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Biomedical subjects

G A Ford

Publications and source records attributed to G A Ford.

At least 55 records · Page 3Linked to original sources

Superficial hand vein responses to NG-monomethyl-L-arginine in post-partum and non-pregnant women.

1. During human pregnancy marked vasodilatation occurs in arterial and venous vascular beds. The mechanisms responsible for this change remain unclear. The contribution of increased nitric oxide activity to vasodilatation associated with pregnancy was determined by examining superficial hand vein responses to NG-monomethyl-L-arginine, an inhibitor of nitric oxide synthase, in post-partum women 24-48 h after delivery when vasodilatation remains at levels present during the third trimester. 2. Seventeen healthy women, 24-48 h post partum, and 13 healthy non-pregnant women were studied. Eight of the post-partum women underwent repeat studies 12-16 weeks after delivery. 3. NG-monomethyl-L-arginine (100 nmol/min) resulted in venoconstriction in non-constricted veins (baseline, 0%; 5 min, 26 +/- 9%; 10 min, 14 +/- 8%; 15 min, 8 +/- 7%; means +/- SEM) and noradrenaline-constricted veins (5 min, 30 +/- 7%; 10 min, 24 +/- 10%; 15 min, 14 +/- 11%). No constrictor response to NG-monomethyl-L-arginine was present in the same women 12 weeks post partum (5 min, 1 +/- 4%; 10 min, 0 +/- 3%; 15 min, 1 +/- 4%) or in the non-pregnant control subjects in non-constricted (5 min, 2 +/- 3%; 10 min, 4 +/- 3%; 15 min, 2 +/- 2%) or noradrenaline-constricted veins (5 min, -2 +/- 7%; 10 min, 1 +/- 9%; 15 min, -5 +/- 7%). 4. These findings indicate that nitric oxide activity is increased in the immediate post-partum period in venous vasculature, and support the hypothesis that increased nitric oxide activity may be responsible for the vasodilatation observed during normal pregnancy.

Adult↗

Effect of oxybutynin on the QTc interval in elderly patients with urinary incontinence.

1. Terodiline, an anticholinergic drug with calcium antagonist properties, is associated with QT prolongation and ventricular arrhythmias. It is not known if oxybutynin, a drug with a similar pharmacological profile, causes QT prolongation. ECGs were obtained before and at least 4 weeks after commencement of oxybutynin (mean daily dose 7.6, range 2.5-10 mg), in 21 elderly (mean age 75, range 58-88 years) patients treated for urinary incontinence. Heart rate, (mean +/- s.d.) 74 +/- 11 vs 69 +/- 11 beats min-1, -6 (-13,2), before vs during oxybutynin therapy, mean difference (95% confidence intervals); PR interval, 168 +/- 27 vs 156 +/- 27 ms, -11 (-26,3); QTc 454 +/- 27 vs 447 +/- 31 ms1/2, -9 (-23,5), and QTc dispersion, QTc max-QTc min, 68 +/- 24 vs 63 +/- 26 ms1/2, -1 (-15,14) were all unaltered by oxybutynin therapy. The lack of an effect on resting heart rate suggests that oxybutynin has little anticholinergic action at cardiac M2 receptors at usually administered doses. Oxybutynin therapy is not associated with QTc interval prolongation and is unlikely to produce ventricular arrhythmias.

Aged↗

Measurement of baroreflex gain from heart rate and blood pressure spectra: a comparison of spectral estimation techniques.

The baroreflex is the physiological control system linking blood pressure and heart rate. Baroreflex gain, alpha, can be estimated from the ratio of heart rate and blood pressure spectra. The aim of this study was to quantify differences in estimates of alpha incurred by using four different spectral analysis techniques. ECG and blood pressure were recorded from 10 healthy subjects. Spectra were estimated using fast Fourier transform (FFT), zero-padded FFT (FFTZ), FFT of the windowed autocovariance function (ACVF), and maximum-entropy (ME) methods. For each subject a mean value of alpha was calculated in the MF (0.05-0.15 Hz) and HF (0.15-0.35 Hz) bands. Mean alpha MF varied between subjects (range 2-10 ms mmHg-1) as did mean alpha HF (range 4-12 ms mmHg-1). Mean differences in alpha MF and alpha HF estimated with different techniques were small. Differences in alpha MF ranged from 0.074 ms mmHg-1 (FFTZ against ME) to 0.298 ms mmHg-1 (FFT against ACVF) and those in alpha HF ranged from 0.057 ms mmHg-1 (FFT against FFTZ) to 0.342 ms mmHg-1 (ACVF against ME). None of these differences were significant. The use of different spectral analysis techniques does not significantly affect estimates of alpha.

