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Biomedical subjects

A Gillies

Publications and source records attributed to A Gillies.

At least 37 records · Page 2Linked to original sources
PubMed1989

Hypertension and asthma: psychological aspects.

Essential hypertensive and asthmatic patients, plus normal non-clinical controls, were compared on a number of psychological measures in order to identify the relationship between psychological distress, coping strategies and compliance behaviour. The hypothesised relationship between chronic clinical ailments and psychological distress was confirmed. The association between the presence of physical symptoms in the symptomatic condition, asthma, and greater psychological distress was also confirmed. The coping strategies adopted by the patients did not discriminate between the two clinical groups. Compliance with medication was negatively correlated with measures of psychological distress. Compliance with an appropriate healthy lifestyle was not correlated with medication compliance, although it too was negatively correlated with other measures of psychological distress.

Adaptation, Psychological↗
PubMed1983

Absorption of retinal and subretinal hemorrhages.

Patients with intra- and subretinal hemorrhages who recovered useful vision from an initially poor visual acuity are described. Three patients with intraretinal hemorrhages all cleared without adverse visual sequelae within four to eight weeks; three patients with subretinal or subpigmental hemorrhages cleared with minimal loss of visual acuity, within three to six months. It seems that the amount of damage done to the retina by an intraretinal or subretinal hemorrhage is related to its size and the ability of ocular tissue to clear the blood. Small amount of hemorrhage in or under the retina is capable of clearing with minimal damage. Subretinal hemorrhage seem to be associated more often with damage to the retina for few possible reasons: (a) direct iron toxicity on the photoreceptors; (b) iron toxicity or mechanical damage to the RPE; (c) cellular migration and proliferation in the subretinal space; (d) proliferation of fibrovascular membrane which may further damage the external retina.

Adult↗
PubMed1982

Changes in "active" and "inactive" renin in the juxtaglomerular apparatuses of rat nephrons and plasma induced by different salt intake.

The juxtaglomerular apparatuses (JGA) of deep and superficial nephrons were isolated by microbiopsy or by microdissection. Inactive renin content was determined by acidification of JGA or plasma to pH 3.0. In rats with low salt intake the renin content of superficial JGA was 13.4 +/- 3.0 ng AI/JGA/h before and 20.4 +/- 3.4 ng AI/JGA/h (n = 9), P less than 0.05) after acidification. The corresponding values for deep JGA were 9.1 +/- 1.2 ng AI/JGA/h and 12.7 +/- 2.7 ng AI/JGA/h (n = 9, P less than 0.01). The plasma renin concentration was 54.1 +/- 15.0 ng AI/ml/h before and 56.0 +/- 10.6 ng AI/JGA/h (n = 7, N.S.) after acidification. In rats with a normal salt intake the superficial renin JGA renin content was 11.6 +/- 2.3 ng AI/JGA/h before and 11.0 +/- 2.7 ng AI/JGA/h (n = 9, N.S.) after acidification. The renin content of deep JGA was 4.6 +/- 0.6 ng AI/JGA/h before and 8.6 +/- 3.1 ng AI/JGA/h (n = 9, P less than 0.005) after acidification. Plasma renin concentration was 34.5 +/- 4.7 ng AI/ml/h and did not change after acidification. In rats with a high salt intake superficial JGA content was 6.8 +/- 1.7 ng AI/JGA/h before and 8.4 +/- 2.1 ng AI/JGA/h (n = 9, N.S.) after acidification. The corresponding values for deep JGA were 5.7 +/- 1.6 ng AI/JGA/h and 6.9 +/- 1.6 ng AI/JGA/h (n = 9, N.S.) respectively. Plasma renin concentration was 13.1 +/- 1.1 ng AI/ml/h and this to 21.8 +/- 2.9 ng AI/ml/h (n = 8, P less than 0.01) after acidification. These results suggest that although the synthesis of active and inactive renin is linked, the secretion of the two forms may be independent.

Animals↗
PubMed1982

Formation and activation of renin in vivo.

