Search PubMed⌕ Search

Biomedical subjects

C G Wathen

Publications and source records attributed to C G Wathen.

At least 55 records · Page 3Linked to original sources
PubMed1986

Direct demonstration of an inhibitor of sodium, potassium dependent adenosine triphosphatase (Na+, K+-ATPase) in plasma from normotensive and hypertensive subjects.

An endogenous inhibitor of Na+, K+-ATPase was extracted from human plasma and sera and concentrated by a novel reverse-phase octadecylsilane chromatography method. The active extracts (eluates) were dried and reconstituted in the minimum volume of the non-adsorbed fraction of the plasma from which they had been derived. Reconstituted eluates, non-adsorbed plasma fractions and native plasma samples were then tested for their ability to inhibit phosphate production in standard Na+, K+-ATPase incubation mixtures. In a pilot study 31 samples of pooled normal human sera were assayed. The eluates gave a significantly lower production of phosphate than the non-adsorbed fractions or the native sera (n = 31, p less than 0.0025). Further concentration of the eluates by repeated chromatography increased the inhibitory power of the eluate proportional to the concentration achieved, as quantified by ouabain dose-equivalents. In clinical studies, samples from 12 normotensive subjects and from 12 untreated patients with essential hypertension were tested. Significant inhibition of the ATPase by the eluates, as compared to the corresponding non-adsorbed fractions was seen for samples from both normotensive (p less than 0.05) and hypertensive (p less than 0.05) subjects. There was no significant difference in incidence or degree of inhibition between the normotensive and hypertensive groups. This study provides direct evidence for the presence of an endogenous inhibitor of Na+, K+-ATPase in human plasma.

Humans↗
PubMed1986

Felodipine as a replacement for minoxidil in the treatment of severe hypertension.

The new calcium antagonist felodipine has been compared with minoxidil in the management of severe hypertension in a group of 17 men. Satisfactory control of blood pressure was achieved in all patients with a combination of beta blocker, loop diuretic and minoxidil after inadequate control on a standard regimen of beta blocker, thiazide and vasodilator. The optimal dose of felodipine was titrated after a placebo phase. In a double blind crossover trial blood pressure on felodipine (150/88 +/- 19/8 mmHg, SD) was the same as on minoxidil (148/87 +/- 23/11 mmHg, NS) and the postural difference was similar (NS) on both drug regimens. Body weight was lower on the felodipine regimen (P less than 0.01), as was supine heart rate (P less than 0.05). There was a small rise in plasma liver enzymes on felodipine therapy (P less than 0.01). Felodipine was well tolerated and may be useful in the management of severe hypertension.

Aged↗
PubMed1986

Pneumonia.

Explore the source record for details and available documents.

Anti-Bacterial Agents↗
PubMed1986

Use of nifedipine as the drug of third choice in management of hypertension.

Nifedipine has been used in the management of hypertension in 36 consecutive patients who could not tolerate, or were not controlled by, atenolol and thiazide diuretics. Mean supine blood pressure was reduced from 193/110 +/- 5/2 (SEM) mmHg to 162/91 +/- 5/2 mmHg at eight weeks and remained at that level for the six months of follow-up. Blood pressure reduction at four weeks was not always a predictor of final BP level. Eight patients could not tolerate atenolol, nine patients could not tolerate thiazide diuretics and four patients could not tolerate nifedipine. No significant changes in plasma urea, creatinine, sodium, potassium urate, 'total CO2' or glucose were observed. We conclude that nifedipine is a well-tolerated drug and may be useful after beta-blockers and thiazide have been tried in the management of hypertension.

Adult↗
PubMed1986

The effect of captopril on blood pressure and glucose tolerance in hypertensive non-insulin dependent diabetics.

