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Biomedical subjects

R J Solomon

Publications and source records attributed to R J Solomon.

At least 37 records · Page 2Linked to original sources
PubMed1986

Urinary kininogen: a possible regulator of kinin formation in normal individuals and subjects with essential hypertension, end-stage renal and liver disease.

Most previous studies have not significantly correlated urinary kallikrein to urinary kinins. We investigated whether urinary kininogen might influence kinin formation within the urine. On an ad-lib diet the 24 hour excretion of total and intact kininogen, kinins and kallikrein was determined in 24 control subjects, 20 untreated essential hypertensives, 12 with end-stage renal disease and 8 subjects with liver disease. Kallikrein and kinins were measured by a direct radioimmunoassay. Total kininogen was determined from the sum of preformed kinins and kinins generated after trypsin (intact kininogen). Cross reactivity between purified human low molecular weight kininogen and bradykinin antiserum was 3%. Total and intact kininogen were significantly correlated with kinins in controls, essential hypertension and liver disease. In essential hypertension, end-stage renal and liver diseases kinins were significantly decreased. This was associated with a reduction in kininogen but not kallikrein in essential hypertension and liver disease, and a reduction in kallikrein but not kininogen in end-stage renal disease. Thus, renal kinin generation in various states may be affected by either or both kininogen and kallikrein.

Humans↗
PubMed1986

Thiazide induced hypotension: the role of plasma volume reduction and the urinary kallikrein system.

The hypotensive response the thiazide diuretics was studied in 15 males with moderate essential hypertension and correlated with serial changes in plasma volume, weight, plasma renin activity, urinary aldosterone, and urinary kallikrein, both total and activity. A greater than 10 mmHg fall in mean arterial pressure after four weeks of treatment defined the responders to therapy (n = 10) while all others were considered non-responders (n = 5). In responders, the fall in mean arterial pressure was accompanied by sustained reduction in plasma volume and weight. No sustained fall in plasma volume was noted in non-responders. Plasma renin activity and urinary aldosterone excretion increased in responders but not in non-responders. Urinary kallikrein, both total and active, increased in the responders but remained unchanged in the non-responders. The results are consistent with the hypothesis that a sustained reduction in plasma volume is necessary for the maintenance of a hypotensive response to thiazides. Stimulation of the renal kallikrein-kinin system may be necessary to balance the antinatriuretic and pressor effects of the renin-angiotensin-aldosterone system. If unopposed, this system would return plasma volume and blood pressure to pretreatment levels.

Aldosterone↗
PubMed1986

Ventricular arrhythmias in patients with myocardial infarction and ischaemia. The role of serum potassium.

An association between low serum potassium concentrations and ventricular arrhythmias has been observed by a number of investigators in patients with both acute myocardial infarction and symptomatic angina. The increased frequency of ventricular fibrillation in patients with low serum potassium concentrations has not been attributable to differences in the size or location of the infarct or concomitant digitalis administration. Although prior diuretic usage is frequently associated with a low serum potassium concentration, diuretic usage in the absence of significant changes in serum electrolytes is not associated with an increase in malignant ventricular arrhythmias. It is not clear whether the alterations in serum potassium are important in the pathogenesis of the arrhythmias or merely a marker for other arrhythmogenic factors. To the extent that changes in serum potassium contribute to the production of serious ventricular arrhythmias, efforts should be directed at the correction of such electrolyte disturbances. Attempts to increase the serum potassium in acute cases do not appear to be successful in preventing ventricular arrhythmias in this setting. Primary prevention of electrolyte disturbances would seem to offer more effective protection against serious arrhythmias. Long term studies with beta-blockers support this premise.

Arrhythmias, Cardiac↗
PubMed1985

The role of urinary kininogen in the regulation of kinin generation.