Aged↗

Management of hypertension in the elderly: attitudes of general practitioners and hospital physicians.

1. The attitudes of general practitioners and hospital physicians to the management of hypertension in the elderly, were examined by responses to a postal questionnaire distributed within the Northern Region, concerning the management of a healthy 75 year old male non-smoker with sustained diastolic or isolated systolic hypertension. 2. Two hundred and fourteen (64%) general practitioners and 127 (70%) hospital physicians responded to the questionnaire. General practitioners stated they would most commonly measure to the nearest 2 mm Hg (47%) as compared with nearest 5 mm Hg (61%) by physicians; P < 0.05. When measuring diastolic blood pressure 16% general practitioners and 31% physicians would use phase IV sounds; P < 0.01. 3. Median levels of hypertension, confirmed by repeated readings, at which antihypertensive therapy would be commenced were similar: 180 (150-230)/100(90-120) mm Hg vs 180 (150-200)/100 (90-120) mm Hg; median (range). The stated use of non-pharmacological methods to lower blood pressure before starting drug therapy was similar (74% vs 63%). General practitioners were more likely to prescribe a thiazide diuretic (70% vs 54%) and less likely to prescribe a calcium channel blocker (14% vs 28%) as first line therapy; data for diastolic hypertension, P < 0.001. 4. Considerable variation exists amongst both general practitioners and physicians in their stated assessment and management of a healthy elderly non-smoking male with sustained hypertension. General practitioners and physicians have similar stated thresholds for treating hypertension but differ in their choice of first line therapy. (ABTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗

Concentration dependent cardiotoxicity of terodiline in patients treated for urinary incontinence.

OBJECTIVE: Terodiline, an antimuscarinic and calcium antagonist drug, was used to treat detrusor instability but was withdrawn in 1991 after provoking serious ventricular arrhythmias associated with increases in the corrected QT interval (QTc). This research was performed to relate drug induced electrocardiographic changes in asymptomatic recipients to plasma concentrations of the R(+) and S(-) terodiline enantiomers. SETTING: Urological and geriatric clinics and wards. SUBJECTS: Asymptomatic patients taking terodiline in stable dose. METHODS: Electrocardiograms (50 mm/s) were collected from patients while they were taking terodiline and compared with ECGs obtained before or after terodiline. QT interval, heart rate corrected QT interval (QTc), and QT dispersion (QTd) were measured. Drug induced electrocardiographic changes were related to plasma concentrations of R(+) and S(-) terodiline. RESULTS: During terodiline treatment mean QTc and QTd were prolonged (491(43) and 84 (35) ms 1/2) compared with measurements made off therapy (443 (33) and 42 (17) ms 1/2, paired t tests, P < 0.002 and P < 0.01 respectively) in the 12 patients in sinus rhythm. The mean (95% confidence interval) drug induced increases were 48 (23 to 74) ms 1/2 for QTc and 42 (13 to 70) ms 1/2 for QTd. These increases correlated with total plasma terodiline (QTc: r = 0.77, P < 0.006, QTd: r = 0.68, P < 0.025) and with plasma concentrations of both terodiline enantiomers. CONCLUSIONS: Terodiline increases QTc and QTd in a concentration dependent manner. It is not clear whether this is a stereoselective effect and, if so, which enantiomer is responsible. The results suggest that drug induced torsade de pointes is a type A (concentration dependent) adverse drug reaction.

Aged↗

Effect of aging on beta 2-adrenergic receptor-stimulated flux of K+, PO4, FFA, and glycerol in human forearms.

