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Biomedical subjects

C C Lang

Publications and source records attributed to C C Lang.

88 records · Page 5Linked to original sources
PubMed1991

Comparison of the effects of ANF 99-126 and ANF 103-126 on captopril-induced renin release in man.

OBJECTIVE: The aim was to examine the effects of atrial natriuretic factor (ANF) 99-126 and ANF 103-126, an N-terminal shortened analogue of the peptide, on the plasma renin activity response to captopril, an inhibitor of angiotensin-converting enzyme. DESIGN: Two protocols were performed. In the first protocol, subjects were studied on three occasions. Captopril 25 mg was given and a 60 minute infusion of 5% D-glucose (placebo), or ANF 99-126 3 or 10 pmol/kg/min, was administered in a single blind randomized manner. The second protocol was divided in two parallel phases comparing ANF 103-126 either 3 or 10 pmol/kg/min to placebo. SUBJECTS: Thirty-three salt-replete healthy male volunteers aged 21-39 years were studied in the supine position. MEASUREMENTS: Plasma renin activity, plasma ANF 99-126 and ANF 103-126 levels, heart rate and blood pressure were measured. RESULTS: Compared to placebo infusion, the rise in plasma renin activity after captopril was attenuated by ANF 99-126 infusion (from 755% of baseline to 294% by ANF 99-126 3 pmol/kg/min and from 755 to 202% by 10 pmol/kg/min; P less than 0.03 and P less than 0.01 respectively). The comparable findings with ANF 103-126 were 492 to 218% (3 pmol/kg/min) and 645 to 364% (10 pmol/kg/min) (P less than 0.01 and P less than 0.01 respectively). CONCLUSIONS: The results, taken in conjunction with previous findings, suggest that atrial natriuretic factor inhibits in a non-selective manner the renin response to all secretagogues so far tested in man. The current results also suggest that the anti-renin action of atrial natriuretic factor does not depend on the first four N-terminal amino acids of the native peptide.

Adult↗
PubMed1990

Effect of atrial natriuretic factor on platelet function in whole blood ex-vivo in man.

Atrial natriuretic factor (ANF) binding sites have been shown to be present on human platelet membranes. We investigated the effect of an infusion of ANF 5 pmol.kg-1.min-1 on platelet aggregation in whole blood ex-vivo in 8 normal volunteers. Spontaneous platelet aggregation, collagen (0.6-2 micrograms.m.-1)-induced or ADP (0.5-2.0 microM)-induced aggregation was not affected by ANF. Plasma aldosterone was however significantly attenuated by ANF. These results show that a pharmacological dose of ANF does not affect platelet aggregation in man. These results suggest that the high plasma levels of ANF normally achieved in chronic heart failure or acute myocardial infarction are unlikely to contribute to the platelet hyperractivity, often observed in these conditions.

Adenosine Diphosphate↗
PubMed1990

Neuroendocrine changes post myocardial infarction: effects of xamoterol.

This study reports the effects of the new beta 1 adrenoceptor partial agonist, xamoterol, on neuroendocrine activity after acute myocardial infarction (AMI). Fifty-one consecutive patients with AMI were randomized to treatment with xamoterol, 200 mg twice a day, or placebo; patients were also stratified as to whether or not diuretic therapy was given for left ventricular dysfunction. Noradrenaline, plasma renin activity (PRA), and atrial natriuretic factor (ANF) were measured over a 10-day period. Noradrenaline concentrations are higher (p less than 0.05) in patients treated with diuretics at the time of admission and fell over the subsequent 10 days (p less than 0.01). Treatment with xamoterol did not affect this noradrenaline response to myocardial infarction. PRA was also significantly higher in the patients treated with diuretics, and there was a nonsignificant trend for xamoterol to blunt the PRA response in these patients. There was no difference in ANF levels between those patients who were treated with diuretics and those who were not; xamoterol did not affect ANF. Thus xamoterol does not further elevate noradrenaline levels as do conventional beta blockers, and it does not activate the renin-angiotensin system as do potent nonselective beta agonists. Furthermore, xamoterol does not increase ANF levels, probably because it is not negatively inotropic. We conclude that xamoterol does not cause deleterious neuroendocrine changes in patients with AMI even in those treated for heart failure.

Adrenergic beta-Agonists↗
PubMed1990

Bioavailability of cefuroxime axetil: comparison of standard and abbreviated methods.