Thirteen hypetensive non-insulin dependent diabetics (9 male, 4 female, mean age 61.6 +/- 6 years) were given 6 weeks treatment with captopril in a dose range 75-150 mg/day. Each patient underwent a standard glucose tolerance test and had blood pressure profiles recorded before and after captopril. Supine systolic blood pressure (mmHg) improved from 181 (+/- 16) to 162 (+/- 17) and diastolic blood pressure from 103 (+/- 11) to 89 (+/- 9). A similar improvement was seen in erect systolic (174 +/- 19 to 156 +/- 19) and diastolic (103 +/- 14 to 87 +/- 11) blood pressures. Following treatment there was no significant change in glucose tolerance although the 120 minute plasma glucose value improved from 15.3 +/- 4.2 to 13.9 +/- 3.4 mmol/l (P less than 0.05). The drug was well tolerated and free of adverse effects. Captopril would therefore appear to be an effective and safe anti-hypertensive agent in non-insulin dependent diabetes and did not result in any deterioration of glucose tolerance.

Aged↗
PubMed1985

Afterload reduction by nifedipine--the acute haemodynamic response to exercise in hypertensive subjects.

In 16 people with essential hypertension, heart rate (HR), blood pressure (BP) and relative cardiac volumes were measured at rest and during submaximal upright exercise before and after 10 mg of sublingual nifedipine using radionuclide ventriculography. In 10 patients who had had no previous therapy (BP 152/103 +/- 5/3 mmHg) nifedipine produced a fall in BP of 6/12 +/- 3/3 mmHg (SEM) and a rise in HR of 15 +/- 5 bpm (P less than 0.001). This was associated with a rise in LVEF of 0.07 +/- 0.02 (P less than 0.005) and in cardiac output of 44 +/- 9%, presumably as a result of ventricular offloading. The cardiac response to exercise given the different starting values, was unchanged by nifedipine. Thus the HR was 101 +/- 6 bpm at rest after nifedipine and on exercise rose to 124 +/- 6 bpm (P less than 0.001): stroke volume was +22 +/- 8% at rest after nifedipine and rose to +43 +/- 12% on exercise. Thus cardiac output which had increased by 44 +/- 9% after nifedipine increased by 100 +/- 10% from the initial value. In 6 patients pre-treated with atenolol (100 mg) and with similar resting BP (158/101 +/- 5/4 mmHg) there was a fall in BP of 32/15 +/- 3/2 mmHg after nifedipine which was greater than in the previously untreated group (P less than 0.01). In this group HR increased by 8 +/- 3 bpm (P less than 0.05). Following nifedipine the exercise response was similar given the different starting values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

End-organ responses to thyroxine therapy in subclinical hypothyroidism.

We studied variables known to change with thyroid hormone status in 18 patients with subclinical hypothyroidism before and during treatment with thyroxine in a dose sufficient to restore the plasma TSH response to TRH to normal. There was an associated increase in both plasma total T4 and free T4 within the normal range but plasma total T3 and free T3 were unchanged. As a result of thyroxine treatment there was a small but significant increase (P less than 0.05) in left ventricular ejection fraction (LVEF) with maximal exercise but no significant changes in LVEF at rest and moderate exercise, continuously monitored mean sleeping heart rate, day/night ratios of urinary sodium excretion, peripheral nerve conduction velocities, fasting serum triglycerides, total cholesterol (TC), high density lipoproteins (HDL) or TC/HDL ratios. On this evidence we do not consider that thyroxine replacement therapy is indicated in patients with subclinical hypothyroidism.

Adult↗
PubMed1985

Are the clinical benefits of oral prenalterol in ischaemic heart failure due to beta blockade? A six month randomised double blind comparison with placebo.

The clinical effects of the oral beta 1 partial agonist, prenalterol, were investigated in 37 patients (29 male, eight female; mean age 57 years) with chronic ischaemic left ventricular failure using a placebo controlled randomised double blind protocol over six months. All patients were limited by dyspnoea (New York Heart Association class III) despite treatment with digoxin and diuretics. Twenty eight patients completed the protocol. Moderate clinical improvement was seen in the prenalterol group, whereas there was little change in the placebo group. Bicycle exercise capacity increased over six months in the prenalterol and placebo groups but only achieved statistical significance for prenalterol when compared with baseline values. Maximum exercise heart rate was significantly reduced in the prenalterol group compared with placebo. Radionuclide left ventricular ejection fraction at rest and during exercise and cardiothoracic ratio showed no significant improvement in either group over six months. Prenalterol was well tolerated and produced no increase in frequency of angina or ventricular arrhythmias. Prenalterol produced clinical benefits and improved exercise tolerance while reducing exercise heart rate. A moderate placebo response was noted. The apparent beta blocking effect of prenalterol may be as important as the beta 1 agonist effect in producing these benefits. Prenalterol has, however, been withdrawn because of side effects in animals.