beta-Adrenergic responses have been shown to decline with aging, particularly in the cardiovascular system. We infused terbutaline, a selective beta 2-adrenoceptor agonist, into the brachial artery of 10 young (mean age 25 yr, range 22-31 yr) and 9 elderly (mean age 73 yr, range 68-81 yr) healthy subjects to examine its effects on nutrient flux. Forearm K+, PO4, free fatty acid (FFA), and glycerol uptake were determined by measurement of forearm blood flow (using dye dilution) and brachial arterial and deep venous plasma substrate concentrations. Elderly subjects were less sensitive to terbutaline-mediated increases in forearm blood flow, net fluxes of K+, and glycerol but not net fluxes of FFA or PO4. The mean fitted slopes of each parameter vs. the log of the terbutaline concentration, a measure of forearm beta-adrenergic sensitivity, for young and elderly groups were 4.9 +/- 1.7 (SD) vs. 2.4 +/- 2.3 for forearm blood flow (P < 0.05), 0.84 +/- 0.46 vs. 0.43 +/- 0.37 for K+ net flux (P < 0.05), -157 +/- 113 vs. -26 +/- 26 for glycerol net flux (P < 0.01), -336 +/- 429 vs. -44 +/- 457 for FFA net flux (P = 0.11), and 0.31 +/- 0.24 vs. 0.18 +/- 0.16 for PO4 net flux (P = 0.14). Terbutaline promoted net uptake of K+ into skeletal muscle less well in the elderly, although net PO4 flux was similar in the two groups. Terbutaline-stimulated vasodilation and net glycerol efflux but not FFA efflux were impaired with aging. These data demonstrate that heterogeneous changes in beta-adrenergic responses occur with aging.

Adult↗

Effect of 'autonomic blockade' on cardiac beta-adrenergic chronotropic responsiveness in healthy young, healthy elderly and endurance-trained elderly subjects.

1. Cardiac chronotropic responses to isoprenaline are reduced with ageing in man. It is unclear whether this is due to reduced cardiac beta-adrenergic sensitivity or to age-associated differences in reflex cardiovascular responses to the vasodilatory effects of isoprenaline. Age-associated changes in physical activity are also reported to influence beta-adrenergic sensitivity. 2. The aim of the present study was to determine the contribution of alterations in reflex changes in para-sympathetic and sympathetic influences and physical fitness to the age-associated reduction in cardiac chronotropic responses to beta-adrenergic agonists. 3. The effect of 'autonomic blockade' with atropine (40 micrograms/kg intravenously) and clonidine (4 micrograms/kg intravenously) on blood pressure, heart rate and chronotropic responses to intravenous bolus isoprenaline doses was determined in eight healthy young (mean age 21 years), nine healthy elderly (72 years) and 10 endurance-trained elderly (69 years) subjects. 4. Elderly subjects had a reduced increase in heart rate after atropine (young, 49 +/- 9 beats/min; elderly, 36 +/- 5 beats/min; endurance-trained elderly, 34 +/- 12 beats/min; P < 0.01) and did not demonstrate the transient increase in systolic blood pressure after clonidine observed in young subjects (young, 11 +/- 10 mmHg; elderly, -12 +/- 16 mmHg; endurance-trained elderly, -18 +/- 11 mmHg; P < 0.01). 5. Cardiac chronotropic sensitivity to isoprenaline after 'autonomic blockade' increased in the young but decreased in the elderly subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Nitric oxide mediated venodilator effects of nebivolol.

1. Nebivolol, a selective beta 1-adrenoceptor antagonist with antihypertensive effects, has haemodynamic effects suggestive of a direct vasodilator action. 2. The dorsal hand vein technique was used to determine whether nebivolol has venodilator action in vivo in man. 3. Nebivolol and atenolol were infused into the phenylephrine preconstricted superficial hand veins of 11 healthy male volunteers. In separate studies L-NMMA (0.1 microgram min-1) was pre- and co-infused with nebivolol to determine whether nitric oxide (NO) mediated mechanisms were present. Further studies with prostaglandin F2 alpha (PGF2 alpha) preconstriction were performed to exclude an alpha-adrenergic antagonistic effect of nebivolol. Effects of L-NMMA infusion on nitroglycerin venodilation were also determined. 4. Nebivolol produced a dose dependent venodilation, (72 +/- 18% maximum), whereas atenolol produced no significant venodilation. At doses of nebivolol producing plasma concentrations comparable with plasma levels achieved after standard oral dosing (10(-13)-10(-12) mol min-1) small (14 +/- 6% and 23 +/- 8%) but significant (P < 0.05) venodilation was observed. 5. The venodilator response to nebivolol was significantly reduced by infusion of L-NMMA (maximum dilation 18% vs 72%, P < 0.01). Venodilator responses to nitroglycerin were unaffected by L-NMMA infusion. A venodilator effect to nebivolol was also seen following preconstriction with PgF2 alpha (40 +/- 20% maximum). 6. Nebivolol has nitric oxide mediated, venodilator effects in man.

