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Biomedical subjects

G Neil-Dwyer

Publications and source records attributed to G Neil-Dwyer.

At least 73 records · Page 4Linked to original sources
PubMed1987

Reduction of stress/catecholamine-induced cardiac necrosis by beta 1-selective blockade.

114 haemodynamically stable patients with acute head injury were randomised, double-blind, to either placebo or atenolol given intravenously (10 mg every 6 h) for 3 days then orally (100 mg daily) for a further 4 days. Both groups were equally stressed as shown by raised arterial noradrenaline levels. In patients receiving placebo, but not in those receiving atenolol, there was a significant (p less than 0.01) positive correlation between arterial noradrenaline and levels of the myocardial isoenzyme of creatine kinase (CKMB). 30% of the placebo group compared with 7.4% of the atenolol group (p less than 0.05) showed CKMB levels greater than 3% of total creatine kinase (compatible with myocardial damage). CKMB levels greater than 6% of total creatine kinase (compatible with acute myocardial infarction) were present in 16.7% of patients receiving placebo but in no patients receiving atenolol (p = 0.053). Atenolol appeared to reduce significantly the likelihood of supraventricular tachycardia and ST-segment and T-wave changes and prevented cardiac necrosis seen at necropsy.

Adolescent↗
PubMed1987

Early intervention with nimodipine in subarachnoid haemorrhage.

Seventy-five consecutive patients with subarachnoid haemorrhage (SAH) were entered into a randomized, double-blind, placebo-controlled trial prior to angiography in order to determine the effect of early intervention with nimodipine on blood pressure (BP), cerebral blood flow (CBF), and clinical outcome. Of these patients, 50 fulfilled the criteria for the final analysis (i.e. SAH due to cerebral aneurysm and receiving 21 days of treatment). There was no difference between the BP recordings of the two treatment groups, but mean CBF decreased slightly in the nimodipine group over the 21-day treatment period. At three months, one patient on nimodipine and six patients receiving placebo had died (P = 0.049, Fisher's exact test), but no significant difference was observed between the two groups, when the 'intent to treat' group of 75 patients was considered. We conclude that nimodipine does not increase CBF or alter BP following SAH, but an improved clinical outcome is evident at three months for patients with SAH due to cerebral aneurysm who had been treated with nimodipine. There were no side-effects due to nimodipine.

Adolescent↗
PubMed1986

Beta-blockers, plasma total creatine kinase and creatine kinase myocardial isoenzyme, and the prognosis of subarachnoid hemorrhage.

Under double-blind randomized conditions the effects of early intervention with oral propranolol or a placebo were studied in 51 cases of subarachnoid hemorrhage. Eleven out of 23 patients randomly assigned to placebo had a poor outcome at 6 months, while 2 of the 28 patients randomly assigned to propranolol had a poor outcome (p less than 0.001). Patients with a poor outcome on the placebo had significantly higher mean plasma total creatine kinase levels (742 IU, standard error of the mean +/- 233 IU) on the fifth day after subarachnoid hemorrhage than patients with a good outcome on the placebo (108 +/- 20 IU; p less than 0.05). A raised plasma creatine kinase myocardial isoenzyme was associated with a particularly poor outlook in patients receiving the placebo, in contrast to those taking a beta-blocker. Clinical outcome and plasma creatine kinase levels in patients taking atenolol (hydrophilic) were similar to those observed in patients receiving propranolol.

Adrenergic beta-Antagonists↗
PubMed1985

Beta-blocker brain concentrations in man.

Patients with subarachnoid haemorrhage (SAH) have been shown to benefit from beta-blockade. SAH patients who came to surgery were investigated if they had been receiving chronic (approximately one week) oral treatment with either hydrophilic atenolol (100 mg/day) or one of the following lipophilic beta-blockers: propranolol (80 mg b.i.d.), oxprenolol (80 mg b.i.d.), or metoprolol (100 mg b.i.d.). Cerebrospinal fluid concentrations of beta-blockers did not reflect their concentrations in the brain. Brain concentrations of the three lipophilic beta-blockers were 10-20 times higher than those of atenolol. The approximate brain/plasma concentration ratios were 26 for propranolol, 50 for oxprenolol, 12 for metoprolol, and 0.2 for atenolol. The brain is thus buffered from peak blood concentrations of atenolol, and this may account for the low incidence of CNS-related side-effects with this hydrophilic beta-blocker.

Adrenergic beta-Antagonists↗
PubMed1985

Beta-blockade benefits patients following a subarachnoid haemorrhage.