Active and acid activated renin was measured in glomeruli of rats obtained by microbiopsy and in rat plasma. Sodium depletion increased total and active renin in the juxtaglomerular apparatus and approximately one third of the renin was in an inactive form in sodium depletion. Sodium loading decreased active and total renin and there was no inactive renin present. In plasma changes in a similar direction occurred for active and total renin but in sodium depletion there was no inactive renin present while with sodium loading approximately 40% was in the inactive form. Haemorrhage caused a release of active renin in both sodium states and did not alter the renin content of the J.G.A. Increased delivery of sodium chloride to the macula densa increased the active renin content of J.G.A. but did not alter the total renin content. These results are compatible with two different roles of the renin angiotensin system. One being concerned with intrarenal regulation of glomerular filtration and renal blood flow and the other with maintenance of vascular tone. The conversion of inactive renin to active renin being of particular importance in the regulation of G.F.R.

Animals↗
PubMed1980

Comparison of piretanide and chlorothiazide in the treatment of cardiac failure.

Piretanide, a diuretic that acts on the loop of Henle, was used to treat patients with cardiac failure. Over a three-day period it caused a significant dose related diuresis and weight loss. It was as effective as chlorothiazide in the control of cardiac failure and was well tolerated by the patients. Potassium loss was less than occurred with chlorothiazide. Its role in the treatment of cardiac failure requires further study and warrants further investigation. The study also showed that many patients with cardiac failure receive diuretic drugs which are not necessary.

Adult↗
PubMed1980

Active and inactive renin in individual juxtaglomerular apparatuses.

1. Renin was measured in individual juxtaglomerular apparatuses before and after acidification in vitro. 2. Active renin increased with delivery of extra sodium by microperfusion to the macula densa and this increase was similar to that achieved with acidification. 3. In rats pretreated with an inhibitor of protein synthesis active renin increased when extra sodium was delivered to the macula densa. 4. Salt intake changed the amount of renin present in the juxtaglomerular apparatus. In rats on a high salt intake the total renin was low and was all in an active form.

Animals↗
PubMed1978

The effect of labetalol in the treatment of severe drug-resistant hypertension.

Twenty-two hypertensive patients from a large clinic, who were resistant to conventional therapy, were entered into this study. Most patients previously had received beta-blocking drugs, thiazide diuretics, alpha-methyl-dopa, or vasodilator drugs (hydrallazine or prazosin) which failed to control their blood pressure. The therapy with vasodilator drugs was discontinued, and the therapy with labetalol (a drug with both alpha-blocking and beta-blocking effect) was commenced. Subsequently, as the blood pressure came under control, other drugs that the patients were taking were also withdrawn. In 13 of the 22 patients, labetalol enabled the blood pressure to be controlled at acceptable levels. In six patients, the response was not considered to be sufficient to justify continuation of labetalol therapy. In three patients, the drug was withdrawn because of postural hypotension in one patient, intractable diarrhoea in another, and an allergic-type skin rash in the third. In certain patients, postural changes in blood pressure were observed, but this rarely produced symptoms. It is suggested that, if blood pressure control is not achieved with a thiazide diuretic and a beta-blocking drug, then labetalol should be introduced and the beta-blocking drug should be withdrawn.

Aged↗
PubMed1978

Hypertension treated by salt restriction.

31 patients with a diastolic blood-pressure between 95 and 109 mm Hg have been treated for two years with a regimen involving a moderate restriction of salt in the diet. The results are compared with those in a control group and in a drug-treated group. Salt restriction has reduced the diastolic blood-pressure by 7.3+/-1.6 mm Hg, a result similar to that in patients treated with antihypertensive drugs. In the untreated group the diastolic blood-pressure rose by 1.8+/-1.1 mm Hg. Most patients did not achieve the desired amount of salt restriction and a stricter adherence to the diet might have caused further falls in blood-pressure. Excessive salt intake is probably a major cause of the epidemic of hypertension in "civilised" countries and a reduction in salt intake may help to control the epidemic. In persons with a diastolic blood-pressure between 90 and 105 mm Hg salt restriction should be tried before drugs.

Blood Pressure↗