Adrenergic beta-Antagonists↗

Omeprazole in the treatment of asthmatics with nocturnal symptoms and gastro-oesophageal reflux: a placebo-controlled cross-over study.

Eleven adult patients with nocturnal asthma, and gastro-oesophageal reflux documented by endoscopy or ambulatory oesophageal pH monitoring completed a double-blind cross-over study (4 week treatment, one week run-in and cross-over periods) comparing the effects of omeprazole 20 mg daily and placebo on asthma control assessed by symptoms, peak expiratory flow rate and bronchodilator usage. Omeprazole treatment did not improve asthma symptoms during the day or night, or peak expiratory flow rate readings. There was no difference in bronchodilator inhaler usage during omeprazole therapy. Treatment of gastro-oesophageal reflux with omeprazole in patients with nocturnal asthma and gastro-oesophageal reflux does not improve asthma symptoms or peak expiratory flow rate. This suggests that gastro-oesophageal reflux does not exacerbate bronchoconstriction in nocturnal asthma.

Aged↗

Effect of aging on changes in plasma potassium during exercise.

BACKGROUND: Exercising skeletal muscle releases large amounts of potassium into plasma. beta-adrenergic receptors enhance reuptake of potassium into muscle. Since beta-adrenergic responses decline with aging in many tissues, the elderly might be predisposed to hyperkalemia during exercise. METHODS: Venous plasma potassium (K+) was measured during graded bicycle exercise (30 W initial workload with 3-minute 30 W increments) in 18 healthy young men (24.0 +/- 2.9 yrs; mean +/- SD), 18 healthy untrained elderly men (70.0 +/- 3.6 yrs), and 7 elderly master athletes (70.0 +/- 4.6 yrs). Subjects exercised to exhaustion. RESULTS: Exercise times and maximal oxygen uptake were: young (N = 14; 19.6 +/- 4.4 min, 42.1 +/- 3.8 ml/kg/min), elderly (N = 13; 11.7 +/- 1.9 min, 26.6 +/- 8.0 ml/kg/min), elderly master athletes (N = 6; 16.8 +/- 2.4 min, 40.2 +/- 10.2 ml/kg/min). The rate of increase in K+ was greater in both elderly (89 +/- 59 mumol/l/min) and elderly master athletes (88 +/- 26) compared with healthy young men (60 +/- 30), p < .05. Despite this greater rate of increase, the elderly group did not achieve higher maximal K+ concentrations than the young because of the much shorter duration of exercise in the elderly group. For subjects performing a maximal exercise test, the maximal increase in K+ was similar in the elderly (1.15 +/- 0.91), but significantly greater in elderly master athletes (1.70 +/- 0.31), compared with healthy young men (1.31 +/- 0.45). CONCLUSIONS: Changes in K+ during short-lasting exercise are similar in untrained healthy elderly men compared with healthy young men, but elderly master athletes have greater changes in K+ during exercise. The greater rate of increase in potassium in healthy and athletic subjects supports the hypothesis of an age-related impairment of the beta 2-adrenergic process that mediates potassium flux into skeletal muscle.

Adult↗

Mechanism of bradykinin-induced venodilation in humans.

Bradykinin, a nonapeptide, dilates vascular smooth muscle at least in part via endothelial cell-dependent mechanisms. The aim of this study was to examine the action of bradykinin in human veins in vivo. Utilizing the dorsal hand vein technique, dose-response curves to bradykinin (maximum dose = 513 ng/min) were constructed in veins preconstricted with the alpha-adrenergic agonist phenylephrine in healthy young volunteers. Bradykinin almost fully dilated the veins back to their baseline diameter. To determine if desensitization of bradykinin-mediated vasodilation occurs, two bradykinin dose-response curves were constructed with a short (10 min) interval between studies. The second dose-response curve showed a diminished response. The EMAX of the first curve was 97.8 +/- 47.4% dilation and the EMAX of the second curve was 64.3 +/- 28.0% dilation (p < 0.05). However, when the two curves were separated by 40 min, there was no loss of responsiveness. To investigate the mechanism by which bradykinin caused vasodilation, we used methylene blue to antagonize endothelium-derived relaxing factor, and indomethacin to block prostaglandin-dependent effects. Methylene blue partially antagonized the vasodilatory response to bradykinin, decreasing the EMAX by 50%. Indomethacin also partially antagonized the vasodilatory response, but to a lesser extent than did methylene blue. The vasodilatory response to bradykinin was not fully antagonized with concurrent infusion of both methylene blue and indomethacin. The mechanism of bradykinin-induced vasodilation involves both EDRF and prostacyclin, and possibly another, as yet unidentified, mediator as well.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Responsiveness of superficial hand veins to alpha-adrenoceptor agonists in insulin-dependent diabetic patients.