The kallikrein-kininogen-kinin system has been postulated to play a role in the regulation of blood pressure and modulation of renal salt and water transport. The activity of this system has usually been determined by measurements of urinary kallikrein excretion. However, urinary kallikrein rarely correlates with simultaneously measured urinary kinins. To further evaluate the factors influencing urinary kinin excretion, we evaluated the role of urinary kininogen in this system. Urines were analyzed from normal subjects and individuals with untreated essential hypertension and end-stage renal disease. Intact urinary kininogen was significantly correlated with urinary kinins in normal subjects (r = 0.65, P = 0.003) and essential hypertensives (r = 0.52, P = 0.026). In both essential hypertension and end-stage renal disease, urinary kinins were significantly decreased (8.00 +/- 1.93, 0.90 +/- 0.18, P less than 0.05, respectively) compared to controls (23.73 +/- 5.20). In essential hypertensives, the reduction in urinary kinins was paralleled by a reduction in intact kininogen with a normal excretion of kallikrein. In end-stage renal disease, the reduction in kinins was paralleled by a reduction in kallikrein with a normal excretion of intact kininogen. This data suggests that kininogen may be an important determinant of urinary kinin excretion in various disease states.

Aldosterone↗
PubMed1984

Elevated nicotine levels in patients undergoing hemodialysis. A role in cardiovascular mortality and morbidity?

The incidence of cardiovascular disease in patients with end-stage renal disease undergoing long-term maintenance hemodialysis is excessively high. The reason for this excess morbidity and mortality has remained unclear. Cigarette smoking is one factor that has been associated with increased cardiovascular risk. To learn more about the effects of tobacco smoking in these patients, nicotine levels were assayed in the serum of 10 patients with end-stage renal disease undergoing maintenance hemodialysis. Specimens were obtained before and after smoking one cigarette and following dialysis or an equivalent period in control subjects. Serum nicotine levels (+/-SEM) in control subjects measured 19.0 +/- 7.2 ng/ml initially, 36.1 +/- 8.2 ng/ml after smoking, and 9.3 +/- 3.5 ng/ml after a period of 4.35 hours. These compare with respective values of 76.6 +/- 16.8 ng/ml (p less than 0.004), 132.9 +/- 19.7 ng/ml (p less than 0.001), and 51.9 +/- 10.5 ng/ml (p less than 0.001) in patients undergoing hemodialysis. These data demonstrate markedly higher nicotine levels in hemodialysis patients compared with control subjects, which may have serious implications regarding morbidity and mortality.

Adult↗
PubMed1984

In vivo effect of volume expansion on rectal gland function. II. Hemodynamic changes.

Intravascular volume expansion causes a 300% increase in the rate of fluid secretion from, and blood flow to, the in vivo rectal gland of the spiny dogfish Squalus acanthias. Similar increases are also observed in explanted rectal glands perfused through a catheter from the dorsal aorta of a volume-expanded dogfish. Stimulation of rectal gland secretion by volume expansion is not associated with a change in the ratio of chloride secreted to oxygen consumed by the rectal gland and the oxygen extraction ratio, suggesting that an increase in blood flow is necessary to support the increased rate of chloride secretion. Perfusion of the explanted gland with bumetanide (10(-4) M) completely inhibits the secretory response to volume expansion but does not prevent the increase in blood flow. Bumetanide also inhibits dibutyryl adenosine 3',5'-cyclic monophosphate- and theophylline-induced increases in chloride secretion but does not inhibit the hyperemic response. Somatostatin inhibits the secretory response of the explanted gland to volume expansion but does not prevent the increase in blood flow. Although an increase in blood flow is necessary to support the increased energy requirement of enhanced transport, the secretory response and the increase in blood flow appear to be independently regulated and mediated, at least in part, by humoral factors.

Animals↗
PubMed1984

Thallium-201 myocardial imaging in patients on chronic hemodialysis.

10 long-term hemodialysis patients had immediate and redistribution thallium-201 myocardial imaging performed after a course of hemodialysis. Subjects had EKGs done on the same day before and after dialysis. 3 of the 10 subjects had resting thallium-201 myocardial imaging obtained on non-dialysis days. 60% of the electrocardiograms showed changes with dialysis. All 13 thallium studies were abnormal, showing multiple transient filling defects at rest. Most subjects had permanent filling defects as well. It is concluded that hemodialysis patients have a high frequency of abnormal thallium-201 myocardial images at rest. The cause of these abnormal studies is uncertain.

