Search PubMed⌕ Search

Biomedical subjects

D J Fitzgerald

Publications and source records attributed to D J Fitzgerald.

160 records · Page 9Linked to original sources

Sphygmomanometers in hospital and family practice: problems and recommendations.

The accuracy and working condition of 210 sphygmomanometers were tested: 100 (50 and mercury and 50 aneroid) models were used in family practices and 100 mercury models in hospitals. Faults in the inflation-deflation system were common and caused mainly by dirt or wear in the control valves. Leakage occurred in 48% of the hospital and 33% of the family practice sphygmomanometers. In the mercury models the mercury or air vents were often in an unsatisfactory condition or the calibrated glass tube dirty. The accuracy of the gauges was examined at 90 and 150 mm Hg: fewer than 2% of the mercury sphygmomanometers but 30% of the aneroid models had errors greater than +/- 4 mm Hg at either pressure. Over half of the cuffs examined had bladders widths less than the recommended size, and 94% had bladders shorter than the length recommended for use on normal adults. Mercury sphygmomanometers should be bought in preference to aneroid models as they are more accurate, less expensive in the long term, and can be maintained by the owner; they should be checked every six to 12 months depending on usage. Replacement parts should be kept readily available.

Equipment Failure↗

Clinical and haemodynamic responses to captopril and hydralazine in chronic congestive heart failure: the importance of preload reduction.

1 Although many vasodilators are effective in the treatment of severe congestive heart failure, there have been few comparative studies of these drugs. We compared the acute haemodynamic effects of captopril and hydralazine in 11 patients with congestive cardiac failure unresponsive to diuretics and digoxin. Both drugs increased resting cardiac index, although this effect appeared more pronounced for hydralazine (33% v 23%). Captopril reduced pulmonary capillary wedge pressure (-8 mm Hg, p less than 0.01) which decreased only slightly on hydralazine. 2 Long-term treatment was then started on the dose found effective during acute administration. Each drug was given for eight weeks. Exercise tolerance improved with both drugs, the increase during the hydralazine phase correlating with the increase in cardiac index at rest (r = 0.75; p less than 0.05). Clinical improvement appeared more definite on captopril than on hydralazine, however. This improvement was maintained during the captopril phase only in those patients who had a greater than 25% reduction in pulmonary capillary wedge pressure in the acute study.

Adult↗

Accuracy of the London School of Hygiene and Remler M2000 sphygmomanometers.

1. The accuracy of the Remler M2000, a semiautomatic portable blood pressure recorder, was assessed with the London School of Hygiene (LSH) and Hawkesley random-zero sphygmomanometers used as reference standards. 2. The Remler gave higher recordings than the LSH sphygmomanometer, the mean systolic and diastolic differences being 5.9 mmHg (P less than 0.001) and 4.7 mmHg (P less than 0.001) respectively. No significant difference was demonstrated between paired Remler and Hawkesley recordings. 3. When simultaneous paired LSH and Hawkesley sphygmomanometer recordings were compared, with LSH gave lower blood pressures: 7.1 mmHg (P less than 0.001) for systolic and 3.6 mmHg (P less than 0.001) for diastolic recordings. 4. The LSH sphygmomanometer underestimates blood pressure, partly due to a calibration error but also because the selection of end points for this device differs from other methods of blood pressure measurement.

Blood Pressure Determination↗

Inhibition of intercellular communication by tumor-promoting phorbol esters.

Cocultures were established of mouse epidermal cells (HEL/37) and mouse fibroblast cells (PG-19) deficient in the enzyme hypoxanthine-guanine phosphoribosyltransferase. Metabolic cooperation between the cocultured cells was detected as labeling of PG-19 cells on incubation of cocultures with [3H]-hypoxanthine. The transfer of label from HEL/37 cells to PG-19 cells was inhibited by the tumor prmoters 12-O-tetra-decanoylphorbol-13-acetate (10(-8) M) and phorbol-12,13-di-decanoate (10(-7) M) but not by nonpromoting derivatives of these phorbol esters. The inhibition was partially prevented by the antiinflammatory steroid fluocinolone acetonide, which is an antagonist of mouse skin tumor promotion, and by prolonged exposure of the cocultures to 12-O-tetradecanoylphorbol-13-acetate.