1. Diabetic autonomic neuropathy causes loss of sympathetic cardiovascular control and is associated with increased vascular sensitivity to catecholamines. Supersensitivity to catecholamines could be due to either a postsynaptic increase in vascular sensitivity or to decreased catecholamine uptake into peripheral sympathetic nerve endings. 2. To differentiate between these possible mechanisms we have measured the responsiveness in vivo to noradrenaline and phenylephrine with local infusions into peripheral veins of diabetic patients with and without symptomatic autonomic neuropathy and of healthy control subjects. The dorsal hand vein compliance technique was used. 3. Symptomatic diabetic patients required significantly lower doses of noradrenaline for half-maximal venoconstriction (ED50) (geometric mean 2.14 ng/min) than control subjects (geometric mean 6.61 ng/min, P = 0.032), but there was no difference in the results from the phenylephrine dose-response curves between the groups. There were no differences in venous responsiveness to noradrenaline or phenylephrine between the asymptomatic diabetic group and the control group. However, in the asymptomatic diabetic group, postural blood pressure change (an index of loss of sympathetic control) was correlated with the ED50 for noradrenaline (r = 0.74, P = 0.014), but not with the ED50 for phenylephrine. In the control group the ED50 values for noradrenaline and phenylephrine were correlated with each other (r = 0.81, P = 0.0005). 4. Both vasopressor drugs act on vascular alpha-adrenoceptors, but only noradrenaline is taken up into peripheral sympathetic nerve endings. Our results suggest that, in diabetic patients, vascular supersensitivity to catecholamines is primarily determined by decreased neuronal catecholamine uptake. A postsynaptic increase in vascular alpha-adrenoceptor stimulation does not appear to be prominent in diabetic autonomic neuropathy.

Adrenergic alpha-Agonists↗

Beta adrenergically mediated cardiac chronotropic and vascular smooth muscle responses during propranolol therapy and withdrawal in young and elderly persons.

Aging is associated with diminished beta-adrenergic responsiveness in a variety of tissues. Desensitization of tissues secondary to the age-associated increase in sympathetic nervous system activity has been proposed as a potential explanation for diminished beta-adrenergic responsiveness. If this hypothesis is correct, then beta-blockade in older people might be expected to reverse the blunted beta-adrenergic responses of tissues having diminished responsiveness. Cardiac chronotropic responses to bolus isoproterenol (ISO) doses and ISO-induced venous smooth muscle dilatation in superficial hand veins were examined in 8 young (26.2 +/- 2.6 yrs) and 9 elderly (68.0 +/- 2.2 yrs) healthy subjects before, during, and 3 and 7 days following 2 weeks of treatment with propranolol. Baseline cardiac chronotropic responsiveness, CD25, was 1.55 +/- 0.77 mcg in the young and 5.97 +/- 2.77 mcg in the elderly subjects (p less than .01), increasing to 84 +/- 56 mcg and 194 +/- 172 mcg during treatment with propranolol. At 3 and 7 days following withdrawal of propranolol, CD25s were respectively 1.24 +/- 0.79 (p = .14) and 1.10 +/- 0.42 (p = .04) in the young and 5.63 +/- 2.34 (p = .31) and 4.85 +/- 2.37 (p = .05) in the elderly subjects. In contrast, there was no decrease in the ED50 or increase in Emax for ISO-induced venodilation of hand veins following propranolol withdrawal. These results demonstrate that both young and elderly subjects have similar increases in cardiac chronotropic responsiveness following discontinuation of beta-blockade and do not support the concept that desensitization is responsible for the diminished beta-adrenergic responsiveness seen with aging.

Adult↗

Bradykinin-induced venodilation is not impaired with aging in humans.

The aim of this study was to determine whether there is an age-related decline in vascular responsiveness to bradykinin, whose vasodilatory action is mediated chiefly through endothelium-derived relaxing factor (EDRF). Dose-response curves for bradykinin were constructed using the dorsal hand vein compliance technique in veins preconstricted with phenylephrine in 27 volunteers (16 male, 11 female) aged 18 to 81 years. At the end of the bradykinin study, 12 subjects had a single infusion of a high dose of isoproterenol. There was no correlation between age and the EMAX or the log ED50 for bradykinin, although the same subjects showed a correlation between age and EMAX for isoproterenol, as previously found. There was no significant difference in either the EMAX or the log ED50 between male and female subjects. The results suggest that bradykinin-induced vasodilation is independent of age or gender.

