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Biomedical subjects

A S Hall

Publications and source records attributed to A S Hall.

At least 55 records · Page 3Linked to original sources
PubMed1995

High resolution magnetic resonance imaging of the anal sphincter using an internal coil.

An internal receiver coil was used to obtain high resolution transverse and oblique coronal magnetic resonance images of the anal sphincter in five normal volunteers and five patients. The internal sphincter had a high signal intensity on T1 weighted, T2 weighted, and STIR sequences whereas the conjoined longitudinal muscle and external sphincter had a low signal intensity. The internal sphincter (but not the external sphincter) showed contrast enhancement after administration of intravenous gadopentetate dimeglumine. The oblique coronal plane was particularly useful for showing the thickness and the relations of the external sphincter. Sphincteric abscesses as well as muscle defects, hypertrophy, and atrophy were clearly shown. The coil was well tolerated by most subjects. It has considerable potential for improving the diagnosis of anorectal disease.

Adult↗
PubMed1995

Clinical background to the use of ACE inhibitor therapy after myocardial infarction.

The rationale for using angiotensin converting enzyme (ACE) inhibitor therapy after acute myocardial infarction has been largely founded on observations made in experimental situations, and in humans before the routine introduction of reperfusion therapies. An important area of ongoing debate therefore continues to be the role of ACE inhibition as an early adjunct to attempts to achieve and maintain patency of infarct-related coronary arteries. Data from clinical trials indicate a substantial survival benefit in patients with impaired ventricular function, but provide little support for the routine treatment of the remaining majority of patients. An important issue in determining whether these agents should be used in a more general and long-term secondary prevention role, is their potential ability to prevent subsequent reinfarction. However, such a strategy is unlikely to be enhanced by either immediate initiation of treatment or withdrawal after just 1 month of therapy.

Angiotensin II↗
PubMed1995

Endoscopic laser ablation of the prostate: MR appearances during and after treatment and their relation to clinical outcome.

OBJECTIVE: Endoscopic laser ablation is a new treatment for benign prostatic hypertrophy. The objectives of this study were to determine the appearances of the prostate on MR images obtained during, 1 week after, and 3 months after this procedure and to determine if a correlation exists between the MR findings and the clinical outcome. Such appearances could then be used to guide the application of laser energy during the procedure in order to optimize the clinical result. SUBJECTS AND METHODS: Eight consecutive men 58-74 years old with symptoms of bladder outflow obstruction caused by benign prostatic hypertrophy underwent endoscopic laser ablation of the prostate under spinal or epidural anaesthesia. Imaging was done on a 0.5-T Picker Asset system with an endorectal receiver coil and conventional T1-weighted spin-echo, T2-weighted spin-echo, and gradient-recalled-echo sequences. T1-weighted magnetization transfer images were obtained in three patients. Images were obtained preoperatively, after ablation of the left-sided quadrants, immediately after completion of the procedure, and 1 week and 3 months later. Preoperative and 3-month postoperative symptom scores, peak urine flow rates, and bladder residual volumes were studied. Images were visually assessed for signal-intensity changes and the presence of cavitation by three radiologists in conference. The results were quantitatively analyzed by measuring prostatic volumes on the gradient-recalled-echo images and by measuring the width and area of regions of signal-intensity change on the T2-weighted images. RESULTS: MR images made immediately after treatment showed an increase in the volume of the prostate (mean, 34%) and a poorly defined, low-signal-intensity region around the urethra on the T2-weighted images in six patients. This probably represented coagulative necrosis. The prostate was smaller on MR images made 1 week after treatment, and after 3 months the prostate returned to its preoperative size. After 1 week, the low-signal-intensity periurethral region on the T2-weighted images was less obvious, and at 3 months it was replaced in four patients by a well-demarcated low-signal-intensity ring on the T2-weighted and gradient-recalled-echo images. No evidence of cavity formation in the prostate was seen on MR images in any patient. Symptom scores and peak urinary flow rates improved after 3 months, with a significant difference between the mean increase in symptom scores in the patients with and without the periurethral changes seen immediately after treatment. However, we found no significant difference between the mean increase in peak urinary flow rates in the patients with and without periurethral changes seen either immediately or at 3 months after treatment. No statistically significant correlation was found between the amount of prostatic swelling and the improvement in symptom scores or peak urine flow rates. CONCLUSION: In patients who have had laser prostatectomy, MR imaging shows significant immediate glandular swelling, which may account for the delayed improvement in symptoms reported with this technique. The presence of the periurethral changes immediately after treatment was correlated with a subsequent improvement in symptom scores. After 3 months, no cavity could be seen in the prostate. This may account for the poorer long-term clinical outcome reported with endoscopic laser ablation of the prostate compared with transurethral prostatectomy.