Previous studies have shown that ECG changes following a subarachnoid haemorrhage are associated with increased catecholamine levels, necrotic myocardial lesions, and a poor prognosis. Furthermore, beta-blockade using propranolol reverses some of the ECG changes and prevents necrotic myocardial lesions. This study was established to assess the affects of adrenergic blockade on morbidity and mortality following subarachnoid haemorrhage. Patients were admitted to the randomized double-blind between-patients study if they presented at the neurosurgical unit within 48 hours of a subarachnoid haemorrhage confirmed by lumbar puncture. Of 224 patients, the first 118 received an alpha-blocker, phentolamine 20 mg three-hourly, and either the beta-blocker propranolol 80 mg eight-hourly, or placebo. The last 106 patients received either propranolol or placebo. Treatment was continued for three weeks. Assessment at four weeks revealed significant improvements in the treated group for neurological deficit (p = 0.003) and death (p = 0.02). More treated patients underwent operation and those that did had a better outcome (p = 0.01). Assessment at one year showed that although patients had improved in both groups, patients in the treated group had significantly fewer neurological deficits (p = 0.003). There were fewer deaths in the treated group but this difference was not significant (p = 0.09). Possible mechanisms for this protective effect of propranolol may include a reduction in plasma renin activity, a reduction in pulmonary oedema, prevention of myocardial infarcts, and a reduction in cerebral oxygen requirements. It is concluded that early beta-blockade benefits patients with subarachnoid haemorrhage, in terms of fewer neurological deficits, for up to one year.

Adolescent↗
PubMed1984

Psychological aspects of patients having multiple operations for low back pain.

The aim of this study was to investigate whether psychological abnormalities were present in patients still complaining of low back pain after more than one operation. It was found that these patients were more psychiatrically disturbed and socially disabled than a matched control group whose back pain responded to one operation. These results suggest that patients requiring assessment for a possible second laminectomy should also be psychiatrically examined.

Back Pain↗
PubMed1983

Progressive change in cerebral blood flow during the first three weeks after subarachnoid hemorrhage.

Cerebral blood flow (CBF) was estimated from each cerebral hemisphere by the 133Xe inhalation method. Daily estimates were made during the first 3 weeks after subarachnoid hemorrhage (1265 studies in 116 patients). Some of the patients were taking adrenergic blocking drugs (propranolol and phentolamine), others were taking tranexamic acid, and the rest were taking no drugs. CBF was also studied in 67 normal subjects. The resting CBF was related inversely to age not only for normal subjects but also for patients after subarachnoid hemorrhage (SAH). The CBF fell progressively during the first 2 weeks after SAH and was abnormally low throughout the 3 weeks after hemorrhage. For any 1 day after SAH, those patients who were fully alert had the smallest reduction in CBF. The progressive changes in CBF occurred whether or not an aneurysm was present on angiograms. For aneurysms situated to one side of the midline, the changes in CBF affected both sides of the brain. The progressive decline in CBF was least in those patients who subsequently made the best clinical recovery. Arterial pCO2 seemed to influence CBF throughout the 3 weeks after SAH. During the 2nd week, CBF was especially low in SAH patients treated with tranexamic acid. The serial changes in CBF are discussed in relation to current views concerning the timing of operation for ruptured aneurysms.

Adult↗
PubMed1983

Collagen deficiency and ruptured cerebral aneurysms. A clinical and biochemical study.

Skin and temporal arterial biopsies were obtained from 17 patients undergoing surgery for ruptured cerebral aneurysm, and specimens were taken from six age- and sex-matched control surgical patients. Radioactively labeled and control tissue collagen patterns were studied by interrupted polyacrylamide gel electrophoresis (PAGE), using the trisborate buffer system or by carboxymethyl cellulose (CMC) chromatography. Type III/I collagen ratios were then measured from autoradiographs of the radioactively labeled samples using the Joyce Loebl gel scanner adapted for flat bed gels. In the case of the CMC labeled material, the ratios were measured by the ratios of the summed radioactively labeled alpha 1(III), alpha 2(II), and alpha 2(I) peaks. Eleven of the 17 patients were Type III collagen-deficient while all of the six control patients had normal collagen ratios. The implications of these findings are discussed.

Adult↗
PubMed1982

Subarachnoid haemorrhage: older patients have low cerebral blood flow.

Daily estimations of hemispheral cerebral blood flow using the xenon-133 inhalation technique was made in 116 patients during the first three weeks after subarachnoid haemorrhage. The patients' cerebral perfusion on average remained less than the normal perfusion expected for their age (based on a single estimation of cerebral blood flow in 67 volunteers). On each separate day after subarachnoid haemorrhage cerebral blood flow was inversely related to the patient's age. Older patients seem especially at risk of developing cerebral ischaemia after subarachnoid haemorrhage. The clinical outcome was more often unfavourable in older patients--that is, in those who tended to have the lowest cerebral blood flow. Present results support the view that episodes of low cerebral blood flow lead to a poor outcome after subarachnoid haemorrhage. Because of the risk of inducing cerebral ischaemia great care should be exercised by physicians administering hypotensive drugs to older patients after subarachnoid haemorrhage.

