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Biomedical subjects

R E Ferner

Publications and source records attributed to R E Ferner.

At least 109 records · Page 6Linked to original sources
PubMed1990

Lack of effect of co-trimoxazole on the pharmacokinetics and pharmacodynamics of nifedipine.

The pharmacokinetics of nifedipine and its primary oxidised metabolite, M-I were studied in nine healthy volunteers following a single oral dose of 20 mg nifedipine alone or after pretreatment with oral co-trimoxazole. Following pretreatment with co-trimoxazole, no significant effect was detected on maximum plasma concentration, elimination half-life, or area under the plasma concentration-time curve of either nifedipine or M-I, nor on the blood pressure response to nifedipine.

Adult↗
PubMed1990

Pharmacokinetics and toxic effects of nifedipine in massive overdose.

A 57-year-old man took 30 x 20 mg nifedipine retarded release tablets. He developed hypotension, tachycardia and flushing, but remained in sinus rhythm. The concentration of nifedipine 10 h after overdose was 604 micrograms 1-1, and of the M-I metabolite 110 micrograms 1-1. Log concentration time curves were linear from 10-72 h for nifedipine, with a half-life of 7.5 h; and for M-I with a half-life of 8.2 h. On this evidence, oral absorption of nifedipine retarded release is complete by 10 h. There was no evidence of saturation of nifedipine or M-I metabolism, even at concentrations ten times above the therapeutic concentration.

Drug Overdose↗
PubMed1989

Drugs in donated blood.

Blood from donors who are or who have been on drug treatment may be hazardous to the recipient. Guidelines are proposed to increase the safety of donated blood without needless rejection of donors, based on the time that should elapse between the last dose and safe blood donation for a range of commonly used drugs.

Blood Banks↗
PubMed1989

Chemical weapons.

Explore the source record for details and available documents.

Chemical Warfare↗
PubMed1989

The effects of intradermal bradykinin are potentiated by angiotensin converting enzyme inhibitors in hypertensive patients.

1. To test the hypothesis that angiotensin converting enzyme (ACE) inhibitors potentiate the tissue effects of bradykinin, the thickness of weals produced by intradermal injections of bradykinin was measured in 17 hypertensive subjects whose antihypertensive regimen included an ACE inhibitor, and in 12 whose treatment did not. 2. Weal thickness increased linearly with the logarithm of the bradykinin dose in both groups (P less than 0.0001). 3. The patients receiving ACE inhibitors showed a mean response of 1.18 +/- 0.08 mm (mean +/- s.e. mean), compared with a mean response of 0.75 +/- 0.08 mm for patients not receiving an ACE inhibitor (P = 0.002). Mean weal response (1.08 +/- 0.9 mm) was not significantly different in patients taking captopril (n = 11) compared with that (1.29 +/- 0.12 mm) in patients taking enalapril (n = 9). 4. Facial flushing during the experiment occurred in six patients taking ACE inhibitors but none who were not. 5. Dermal responses to bradykinin are enhanced in patients taking ACE inhibitors as routine antihypertensive therapy. This study supports the hypothesis that bradykinin may be responsible for some of the adverse effects of these drugs.

Adult↗
PubMed1989

Plasma exchange for Guillain-Barré syndrome.

The impact of plasma exchange (PE) on the treatment of severe Guillain-Barré syndrome (GBS) was studied by comparing all the 16 patients treated with PE in a London teaching hospital between January 1985 and August 1987, with 64 historical controls drawn from a series of patients observed during a prospective study in South East England in 1983 and 1984. There were no GBS-related deaths in the PE treated group but seven in the historical controls (2P = 0.39). The median duration of ventilation was only 20 days (range 7-64) in the PE group compared with 36 days (range 14-365) in the surviving patients in the control group (2P = 0.06, 95% confidence interval of difference in medians -36 to 0 days). The PE group walked earlier without aid (median 55.5 compared with 86 days, 2P = 0.04, 95% confidence interval of difference in medians -88 to -2 days). Three months after the onset of neuropathy all PE treated patients were able to walk with support or better, whereas 19 of the surviving historical controls were unable to walk even with support (2P = 0.009). The costs of PE were offset by savings in intensive care unit and hospital expenditure.

Adult↗
PubMed1989

Pharmacokinetics and toxic effects of diltiazem in massive overdose.

