Search PubMed⌕ Search

Biomedical subjects

M R Lee

Publications and source records attributed to M R Lee.

At least 163 records · Page 9Linked to original sources

Hypertension and hyperkalaemia responding to bendrofluazide.

A 33-year-old man is described with hyperkalaemia, hypertension and acidosis. The blood pressure was 160 to 200 mmHg systolic and 90 to 110 mmHg diastolic and the plasma potassium was between 6.0 and 7.0 mmole per litre. There was no renal disease and creatinine clearance was 103 ml per minute. Plasma renin activity was low and plasma aldosterone was at the lower limit of normal. Sodium deprivation or oral frusemide had little effect on blood pressure, plasma potassium, renin, aldosterone or arginine vasopressin. However, bendrofluazide caused a rapid fall of blood pressure and plasma potassium, and rise of plasma renin, aldosterone and plasma arginine vasopressin. Hypertension and hyperkalaemia is rare in the absence of renal failure. Four similar patients reported previously are reviewed. We suggest that our patient, and perhaps some of those reported earlier had primary abnormality of renal tubular function with impaired secretion of potassium and excessive tubular reabsorption of sodium. The plasma renin activity could be due to volume expansion and the low plasma aldosterone was probably caused by the antagonistic effects of low renin depressing synthesis and hyperkalaemia increasing it. A minor similar tubular abnormality might be the explanation in some of the patients with essential hypertension who have low plasma renin activity.

Adult↗

Severe hyponatraemia. A study of 17 patients.

17 patients with severe hyponatraemia (none had cardiac failure or had lately had an operation) all had excessively high plasma-antidiuretic hormone (A.D.H.). Only 13 had features typical of the syndrome of inappropriate secretion of A.D.H. (S.I.A.D.H.). Plasma-A.D.H. was not related to either plasma-sodium or diagnosis. There were as many patients with chest infection as with carcinoma of the lung. Plasma-sodium and plasma-A.D.H. returned rapidly towards normal in the patients with chest infection or volume depletion but these concentrations corrected much more slowly in patients with carcinoma of the lung. The increase in plasma-sodium in patients with chest infection was too rapid to be produced by water-deprivation treatment and was due to return of plasma-A.D.H. to normal. The term S.I.A.D.H. implies an understanding of pathophysiology that does not exist. As a diagnosis it does not help in management or prognosis. A simpler, more descriptive terminology such as "hyponatraemia with carcinoma of the lung" would be more useful and less confusing in the clinical situation.

Aged↗

Effect of carbamazepine on plasma and urine arginine-vasopressin.

1. Five normal subjects were studied before and during treatment with carbamazepine. 2. Plasma sodium, plasma and urine arginine-vasopressin and urine osmolality were measured during a day of water deprivation, before and during drug treatment. 3. During treatment with carbamazepine plasma sodium increased wheras plasma and urine arginine-vasopressin and urine osmolality decreased. Plasma and urine arginine-vasopressin were signifi"antly correlated with urine osmolality. However, carbamazepine did not affect the osmolality of urine produced by the kidney, in response to endogenous arginine-vasopressin. 4. Plasma and urine arginine-vasopressin were significantly correlated with plasma sodium on both control and drug-treatment days, but the relationships of plasma and urine arginine-vasopressin to plasma sodium were different during carbamazepine treatment, as compared with the control period. 5. It is suggested that the threshold of the hypothalamic osmoreceptors for release of arginine-vasopressin is modified by carbamazepine, and that this may be either a direct action or secondary to another action of the drug.

Adult↗

Urinary dopamine in man and rat: effects of inorganic salts on dopamine excretion.

1. Plasma and urine free dopamine (3,4-dihydroxyphenethylamine) were measured in six normal male volunteer subjects and the urinary clearance of dopamine was calculated for each subject. 2. The excretion rates for free dopamine in man were greater than could be explained by simple renal clearance. It was concluded that free dopamine must, therefore, be formed in the kidney. 3. Changes in urinary dopamine excretion were studied in four groups of rats initially maintained on low sodium diet and then given equimolar dietary supplements of NaCl, NaHCO3, KCl or NH4Cl, to study the specificity of the previously observed increase in dopamine excretion after increased dietary NaCl. 4. The mean dopamine excretion increased significantly in rats given NaCl, KCl and NH4Cl, whereas dopamine excretion decreased in those given NaHCO3. 5. The failure of dopamine excretion to rise in response to loading with NaHCO3 was unexpected, and argues against a simple effect of volume expansion by the sodium ion. The increase in dopamine excretion with KCl and NH4Cl showed that this response was not specific to the sodium ion.

Adult↗

Treatment of Bartter's syndrome in early childhood with prostaglandin synthetase inhibitors.

The diagnosis of Bartter's syndrome was made in a 9-month-old boy investigated for poor weight and height gain. Initial treatment with oral potassium supplements and later spironolactone had little or no effect on his growth, although plasma potassium rose to normal after spironolactone. At 33 months indomethacin therapy was started with dramatic results. His symptoms went and his height and weight accelerated into the normal range. In view of the toxicity of indomethacin it was replaced after 12 months by another prostaglandin synthetase inhibitor, ketoprofen, with a satisfactory result. During the change-over period from indomethacin to ketoprofen the expected deterioration in clinical well-being was observed, accompanied by a rise in urinary prostaglandins and plasma renin activity. Prostaglandin synthetase inhibitors provide the best available treatment for Bartter's syndrome.