Adult↗
PubMed1984

Ventricular arrhythmias in patients with myocardial infarction and ischaemia. Relationship to serum potassium and magnesium.

Alterations in serum electrolytes may frequently accompany ischaemic heart disease. Many of these patients are hypertensive and receive diuretic therapy which results in chronic lowering of serum potassium and magnesium. In addition, acute catecholamine-induced shifts of potassium into cells may also occur in the setting of acute myocardial ischaemia. An association between low serum potassium concentrations and ventricular arrhythmias has been observed by a number of investigators in patients with acute myocardial infarction. The increased frequency of ventricular fibrillation with low serum potassium concentrations is particularly relevant as this arrhythmia is associated with poor prognosis, even in the setting of a coronary care unit. Ventricular fibrillation also occurs with increased frequency in patients with angina who have low serum potassium levels. The possibility that low serum potassium concentrations may be a risk factor in the increased incidence of sudden death in such patients should be considered. Diuretic-induced magnesium deficiency may be yet another factor favouring the emergence of ventricular arrhythmias in patients with ischaemic heart disease. While such electrolyte disturbances do not account for all of the ventricular irritability seen in patients with ischaemic heart disease, they represent easily identifiable and treatable risk factors. Primary prevention of these electrolyte disturbances in patients at risk for coronary ischaemia is recommended.

Acute Disease↗
PubMed1983

Cimetidine-induced interstitial nephritis with response to prednisone therapy.

Acute renal failure developed in a patient after she received cimetidine therapy. A renal biopsy specimen showed acute interstitial nephritis. Withdrawal of cimetidine therapy led to improvement of renal function. Rechallenge with cimetidine occurred during prednisone therapy. Renal function continued to improve, but worsened when the treatment with these steroids was discontinued.

Acute Disease↗
PubMed1982

Ketone body effects on glutamine metabolism in isolated kidneys and mitochondria.

beta-Hydroxybutyrate (but not acetoacetate) caused marked inhibition of ammonia production and glutamine extraction in isolated perfused kidneys from normal rats. Glutamine synthesis was not affected by beta-hydroxybutyrate (BHB). Measurement of metabolite levels in freeze-clamped kidneys showed that BHB increased glutamine concentration, decreased ammonia concentration, and reduced the mitochondrial NAD+/NADH ratio (calculated) in perfused kidneys. BHB inhibited flux through the glutamate dehydrogenase pathway, probably as a result of reduction in the NAD+/NADH ratio, in isolated renal mitochondria. In isolated perfused kidneys from acidotic rats, ammonia production and mitochondrial NAD+/NADH were both elevated and BHB did not inhibit renal ammoniagenesis. Although ammonia production in the acidotic kidneys was not directly related to the mitochondrial NAD+/NADH ratio, the elevation of this ratio may have permitted a normal rate of oxidation of glutamine end products--which is essential for maintaining the elevated ammoniagenesis--to take place in the presence of BHB.

3-Hydroxybutyric Acid↗
PubMed1982

Phantom urinary symptoms in hemodialysis patients.

Phantom urinary symptoms were reported by 12 or 24 hemodialysis patients surveyed. The symptoms were present in all age groups. The absence of any correlation between the occurrence of these symptoms and length of time and dialysis suggest that urinary phantoms in hemodialysis patients may persist over time in contrast to the gradual disappearance of phantoms symptoms resulting from amputation. No correlation was found between occurrence of phantom symptoms and sexual impairment, actual voiding of urine or symptoms of peripheral neuropathy.

Adult↗
PubMed1981

Importance of potassium in patients with acute myocardial infarction.