A 50-year-old man with ischaemic heart disease took 98 tablets of diltiazem 60 mg with alcohol. He developed a junctional bradycardia, hypotension and reduced cardiac function refractory to intravenous calcium gluconate. He survived with temporary cardiac pacing and infusion of dopamine. As much as half the dose was vomited back, but nonetheless the plasma diltiazem concentration reached 6090 micrograms/l before falling mono-exponentially with a half-life of 8.6 h. Sinus rhythm returned when the plasma concentration of diltiazem was around 750 micrograms/l. Standard resuscitative procedures sufficed to treat massive diltiazem overdosage.

Adult↗
PubMed1988

Oral hypoglycemic agents.

The sulfonylureas remain the most important oral agents, although their chronic hypoglycemic actions are still unexplained and the evidence on their relative efficacy is inconclusive. Data on relative safety suggest that chlorpropamide is the most toxic sulfonylurea but glyburide causes dangerous hypoglycemia as often as chlorpropamide. For many patients, good blood glucose control will be achieved by taking tolbutamide or another sulfonylurea 30 minutes before breakfast and the main evening meal. The biguanide metformin, which is as safe as glyburide, is of use in treating overweight diabetic patients who do not have cardiovascular, hepatic, or renal dysfunction.

Administration, Oral↗
PubMed1988

Reversal of histamine-induced bronchoconstriction by the H1-receptor antagonist levocabastine: a potential model for efficacy in anaphylaxis.

1. The rate of onset and magnitude of the effect of levocabastine, a potent H1-receptor antagonist, in reversing histamine-induced bronchoconstriction were determined in a double-blind cross-over trial against saline placebo. Histamine was administered by nebuliser so that forced expiratory volume in 1 second (FEV1) was reduced to 80-75% of baseline FEV1 in 10 men with mildly or moderately responsive airways and the effects of intravenous injection of saline or saline + 200 micrograms levocabastine were studied. 2. The maximum rate of recovery of FEV1 was 7[2-10]% min-1 (median [range]) in the first 5 min after levocabastine injection, but only 4[1-7]% min-1 after saline alone (P less than 0.05). 3. The median area under the recovery curve of FEV1 from 0 to 30 min after injection was 405 [228-498]% basal FEV1 X min after levocabastine and 301[98-502]% basal FEV1 X min after saline alone (P less than 0.002). 4. FEV1 returned to 90% of baseline within 30 min in all subjects after levocabastine, but not after saline alone (P less than 0.002). 5. Histamine-induced bronchoconstriction was relieved more quickly by levocabastine than saline alone. This model may have application to the study of drugs used in the treatment of anaphylaxis.

Adult↗
PubMed1988

Allopurinol kinetics after massive overdosage.

A 15-year-old girl with normal renal function took 75 tablets of allopurinol 300 mg. She did not suffer any ill-effects. Samples obtained over 84 h showed prolonged elimination of allopurinol, with a half-life of 3.6 h, and oxipurinol, with a half-life of 26 h.

Adolescent↗
PubMed1988

Impaired beta-cell responses improve when fasting blood glucose concentration is reduced in non-insulin-dependent diabetes.

Pancreatic beta-cell responses to a controlled intravenous glucose stimulus in 18 untreated non-insulin-dependent diabetic patients were compared with those in seven healthy control subjects. The patients' first-and second-phase responses were only 10 to 20 per cent of those of the normal subjects. However, when normal subjects had been hyperglycaemic for two hours, their first-phase responses were similar to those of the patients. Six patients were subsequently treated by diet alone, six by diet and tolbutamide and six by diet and metformin. There was no improvement in first-phase responses after treatment, but second-phase responses doubled. Improved responses were seen with all treatments, and correlated with the fall in fasting blood glucose concentration during treatment. This study supports the view that hyperglycaemia impairs beta-cell function and suggests that first-phase responses are more sensitive to hyperglycaemia than second-phase responses.

Adult↗
PubMed1987

Effects of intradermal bradykinin after inhibition of angiotensin converting enzyme.

Inhibitors of angiotensin converting enzyme may cause angio-oedema. To see if this might be due to potentiation of the tissue effects of bradykinin the thickness of weals raised by intradermal injection of saline or 1, 3, or 10 micrograms bradykinin was measured before and three times after single doses of captopril, enalapril, or placebo. The mean thickness increased with increasing doses of bradykinin. It did not change with time after the administration of placebo or captopril but increased from 0.61 mm before enalapril to 1.12 mm two and a half hours and 1.06 mm five hours after enalapril was given. Five subjects flushed when given bradykinin after captopril and four after enalapril, but none flushed when given bradykinin after placebo. It is concluded that angiotensin converting enzyme inhibitors potentiate the effects of intradermal bradykinin in vivo and that this may partially explain why they cause angio-oedema in susceptible patients.

Adult↗