Adolescent↗

An Eudragit-coated prednisolone preparation for ulcerative colitis: pharmacokinetics and preliminary therapeutic use.

Prednisolone metasulphabenzoate, a steroid with poor colonic absorption, was coated with the pH-dependent acrylic resin Eudragit S, as a means of delivering an orally administered preparation to the proximal colon. The therapeutic potential of delivering this steroid with potentially less systemic side-effects to the proximal colon was assessed in extensive ulcerative colitis. Plasma and urine prednisolone profiles in 6 healthy volunteers confirmed minimal absorption from Eudragit S-coated prednisolone metasulphabenzoate compared to prednisolone acetate: peak plasma prednisolone concentrations 29 +/- 21 ng/ml vs. 570 +/- 185 ng/ml (P less than 0.01), area under curve measurements 204 +/- 214 vs. 2724 +/- 1236 ng.h/ml (P less than 0.01). Prednisolone metasulphabenzoate coated with Eudragit S (30-60 mg daily) was then administered for 12 weeks to 12 patients with colonoscopically proven extensive ulcerative colitis in relapse. Symptoms, sigmoidoscopic appearances and rectal histological abnormalities all improved during therapy. Complete clinical remission occurred in 7 patients, a partial response in 2 patients and no response in 3 patients. Cortisol responses to tetracosactrin demonstrated no significant adrenal suppression following treatment. Eudragit S-coated prednisolone metasulphabenzoate may be a useful treatment for extensive ulcerative colitis, without risk of systemic steroid side-effects.

Acrylic Resins↗

Age-related changes in adenosine and beta-adrenoceptor responsiveness of vascular smooth muscle in man.

1. Ageing is associated with a decline in beta-adrenergic responsiveness in several tissues. Reduced beta-adrenoceptor mediated smooth muscle relaxation in aged man has been demonstrated using the dorsal hand vein technique. Isoprenaline and adenosine activate adenylate cyclase through separate membrane bound receptors to induce vasodilatation. 2. To determine the specificity of reduced beta-adrenergic responsiveness in smooth muscle of aged man, and possible sites of the defect responsible, venodilatory responses to isoprenaline, a beta-adrenoceptor agonist and adenosine were determined in nine young (age 26 +/- 3 years: mean +/- s.d.) and eight elderly (age 70 +/- 5 years), healthy male volunteers. Veins were partially constricted with the alpha 1-adrenoceptor agonist phenylephrine and increasing doses of adenosine (5 to 1220 micrograms min-1) or isoprenaline (271 ng min-1) were infused. 3. Maximal dilatation induced by isoprenaline was 83 +/- 26% in the young and 51 +/- 34% in the elderly, P = 0.02. Maximal dilatation induced at the highest dose of adenosine (1220 micrograms min-1) was similar in young and elderly: 79 +/- 25% vs 88 +/- 28%, P = 0.26. 4. Adenosine venodilatation was measured before and after infusions of theophylline (6.8 to 135 micrograms min-1) for 30 min in six subjects. Adenosine responsiveness was unchanged following theophylline: 48 +/- 16% to 49 +/- 40%, P = 0.44. 5. The results suggest that the age-associated reduced responsiveness of the beta-adrenergic system in human vascular smooth muscle is not shared by venodilatation mediated by adenosine.

Adenosine↗

Use of the SeHCAT test in the investigation of diarrhoea.

The SeHCAT test was used to investigate possible bile acid malabsorption in 166 patients presenting to a district general hospital with chronic diarrhoea of uncertain cause. Eighty-four (51%) patients had impaired SeHCAT retention. These included 23 of 28 patients with a possible type I abnormality (terminal ileal resection or disease, previous pelvic radiotherapy), 20 of 74 with a possible type II abnormality (idiopathic diarrhoea), 32 of 45 with a possible type III abnormality (post-cholecystectomy, post-vagotomy), and 9 of 19 with diarrhoea associated with diabetes. Patients with severe bile acid malabsorption demonstrated a good response to cholestyramine whereas the response in patients with a mildly abnormal SeHCAT retention was variable. Bile acid malabsorption is an important cause of diarrhoea in patients presenting with unexplained chronic diarrhoea.

Adolescent↗