A randomized cross-over study comparing serum and urinary concentrations of cefuroxime after a 750 mg intravenous dose of cefuroxime and a 500 mg oral dose of cefuroxime axetil was conducted to evaluate the bioavailability of the current marketed formulation of cefuroxime axetil. The absolute bioavailability was compared with various abbreviated methods of assessing bioavailability. The peak concentrations (Cmax) and times to peak (Tmax) varied considerably (range 4.7-12.0 mg/l and 1.5-4 h respectively). The absolute bioavailability was 67.9%. The urine recovery after oral dosage and urine bioavailability were 38.6% and 50.3% respectively. The mean AUC0-6 h after the oral dosage was 27.7 mg/l.h. Both urine recovery and urine bioavailability were poor indicators of bioavailability (r = 0.54, r = 0.33 respectively). Although AUC0-6 h after the oral dose was positively correlated with absolute bioavailability, the coefficient of determination (r2) indicated that only 56% of the variation in absolute bioavailability was explained by AUC0-6 h. This study demonstrated that the current formulation of cefuroxime axetil is reliably absorbed although there is considerable variation in Cmax and Tmax. Because of this variation and because the abbreviated methods were unsatisfactory, we recommend that bioavailability of cefuroxime axetil in patients should be measured by formal intravenous/oral cross-over serum concentration studies.

Biological Availability↗
PubMed1990

Gall-bladder perforation after long-term dapsone therapy.

A 65-year-old man on maintenance dapsone therapy for dermatitis herpetiformis for 30 years was admitted to hospital with acute abdominal pain and vomiting. Investigations revealed a Heinz body haemolytic anaemia. Worsening symptoms prompted an emergency laparotomy that revealed a perforated gall bladder with pigmented biliary calculi. In previous reviews of the haematological abnormalities associated with dapsone therapy, life-threatening cholecystitis has not been described.

Abdomen, Acute↗
PubMed1990

Physicians' attitudes to the treatment of elevated serum cholesterol.

A questionnaire was sent to 457 physicians (328 general practitioners, 129 hospital doctors) to assess their attitudes to and their knowledge and practice of the management of raised serum cholesterol. Replies were returned by 206 (63%) general practitioners and 95 (74%) hospital doctors. While smoking, hypertension, diabetes mellitus and elevated total serum cholesterol were recognised as major risk factors for coronary heart disease, a significant number of respondents considered serum triglycerides to be less important. Both groups of physicians start dietary management at similar total serum cholesterol levels, but hospital doctors were more likely to use dietetic services. The two groups had a similar threshold for the addition of drug therapy. A bile acid sequestrant was the favoured first choice as a cholesterol lowering agent, although a wide variety of other drugs were also chosen. The screening of high risk patients was preferred to whole population and opportunistic screening for identifying hypercholesterolaemic individuals. The findings have important implications in the delivery of services to hypercholesterolaemic patients.

Anticholesteremic Agents↗
PubMed1989

A survey of current use of angiotensin-converting-enzyme inhibitors by Scottish physicians in the treatment of chronic cardiac failure.

318 consultant physicians in Scotland were sent a questionnaire on their use of angiotensin converting enzyme (ACE) inhibitors to treat chronic heart failure (CHF). 229 (72%) replies were received. Of these 91% used ACE inhibitors for CHF; 22% were geriatricians, 58% general physicians and 20% cardiologists. All groups reserved ACE inhibitors for patients uncontrolled by diuretics alone. Compared to general physicians, cardiologists used ACE inhibitors in preference to other vasodilators and digoxin, used higher doses and commenced treatment more often on a day-patient basis. Cardiologists also commonly started treatment with captopril even if continuing with enalapril. Geriatricians used ACE inhibitors as frequently as cardiologists but at lower doses; they did not report side-effects more frequently. Further investigation of the safety and possible cost savings of supervised day-patient rather than in-patient, introduction of ACE inhibitors for CHF is now merited. To avoid an extended period of patient observation after the first dose of ACE inhibitor, captopril might also be given as the initial therapy, even if continuing with enalapril. This policy would also reduce the risk of any hypotensive response being prolonged.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Diagnosis of type 1a and type 1c glycogen storage diseases in adults.

The hepatic glucose-6-phosphatase system was studied with a novel microanalytical technique in adult patients undergoing liver biopsy. 4 patients were diagnosed as having type 1 glycogen storage disease (GSD). 3 of these patients, who had hypoglycaemic symptoms, had variations of type 1a GSD, which is caused by a defect in the hepatic microsomal glucose-6-phosphatase enzyme. The fourth, with hepatomegaly and no hypoglycaemic symptoms, had a normal glucose-6-phosphatase enzyme but a defect in the hepatic microsomal phosphate/pyrophosphate translocase T2; this is the first report of an adult with type 1c GSD. Adult type 1 GSD should be considered in patients with unresolved hypoglycaemic symptoms and/or unresolved hepatomegaly.

Adult↗
PubMedDate not supplied

Cyclosporin-induced nephrotoxicity and hypertension.

The use of cyclosporin in therapeutics is increasing. Unfortunately, cyclosporin has important detrimental effects on kidney function and blood pressure. Based on the pathogenesis of these side effects, different drug groups have been studied, but with variable success.

Angiotensin-Converting Enzyme Inhibitors↗