Aged↗
PubMed1994

Context of consent.

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Clinical Trials as Topic↗
PubMed1994

Octreotide does not alter endotoxin lethality in mice or endotoxin-induced suppression of human leukocyte migration.

Octreotide, a somatostatin analog, was evaluated for its effects on long-term survival in a mouse model of endotoxemia and for its effects on endotoxin-induced suppression of human leukocyte migration. Swiss Webster mice were simultaneously rendered endotoxemic with a single intraperitoneal injection of 800 micrograms E. coli Lipopolysaccharide (LPS) and treated with one of four doses of subcutaneous (s.c.) octreotide (1.0 mg/kg in 0.4 ml saline, 0.1 mg/kg in 0.4 ml saline, 0.1 mg/kg in 0.04 ml saline, or 0.001 mg/kg in 0.04 ml saline) or saline alone (fluid-resuscitated control group: 0.4 ml saline s.c.; or non-fluid-resuscitated control group: 0.04 ml saline s.c.). Octreotide was continued with or without supplemental s.c. fluid resuscitation (0.4 ml saline) at eight hour intervals for either twenty-four or forty hours. There was no statistical significance to differences in long-term survival between comparable groups of octreotide treated vs saline treated animals during the entire fourteen day period of observation. Fluid resuscitation during the first forty hours following endotoxemia induction delayed death, but did not significantly improve long-term survival. In vitro work was conducted to determine the effect of octreotide on endotoxin-induced suppression of human leukocyte migration. Octreotide at concentrations ranging from 3.05 x 10(-5) Molar to 3.05 x 10(-11) Molar had no significant effect on leukocyte migration. In this study octreotide treatment failed to improve long-term survival in mice with endotoxemia and did not alter endotoxin-induced suppression of leukocyte migration.

Animals↗
PubMed1994

Inhibition of ACE/kininase-II, acute myocardial infarction, and survival.

Three major trials, in patients with chronic heart failure, have shown that treatment with an ACE inhibitor reduces mortality. However, at the time of writing this review there continue to be strong grounds for uncertainty as to the role of these drugs after acute myocardial infarction in man. This uncertainty is exemplified by the findings of two recently published mortality trials, the CONSENSUS II and the SAVE investigations. Despite virtually identical premises, though widely differing therapeutic approaches, the observations reported in these two papers contrast markedly. In this review we have sought to analyse the possible reasons why the findings of the two trials differ. In our attempt to understand this important issue we have necessarily turned to smaller clinical studies, and also to investigations performed in animals. Furthermore, we review the investigational strategies which have been employed by other, currently unreported, large scale survival studies, as these will certainly hold many of the answers to the questions which the SAVE and CONSENSUS II trials have raised.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

ACE inhibition, atherosclerosis and myocardial infarction--the AIRE Study in practice. Acute Infarction Ramipril Efficacy Study.