The records of 151 patients entering a coronary care unit and subsequently diagnosed as having an acute myocardial infarction were reviewed. The prevalence of hypokalemia, its relationship to diuretic treatment and the development of either ventricular tachycardia or ventricular fibrillation were studied. At admission, 14% of patients were hypokalemic. The presence of hypokalemia was related to previous diuretic therapy. Twenty-three percent of patients receiving diuretics as compared to 7% of patients not taking diuretics had a serum potassium of 3.5 mEq/L or less. Thirty-seven patients experienced either ventricular tachycardia or ventricular fibrillation. The presence of hypokalemia was associated with an increased frequency of both of these arrhythmias. Sixty-seven percent of patients with a serum potassium of less than 3.1 mEq/L had these serious ventricular arrhythmias compared to 40% of patients with a serum potassium between 3.1 and 3.5 mEq/L and 20% of normokalemic patients. The prevalence of premature ventricular beats was not correlated with the presence of hypokalemia. We conclude that hypokalemia is not only a common problem in patients with acute myocardial infarction but a clinically significant factor in the development of life threatening arrhythmias. Primary prevention of hypokalemia and its prompt treatment are indicated in these patients.

Arrhythmias, Cardiac↗
PubMed1981

Electrocardiographic changes following dialysis.

We investigated electrocardiographic changes occurring after hemodialysis in 20 male patients with chronic renal failure. Changes in the configuration of T wave, ST segment and R wave consistent with ischemia were found in 30, 45, and 75%, respectively. Contrary to prior speculation the R wave height did not vary with the volume changes of body fluid occurring in dialysis. It is concluded that ischemic-appearing changes of uncertain significance are common in the postdialysis population.

Adult↗
PubMed1979

Disseminated Mycobacterium chelonei infection: response to sulfonamides.

A disseminated infection due to Mycobacterium chelonei occurred in a hemodialysis patient after rejection of his second renal transplant. Painful subcutaneous nodules and abscesses were found on both legs. Therapy with sulfisoxaxole and kanamycin produced a prompt response twice, as did sulfisoxazole alone on 2 additional occasions, despite resistance in vitro to both drugs. Clinical relapses occurred 3 times when administration of sulfisoxazole was discontinued.

Administration, Oral↗
PubMed1975

Bartter's syndrome. New insights into pathogenesis and treatment.

Discussed here is a patient with normotension, hypokalemic alkalosis, hyperreninemia, hyperaldosteronism, juxtaglomerular cell hyperplasia and insensitivity to the pressor effects of angiotensin (Bartter's syndrome). The hyperreninemia and hyperaldosteronism were both suppressible with volume expansion. Hypokalemia was correctible both short-term with potassium chloride infusions and long-term with spironolactone. Nevertheless, the abnormal pressor response to infused angiotensin could not be corrected by these maeuvers, suggesting that this defect is likely to be of primary pathophysiologic significance. We found that potassium loading markedly stimulated aldosterone excretion. This may explain the inadequacy of potassium supplementation alone to correct the hypokalemia and the observed "escape" from the potassium conserving effects of spironolactone seen in patients with Bartter's syndrome. The administration of propranolol in large doses only partially suppressed the marked hyperreniemia of our patient and failed to prevent a subsequent rise in the renin level which was associated with spironolactone therapy. In contrast, suppression of the renin level to normal was demonstrated by sodium loading. It is suggested that patients with Bartter's syndrome be treated simultaneously with large doses of spironolactone and a high sodium intake.

Adult↗
PubMed1975

Thiocyanate inhibition of ATPase and its relationship to anion transport.

Adenosine triphosphatase activity not dependent on sodium or potassium but inhibited by thiocyanate is present in broken-cell homogenates of eel gill and rat kidney. This enzymatic property is predominantly associated with mitochondria, although thiocyanate-inhibited ATPase can also be detected in microsomes with little or no mitochondrial contamination as measured by the activity of the mitochondrial marker enzyme succinic dehydrogenase. When eels are transferred from fresh to salf water, thus increasing active outward transport of chloride across the gill, the thiocyanate-inhibited ATPase of gill microsomes does not change, though the activities of succinic dehydrogenase and Na-K-ATPase in gill homogenates are augmented. The thiocyanate-inhibited ATPase of homogenates of outer renal medulla does not differ from that of renal cortex, in contrast to Na-k-atpase which is higher in renal medulla than in cortex. The data do not support a role for thiocyanate-inhibited ATPase in active chloride transport by epithelial tissues.

Adenosine Triphosphatases↗