Adult↗
PubMed1982

Beneficial effects of adrenergic blockade in patients with subarachnoid haemorrhage.

A total of 148 patients presenting within 48 hours of subarachnoid haemorrhage were assigned at random to receive standard management only or standard management and treatment with the adrenergic-blocking agents propranolol and phentolamine (or propranolol alone) for three weeks. One hundred and thirty-four patients completed the study. Assessment at four weeks showed a strong trend for less neurological deficit in the treated group, almost statistically significant (p=0.053) in the women. During the first month the treated group suffered fewer episodes of clinical deterioration consistent with cerebral arterial spasm: thus more treated patients underwent operation and those who did had a better outcome (p=0.030). At one year fewer were dead or disabled (unable to work) in the treated group; a significant difference for women (p=0.030). Possible mechanisms for these actions may include a reduction in pulmonary oedema, prevention of myocardial infarcts, a reduction in plasma renin activity, nd a reduction in cerebral oxygen requirements. It is concluded that early adrenergic blockade benefits patients (particularly women) with subarachnoid haemorrhage for up to one year in terms of lesser neurological deficit. Beta-blocker rather than alpha-blockade appears to be the useful component. A randomised, blind extension of the present study using long-acting propranolol and placebo has shown a significant (p=0.026) decrease in deaths and significantly (p=0.003) fewer poor results in the treatment group.

Adolescent↗
PubMed1982

Cardiac sequelae of acute head injury.

An intensive 72 hour study of the cardiovascular effects of severe diffuse brain injury was made in seven patients. No other major injury was present. Patients received optimal care very rapidly after injury and intracranial pressure, which was continuously monitored, was maintained at or just above normal by elective positive pressure ventilation techniques. Three patients showed evidence of progressive myocardial ischaemia on continuous electrocardiographic monitoring. Two of these patients died. Ventricular arrhythmias were uncommon but one of the patients with ischaemia developed ventricular tachycardia. Heart rate patterns were very abnormal but did not predict complications. Blood pressure did not vary greatly and cardiac outputs were usually normal. Pronounced excesses of urinary catecholamines and serum creatine kinase 2 isoenzyme (CK MB) as well as total creatine kinase were found. Histological evidence of myocardial damage could be shown at necropsy in the one case whose heart was available for study. This study shows that the cardiac effects of isolated diffuse cerebral injury may be harmful and even fatal despite correction of secondary factors such as anoxia and raised intracranial pressure. The findings suggest that evaluation of the potential benefits of sympathetic blockade is warranted. Cardiac complications of cerebral damage deserve wider recognition by intensive care personnel, neurologists, and neurosurgeons.

Adolescent↗
PubMed1981

Some patients with cerebral aneurysms are deficient in type III collagen.

Polyacrylamide gel electrophoresis of pepsin-digested skin biopsy specimens and carboxymethyl cellulose chromatography of radioactively labelled collagens produced by cultured fibroblasts demonstrated that 7 of 12 patients with congenital cerebral aneurysms were type III collagen deficient. This suggests that some cerebral aneurysms resemble various inherited defects of connective tissue-i.e., Ehlers-Danlos syndrome type IV-in which type III collagen deficiency causes arterial fragility.

Cerebral Hemorrhage↗
PubMed1981

Beta-adrenoceptor blockers and the blood-brian barrier.

1 This study on 21 neurosurgical patients was set up to investigate the extent to which four chronically administered beta-adrenoceptor blockers, propranolol, oxprenolol, metoprolol and atenolol, cross and blood-brain barrier and enter the cerebrospinal fluid (CSF) and brain tissue. The concentration in the CSF of the three lipophilic beta-adrenoceptor blockers, propranolol, oxprenolol and metoprolol, approximated to the free drug concentration in the plasma, and was a poor predictor of brain concentration. These three lipophilic beta-adrenoceptor blockers appeared in brain tissue at concentrations 10-20 times greater than that of hydrophilic atenolol. The approximate brain/plasma ratio for propranolol was 26, for oxprenolol 50, for metoprolol 12 and for atenolol 0.2. 2 The low concentration of atenolol in brain tissue is possibly responsible for the low incidence of central nervous system-related side effects in patients on this agent compared to lipophilic beta-adrenoceptor blockers.

Adrenergic beta-Antagonists↗