Unlike most cell-types in the body, cardiomyocytes do not replicate in adult life. Consequently myocardial infarction produces irreparable damage to the heart which in turn increases the likelihood of premature death. Recent trials indicate that immediate aspirin and thrombolytic therapy beneficially modify the natural history of myocardial infarction, reducing both short- and long-term mortality rates. However, the occurrence of early heart failure in as many as one third of patients continues to carry with it a particularly poor prognosis. Recent trials with ACE inhibitors indicate that delayed initiation (beyond 24 h) and long-term maintenance treatment of patients selected on the basis of either heart failure (AIRE Study) or an ejection fraction of less than 40% (SAVE Study) result in large reductions in all-cause mortality. Although the exact mechanism of this benefit remains uncertain the reduction of further myocyte death due to reinfarction or gradual toxic attrition has been suggested. The currently unreported ISIS-4 and GISSI-3 should provide additional information as to whether the clinical indications for ACE-inhibitor therapy should be extended to other patient groups.

Coronary Artery Disease↗
PubMed1994

Cardiac remodelling.

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Adaptation, Physiological↗
PubMed1994

ACE-inhibitor therapy after myocardial infarction--a new treatment strategy.

Potential benefit or harm of drug therapy in patients with chronic congestive heart failure and those later presenting to hospital after an acute myocardial infarction (AMI) have been studied in a number of large-scale survival studies during the last few decades. Currently available data are reviewed in order to consider both methodology and also the clinical relevance of findings with emphasis on trials with ACE-inhibitors like CONSENSUS-II, the ISIS-4, GISSI-3 and Chinese mega-trials, TRACE, SAVE and AIRE. Results of SAVE and AIRE show a clear survival benefit for the patients. Furthermore, the benefit of both trials was in addition to any other benefit which resulted from aspirin, thrombolytic and beta-blocker therapies. In absolute terms, treatment of 1,000 patients with ramipril (AIRE) for 1 year would be expected to result in the prevention/delay of 40 premature deaths. The beneficial effects of ramipril were clearly apparent by 30 days though additional benefit beyond this point was also present. Furthermore, prespecified subgroup analysis revealed significant benefit for patients at risk like women and the elderly. A selective approach is argued for the treatment of patients with ACE-inhibitors after myocardial infarction.

Aged↗
PubMed1993

Phenoxybenzamine mediated inhibition of the vascular dopamine D1 receptor.

Cultures of rat mesenteric artery vascular smooth muscle cells express both vascular dopamine D1 receptors and beta 2-adrenoceptors but not alpha 1- or alpha 2-adrenoceptors, permitting direct investigation of the dopamine D1 receptor antagonist activity of phenoxybenzamine. After incubating cells with phenoxybenzamine (10(-5) M) for 20 min, an 80% inhibition of dopamine-induced (10(-4) M) cAMP formation was observed. Isoprenaline-induced (10(-5) M) cAMP formation remained unaffected by phenoxybenzamine. Inhibition of the dopamine response following 20 min incubation with phenoxybenzamine, was concentration-related and could not be reversed by repeated washing. Mean IC50 (95% confidence limits) = 4.68 x 10(-6) M (3.86-5.01). Exposure of cells to the selective dopamine D1 receptor partial agonist (+)-SKF 38393 (10(-6) M) prior to phenoxybenzamine incubation, resulted in protection of dopamine-induced cAMP formation. Exposure of cells to the stereo-enantiomer (-)-SKF 38393 (10(-6) M) did not produce any protective effect. The concentration-effect curve for (+)-SKF 38393 mediated protection had a mean EC50 value of 0.11 x 10(-6) M (0.10-0.11), which is comparable with the Ka apparent value (0.06 x 10(-6) M) for this compound when acting as an agonist to induce cAMP formation via the vascular dopamine D1 receptor. Previous studies of the vascular dopamine D1 receptor are likely to have been influenced by the frequent use of phenoxybenzamine, which we have shown to act as a potent antagonist at this site.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Pharmacological characterization of the dopamine receptor coupled to cyclic AMP formation expressed by rat mesenteric artery vascular smooth muscle cells in culture.

