmonary hypertension, and pulmonary microvascular injury in this fulminant model of porcine Pseudomonas ARDS.
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PMID:Successful treatment of adult respiratory distress syndrome by histamine and prostaglandin blockade in a porcine Pseudomonas model. 311 84

Between March 1981 and March 1986, 200 orthotopic heart transplantations were performed at the University of Pittsburgh. Fourteen of those procedures were carried out in children 2 to 16 years of age. Two children received combined liver and heart transplants; one because of familial hypercholesterolemia with associated ischemic heart disease, and the other because of dilated cardiomyopathy associated with intrahepatic biliary atresia. Eight patients had dilated cardiomyopathy, and two had myocarditis. Two had heart transplantations for congenital heart disease: one had multiple muscular ventricular septal defects repaired in infancy and had an associated cardiomyopathy, and the other developed a cardiomyopathic ventricle from a congenital right coronary artery to right atrial fistula. Chronic immune suppression consisted 0.2 to 0.5 mg/kg/d of prednisone and 5 to 50 mg/kg/d cyclosporine, with the addition of antithymocyte globulin for unresolved moderate or severe acute rejection. There were three early postoperative deaths: one from intracranial bleeding, one from Pseudomonas mediastinitis, and one from ischemic injury to transplanted organs. Early postoperative complications included reversible renal failure, hypertension, and seizures. Late problems were related to allograft rejection and side effects of cyclosporine and corticosteroids. Significant rejection episodes occurred in all patients surviving longer than 2 weeks, with seven requiring antithymocyte globulin. Two patients died 8 months following transplantation of severe acute and chronic rejection; another patient required retransplantation for ischemic cardiomyopathy resulting from chronic rejection but subsequently died of recurring rejection 3 months after the second transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experience with heart transplantation in children. 354 Aug 34

Pulmonary microvascular injury during sepsis after injury appears to be amplified with plasma fibronectin deficiency, but the degree of injury relative to the extent of sepsis has not been defined. We evaluated pulmonary vascular permeability in sheep as influenced by various levels of postoperative Pseudomonas sepsis during a period of plasma fibronectin deficiency. The hemodynamic response to Pseudomonas was very similar regardless of the intensity of septic challenge and characterized by systemic arterial hypotension, decreased cardiac output, and pulmonary arterial hypertension. In contrast, increased pulmonary microvascular permeability was observed with increments in the bacterial challenge. Thus, lung protein clearance (LPC) or so called pulmonary transvascular protein clearance (TPC) used as an index of lung vascular permeability was 9.1 +/- 1.9 ml/hr, 15.1 +/- 1.7 ml/hr, and 19.3 +/- 3.0 ml/hr 2 hr after low (3 X 10(9) i.v.; 1 X 10(10) i.p.), medium (3 X 10(9) i.v.; 3 X 10(10) i.p.), and high (5 X 10(9) i.v.; 5 X 10(10) i.p.) dose Pseudomonas challenges, respectively. Thus, the extent of the altered pulmonary microvascular integrity in sheep during sepsis after surgery in the presence of fibronectin deficiency is dependent on the degree of bacterial sepsis. In addition, infusion of cryoprecipitate was an effective means of reversing the plasma fibronectin deficiency. Accordingly, this may be used as a model to investigate the mechanism of altered lung fluid balance during postoperative septic shock and the effect of fibronectin on this response.
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PMID:Lung fluid and protein flux during postoperative sepsis. 405 99

Pulmonary effects, lung clearance, and tissue retention of blood-borne Pseudomonas aeruginosa were compared in dogs (n = 5) and pigs (n = 5) during continuous 6-hour intravenous infusion of 1.2(10(9)) bacteria/min/20 kg. Control pigs received an equal volume of sterile saline. In contrast to controls, experimental pigs developed pulmonary artery (PA) hypertension (mean, 30 +/- SE 3; baseline, 17 mm Hg) and pulmonary failure manifested by hypoxemia (mean PaO2, 49 +/- 4; baseline, 78 +/- 2 mm Hg; p less than 0.001), increased intrapulmonary shunting (40 to 50%), noncardiogenic pulmonary edema, and congestive atelectasis, a pattern of pulmonary failure very similar to sepsis-induced ARDS in humans. In dogs, PA pressures wee unchanged from baseline, no edema was detected, and comparable hyperventilation was associated with an increase in PaO2 from 77 +/- 4 (baseline) to 87 +/- 2 mm Hg (p less than 0.001). Tissue retention of viable blood-borne organisms in pigs was greatest in the lungs. In dogs, lung retention was minimal and greatest tissue retention occurred in the liver and spleen. We conclude that both lung clearance of blood-borne organisms and bacteremia-induced pulmonary failure are quite host dependent.
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PMID:Bacteremia: host-specific lung clearance and pulmonary failure. 678 63


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