Animals↗

A rapid agglutination assay to detect anti-streptokinase antibodies.

BACKGROUND: Streptokinase resistance may cause suboptimal thrombolytic therapy. AIM: To develop a rapid latex-bead assay to detect streptokinase antibodies. METHODS: Sera were obtained from 16 patients presenting with acute myocardial infarction (MI) before treatment with streptokinase and 1 and 6 months post treatment, and from 100 controls. Sera were assayed for anti-streptokinase antibodies using a functional streptokinase-neutralising assay. RESULTS: Streptokinase-neutralising activity was low in controls (54 +/- 5U/ml) and patients prior to treatment (101 +/- 18), increasing to 2,110 +/- 823 and 1,017 +/- 169 at 1 and 6 months (mean +/- SEM). The latex assay had a sensitivity of 94% and a specificity of 93% for detecting individuals with > 350U/ml of streptokinase resistance, which is sufficient to neutralise the drug clinically. CONCLUSIONS: Estimation of streptokinase resistance using an enzyme immunoassay and a latex bead assay correlated well with serum neutralising activity. This assay can rapidly identify patients who have a high level of streptokinase-neutralising activity.

Agglutination Tests↗

Non-steroidal anti-inflammatory drugs (NSAIDs) and gastro-intestinal toxicity: current issues.

Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most widely used drugs and their widespread use is associated with increased gastro-intestinal toxic effects such as ulceration, haemorrhage, perforation and death. They result in these complications mainly by reducing cytoprotective prostaglandins (PGE2 and PGI2) in the stomach, through the inhibition of cyclo-oxygenase (COX) enzyme. The increased morbidity and mortality, in addition to enormous cost, associated with NSAID-associated side effects, necessitates a need for safer GI-friendly NSAID. Various approaches have been used to counteract NSAID associated side effects with varying degrees of success and acceptance. These include the use of alternative analgesia, anti-acid secretory agents like proton pump inhibitors, sucralfate and prostaglandin analogues. In addition, new types of NSAIDs are being developed, based on new understanding of their mechanism of action and the pathogenesis of inflammation. These include a new class of NSAIDs called "selective Cox-2 inhibitors". These agents preserve the COX-1 that is responsible for the production of cytoprotective prostaglandins in the stomach and selectively inhibit COX-2 induced at the sites of inflammation. Selective COX-2 inhibitors exert the same analgesic and anti-inflammatory effects as the existing NSAIDs but may be less toxic to the stomach. In this review the background development and well-structured clinical trials on this new generation NSAIDs are discussed.

Anti-Inflammatory Agents, Non-Steroidal↗

Okadaic acid and phorbol esters: comparative effects of these tumor promoters on cell transformation, intercellular communication and differentiation in vitro.

Okadaic acid is a non-12-O-tetradecanoylphorbol-13-acetate (TPA)-type tumor promoter in the mouse skin carcinogenesis system. Here we report on the in vitro activity of okadaic acid in 3 assay systems: BALB/c 3T3 cell transformation, gap junctional intercellular communication (GJIC) in various cell types, and inhibition of induction of differentiation of Friend virus-transformed murine erythroleukemia (MEL) cells. The activity of okadaic acid was compared to that of the phorbol ester tumor promoters TPA and phorbol-12,13-didecanoate (PDD). In a test system involving a 2-week exposure of BALB/c 3T3 cells following 3-methylcholanthrene initiation, okadaic acid at a concentration of 10 ng/ml was equipotent to PDD as a promoter of cell transformation (4.9 and 3.7 foci/dish, respectively). Longer exposures to okadaic acid resulted in cytotoxicity. Okadaic acid-generated as well as PDD-generated transformed foci displayed a selective lack of GJIC between focus cells and surrounding normal cells, i.e., transformed cells communicate among themselves but not with surrounding cells. However, in contrast to TPA, there was no inhibition by okadaic acid, except at toxic doses, of homologous GJIC in BALB/c 3T3 cells or human and mouse keratinocytes. Furthermore, okadaic acid, unlike TPA, did not inhibit MEL cell differentiation. Together, these results indicate that okadaic acid acts as a promoter of cell transformation but that its mechanism of action is different from that of the phorbol ester tumor promoters.

Animals↗