Bartter Syndrome↗

Sodium losing renal disease: Two cases and a review of the literature.

Two patients with sodium-losing renal disease were studied in detail. Both presented with shock and hypotension which was attributed at first to other causes, as was the recurrent hyponatraemia in one of them. In both patients the cause of the sodium loss was probably unrelieved urinary obstruction which has been reported previously to cause water loss but not sodium loss. Both patients had severe hyponatraemia when they were sodium depleted, which has previously been attributed to water retention from excessive secretion of antidiuretic hormone. Plasma arginine vasopressin concentrations were raised in one patient but not in the other. The cause of the water retention in the other patient is not known. One of the patients, like others described in the literature, was only able to vary his sodium excretion within narrow limits. He became sodium depleted on a normal intake and oedematous when he was given saline intravenously. We suggest that the term sodium-losing renal disease should be replaced by the term 'fixed sodium' excretion renal disease.

Adult↗

Failure of saralasin to predict a response to surgery in renovascular hypertension.

Arteriography in two patients with renovascular hypertension suggested fibromuscular hyperplasia, mainly affecting the right renal artery. When saralasin was infused intravenously there was no fall in blood-pressure in either patient. However, both had a raised renal-vein plasma-renin activity on the affected side, relative to the unaffected kidney. Auto-transplantation resulted in a sustained reduction in arterial pressure in both patients. A negative saralasin test should not necessarily exclude further investigation of young patients with severe hypertension.

Adult↗

Internal proteins of influenza virus: 35S-methionine peptide maps as genetic markers.

Methods are described for the preparation in vivo of 35S-methionine-labelled influenza viruses, the purifiction of the nucleoprotein (NP) and matrix (M) proteins and the separation of peptides obtained by protease digestion by two-dimensional thin-layer chromatography. The maps of the M proteins of A/Okuda/57(H2N2) and A/Finland/4/74(H3N2) were very similar overall but differed in three peptides. Hence they could be clearly distinguished. Maps of the NP proteins of the same strains showed a greater number of differences. A recombinant strain having the haemagglutinin and neuraminidase of the A/Finland/4/74 parent and the virulence of the A/Okuda/57 parent was shown to have the M and P proteins of A/okuda/57.

Chromosome Mapping↗

The effect of carbidopa administration on urinary sodium excretion in man. Is dopamine an intrarenal natriuretic hormone?

1 Carbidopa, a known inhibitor of the peripheral conversion of dopa to dopamine, was given to six normal volunteers to examine the effect of interference with dopamine synthesis on urinary sodium excretion. 2 On the first day of administration, carbidopa caused a significant fall not only in urinary dopamine excretion (P less than 0.01) but also in urinary sodium excretion (P less than 0.05). 3 A highly significant correlation was also found between mean sodium excretion and mean dopamine excretion in the days prior to and during carbidopa administration (r = 0.617, P less than 0.001; 4 = 0.764, P less than 0.001 respectively). 4 The significance of these findings is discussed and it is proposed that dopamine may be an important intrarenal natriuretic hormone.

Adult↗

Evaluation of the rapid hippurate hydrolysis test with enterococcal group D streptococci.

The rapid hippurate hydrolysis test was evaluated with the conventional test, using 17 group A streptococci, 9 non-enterococcal group D streptococci, 108 enterococcal group D streptococci, and 2 strains of Listeria monocytogenes. There was complete correlation between the rapid and conventional tests with all organisms except enterococcal group D. The rapid hippurate hydrolysis method was more sensitive with the enterococci; 95.4% were positive with the rapid method, and 9.3% were positive with the conventional method. Thin-layer chromatography (TLC) was performed on all isolates to determine if the end product of hydrolysis, glycine, was indeed present. The TLC results were in agreement with the rapid and conventional methods for group A streptococci, nonenterococcal group D streptococci, and L. monocytogenes. TLC results were in total agreement with the rapid hippurate hydrolysis test for the enterococcal group D isolates, thus verifying the accuracy of this more sensitive test. Trace amounts of glycine were found in the substrate, indicating the need for including an uninoculated substrate control as well as stock strains of group A and B beta-hemolytic streptococci (negative and positive controls, respectively) each time the rapid hippurate hydrolysis test is performed.

Amidohydrolases↗

Renin and aldosterone relationships in manic depressive psychosis.

The paper describes a two-month period of study in four bipolar manic-depressive patients in a metabolic ward. Plasma renin activity, packed cell volume, plasma sodium and potassium were determined at intervals. Twenty-four-hour urinary sodium, potassium and creatinine were also estimated daily. Aldosterone production rate was measured on two occasions for each patient. Three of the patients showed at least one episode each of mania and depression during the study, while the fourth patient, who was receiving prophylactic lithium throughout, had one ten-day depressive episode but was otherwise normal. No obvious relationship between mood and plasma renin activity was observed, but the group showed a high resting renin activity, a blunted renin response to posture, and inappropriate aldosterone production rates for the renin activity found. It is postulated that a primary defect in the aldosterone-renin system may be present in bipolar manic-depressive psychosis.

Adult↗