1. Mesenteric artery vascular smooth muscle cells derived from male Wistar rats and grown in culture were prelabelled with [3H]-adenine and exposed to a range of dopamine receptor agonists and antagonists. Resultant [3H]-cyclic AMP formation was determined and concentration-effect curves constructed, in the presence of propranolol (10-6) M) and the phosphodiesterase inhibitor IBMX (5 x 10(-4) M). 2. Ka apparent values for D1/DA1 dopamine receptor agonists SKF 38393, fenoldopam, 6,7-ADTN, and dopamine were 0.06, 0.59, 4.06 and 5.77 x 10(-6) M respectively. Although fenoldopam and SKF 38393 were more potent than dopamine, they were partial agonists with efficacies, relative to dopamine of approximately 48% and 24% respectively. 6,7-ADTN, in contrast, behaved as a full agonist. 3. Dopamine-stimulated cyclic AMP formation was inhibited in a concentration-dependent manner by the D1/DA1 dopamine receptor selective antagonists, SCH 23390 and cis-flupenthixol (Ki values 0.53 and 36.1 x 10(-1) M respectively). In contrast, the D2/DA2 dopamine receptor selective antagonists, domperidone and (-)-sulpiride, were less potent (Ki values 2.06 and 5.82 x 10(-6) M respectively). Furthermore, the stereoisomers of SCH 23390 and cis-flupenthixol, SCH 23388 and trans-flupenthixol, were at least two orders of magnitude less potent (Ki values 0.14 and 13.2 x 10(-6) M respectively) indicating the stereoselective nature of this receptor. 4. Our results indicate that rat mesenteric artery vascular smooth muscle cells in culture express a dopamine receptor coupled to cyclic AMP formation, which has the pharmacological profile, characteristic of the D1 dopamine receptor subfamily.

Animals↗
PubMed1993

Validation of primary and secondary outcomes and classification of mode of death among patients with clinical evidence of heart failure after a myocardial infarction: a report from the Acute Infarction Ramipril Efficacy (AIRE) Study Investigators.

The AIRE study--a trial involving over 2,000 patients with clinical heart failure after myocardial infarction--assessed different outcomes. The primary outcome was total mortality. The secondary outcome was time to death, or progression to severe/resistant heart failure, reinfarction or stroke. Tertiary analyses included hospitalization and mode of death. To obtain maximum quality in the validation of outcomes and to optimize the quality of the data in the study, an end-points committee reviewed all data following preset definitions prior to code break. All definitions used are reported here. Experience of the validation process demonstrated that there are wide variations in clinical practice and terminology not only among countries but also among individual investigators. Variation in the clinical handling and treatment of patients makes it imperative to validate outcomes centrally on the basis of available facts.

Cause of Death↗
PubMed1992

Thiol group identification at or near the agonist binding site of the vascular dopamine receptor.

Cultured mesenteric artery vascular smooth muscle cells derived from male Wistar rats, expressing both beta 2-adrenoceptors and dopamine DA1 receptors, were prelabelled for 2 h with [3H]adenine. [3H]cAMP formation stimulated by the addition of dopamine (plus propranolol 10 microM), isoprenaline or forskolin, in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) (0.5 mM) was then determined. Exposure of cells to the thiol-oxidizing agent DTNB (5,5'-dithiobis-2-nitrobenzoic acid) following prelabelling, and prior to cAMP assay, resulted in a time-dependent inhibition of dopamine (0.1 mM)-induced cAMP formation, which obeyed the rules of first-order kinetics, being complete by 60 min. This inhibitory effect was observed to be dose related with 50% inhibition achieved at a concentration of 0.5 mM. Exposure to DTNB (5 mM) for 45 min abolished the cAMP response to dopamine (0.1 mM) with little effect on the response to forskolin (10 microM) or isoprenaline (10 microM). Prior addition of the dopamine DA1/D1 receptor selective partial agonist (+)-SKF 38393 (1 microM) preserved the dopamine induced cAMP formation despite DTNB exposure, while its stereo-enantiomer (-)-SKF 38393 (1 microM) protected only 25% of the response. Sequential exposure of cells to DTNB (5 mM) and then either vehicle or DTT (DL-dithiothreitol; 1 mM), each for 20 min periods, resulted in a 70% inhibition of dopamine induced cAMP formation which was almost completely reversed by the disulphide bridge cleaving compound DTT.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