Adrenergic beta-Agonists↗
PubMed1985

Right ventricular performance during exercise in chronic obstructive pulmonary disease. The effects of oxygen.

Radionuclide ventriculography allows non-invasive assessment of right ventricular performance. This study has confirmed that there is a modest reduction in right ventricular ejection fraction (RVEF) in patients with chronic obstructive pulmonary disease (COPD), as compared to normal subjects. However, occult right ventricular dysfunction also becomes apparent in these patients during exercise. The change in RVEF during exercise is related to the corresponding fall in arterial oxygen saturation in patients with COPD. Oxygen improves the response of the right ventricle to exercise, although the mechanism remains unclear. Long-term oxygen therapy, in patients with respiratory failure, does not appear to have any significant effect on RVEF.

Adult↗
PubMed1985

Effects of felodipine on resistance and capacitance vessels in patients with essential hypertension.

The acute cardiovascular effects of oral felodipine (0.05 mg/kg and 0.1 mg/kg) were studied using radionuclide methods in 14 hypertensive patients. Eight were previously untreated and 6 had been treated with atenolol 100mg daily for a least 1 month. The maximal effects were observed 60 minutes after the first oral dose and no greater effect was observed with the higher dose. Felodipine caused a reduction in systemic vascular resistance, with a fall in blood pressure and an increase in cardiac output and left ventricular ejection fraction. Those responses were presumably mediated by the reduction in afterload, as they were not modified by pretreatment with atenolol. There were no changes in venous capacitance and the overall pattern of response was similar to that noted with hydralazine. Thus, in hypertensive subjects felodipine acts as a potent arteriolar vasodilator. The results suggest the drug may be an effective means of controlling hypertension, particularly when given in combination with other antihypertensive therapy.

Adult↗
PubMed1985

Felodipine can replace minoxidil in the treatment of refractory hypertension.

In a group of 15 men with severe hypertension in a double-blind crossover trial, the new calcium antagonist felodipine has been shown to lower blood pressure as effectively as minoxidil when used in combination with a beta-blocker and a loop diuretic. Felodipine was well tolerated and may have a role in the management of severe hypertension.

Aged↗
PubMed1985

Left ventricular performance in subclinical hypothyroidism.

Normal plasma thyroid hormones with elevation of thyrotrophin levels in asymptomatic patients is known as subclinical hypothyroidism. Radionuclide angiography was used to study left ventricular function in 10 such patients before and after establishment of normal thyrotrophin levels with thyroxine. Resting left ventricular ejection fraction was similar in both states but exercise left ventricular ejection fraction was less in the subclinical hypothyroid (61 +/- 3 per cent) compared with the euthyroid (68 +/- 3 per cent; p less than 0.025) state. Sodium nitroprusside caused similar increases in resting cardiac output but in subclinical hypothyroidism this resulted from a large increase in heart rate (26 +/- 4 beats/min) and reduction in stroke volume (11 +/- 4 per cent) whereas in the euthyroid state, the heart rate increment was less (14 +/- beats/min) and stroke volume was unchanged. Analysis of left ventricular pressure-volume relationships at end-systole during exercise showed a steeper pressure-volume slope in the euthyroid compared with the subclinical hypothyroid state (p less than 0.05). Subtle impairment of left ventricular function is detectable in subclinical hypothyroidism and may justify use of hormone replacement.

Adult↗
PubMed1984

The effect of in vitro captopril and angiotensin II on plasma renin activity.

Samples of plasma from ten normotensive volunteers and ten hypertensive patients were assayed for plasma renin activity before and after the addition of either captopril or captopril and angiotensin II. The study was repeated after treating portions of the same specimens with trypsin, to activate the inactive renin component. The results indicate that inactive renin is not converted to the active form by captopril in vitro, nor does the addition of angiotensin II inactivate the active form. These data are consistent with the in vivo findings that changes in active and inactive renin occur independently under conditions of challenge by captopril or angiotensin II analogues.

Angiotensin II↗