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Biomedical subjects

T Morgan

Publications and source records attributed to T Morgan.

At least 127 records · Page 7Linked to original sources
PubMed1986

Results of a randomized trial of end-to-side portacaval shunt and distal splenorenal shunt in alcoholic liver disease and variceal bleeding.

Since 1976, we have compared the end-to-side portacaval shunt (PCS) with the distal splenorenal shunt (DSRS) in patients with alcoholic liver disease and recurrent variceal bleeding. Fifty-four patients were randomly assigned to receive either shunt procedure. There were 27 patients in each group and both groups were highly comparable in clinical and laboratory characteristics. Median follow-up was 31 mo in each group. Postoperative complications and operative mortality (7% after PCS, 12% after DSRS) were comparable. Spontaneous portasystemic encephalopathy developed in 32% of the patients at risk after PCS and in 39% after DSRS. Rebleeding from varices occurred in 4% of the patients after PCS and in 27% after DSRS. Cumulative survival was not significantly different between groups (5-yr survival: 31% after PCS, 43% after DSRS). We have failed to demonstrate superiority of DSRS in our patients with alcoholic liver disease with respect to postoperative encephalopathy or survival, and have experienced an unusually high rate of variceal rebleeding after DSRS.

Adult↗
PubMed1986

Trauma center and the OR. A cooperative approach to caring for the massively injured.

Communication must be established between the operating room and trauma center. At SNJRTC, perioperative nurses rotate through the trauma center and are part of nursing grand rounds on trauma patients. This system has improved interdepartmental relations, educational development, and most importantly, established a system in which patients have the best chance of survival as a result of the cooperative approach to the care of the massively injured.

Communication↗
PubMed1986

The role of sodium restriction in the management of hypertension.

More than 50 studies have investigated the effect of altered sodium intake on blood pressure. A regression line drawn through the change in blood pressure and change in sodium intake indicates that blood pressure alters about 10 mmHg (1 mmHg = 133.322 Pa) for every 100 mmol/day alteration in sodium intake, a change similar to that observed in between-population "studies." The studies that have failed to show a change in blood pressure have usually been in people with a blood pressure less than 130/90 mmHg. Normotensive people appear to tolerate a higher intake of sodium before blood pressure rises, but if increased sufficiently, blood pressure rises in most people. Sodium restriction reduces blood pressure in people with severe hypertension, moderate hypertension and mild hypertension. It may be the cause of blood pressure increase associated with age and the reason for the higher prevalence of hypertension and vascular disease in Western communities. Sodium restriction should be used to treat people with elevated blood pressure.

Blood Pressure↗
PubMed1986

Factors that determine the response of people with mild hypertension to a reduced sodium intake.

One hundred and eighty-six males who had had 3 run-in visits entered the study with a supine diastolic BP 95-110 mm Hg. This was followed by 3 pretreatment and 3 post-treatment visits. One hundred and sixty patients were given advice to reduce sodium intake after visit 3, and twenty-six patients served as control. In the control group there were relatively insignificant changes between the pre and post visits. In the diet group blood pressure fell by 13/9 mm Hg; urine sodium from 168 to 85 mmol/day and plasma renin activity rose from .50 to .77 ng AI/ml/h. Regression analysis showed that the only cross-sectional correlations were PRA with age, urine sodium and plasma potassium. There were highly significant correlations between the change in urinary sodium and the change in blood pressure and between the changes in blood pressure and plasma renin activity. Multiple Regression Analysis indicated that the final diastolic blood pressure achieved depended upon the initial diastolic blood pressure, the fall in sodium intake, and was reduced by the rise in plasma renin activity. Patients who responded to sodium restriction had a lower initial renin value than other patients. This study emphasises the importance of the interaction between sodium, potassium and renin in the determination of blood pressure levels.

Adult↗
PubMed1986

The role of the macula densa in renin release: studies by microperfusion.

The role of the macula densa in control of renin release and in mediation of tubulo-glomerular feedback was investigated following orthograde microperfusion in Munich Wistar rats. Tubules of surface glomeruli were perfused, drip-fixed with glutaraldehyde and biopsy cores taken containing perfused and non-perfused glomeruli. Serial sections were examined by light and electron microscopy. In some animals dilated basolateral spaces were observed between cells in control maculae densa but no spaces were found following microperfusion with hypertonic NaCl, isotonic mannitol or hypotonic NaCl containing 1 mg/l frusemide. In other animals no spaces were found in control cores, and perfusion with the above solutions had no effect. However, in such animals, tubules perfused with hypotonic NaCl (71 mmol/kg H2O) had prominent basolateral spaces in their maculae densa. The presence of dilated basolateral intercellular spaces is generally associated with osmotically driven water flow. The extent of dilatation of such spaces in the macula densa is correlated with transepithelial osmotic or ionic gradients and may indicate activity of these cells in the recognition of distal tubular fluid composition.

Animals↗
PubMed1986

Australian National Health and Medical Research Council dietary salt study in mild hypertension.

Two-hundred-and-twelve untreated subjects (mean age 52.3 +/- 0.8 years; 181 males and 31 females) with a diastolic blood pressure between 90 and 100 mmHg were recruited to the study. Subjects were seen fortnightly and, after 4 pre-diet visits, were randomized into a normal diet group (A, 55 subjects), a high-potassium diet group (B, 52 subjects receiving greater than 100 mmol K+/day) a reduced-sodium diet group (C, 52 subjects receiving 50-75 mmol Na+/day) or a high-potassium and low-sodium diet group (D, 53 subjects receiving same Na+ and K+ as groups B and C). Two-hundred subjects completed the diet phase of 12 weeks. Urine sodium fell to 86 +/- 7 mmol/day in group C and 73 +/- 6 mmol/day in group D, while daily potassium excretion rose to 96 +/- 5 mmol in group B and 87 +/- 4 mmol in group C. Systolic and diastolic blood pressure fell by 3.8 +/- 1.0 and 1.6 +/- 0.6 mmHg respectively in the normal diet group. The falls in systolic and diastolic blood pressures (mmHg) in the diet phase were 7.7 +/- 1.1 and 4.7 +/- 0.7 (B), 8.9 +/- 1.0 and 5.8 +/- 0.6 (C) and 7.9 +/- 0.9 and 4.2 +/- 0.7 (D). These falls were all greater than those in the control group on an intention-to-treat analysis (P less than 0.005) but did not differ from each other. Factorial analysis confirmed that the falls in pressure attributable to the low-sodium diet and high-potassium diet were not additive.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1984

Adverse reactions to long-term diuretic therapy for hypertension.

Diuretics are important drugs used in therapy for hypertension. Diuretics have a number of side effects, some of which have long-term consequences. In this study diuretics were used to treat individuals with mild hypertension. Patients receiving diuretics as sole therapy had an increased mortality due to an excess number of deaths from myocardial infarction or sudden death. In patients given alpha-methyldopa or propranolol as well as a diuretic drug, this effect was not observed. The increased mortality may be due to an increased susceptibility to arrhythmias in individuals receiving diuretics, and this was prevented by drugs that interfere with the effects of the sympathetic nervous system.

Adrenergic beta-Antagonists↗
PubMed1984

The role of sodium and potassium in the control of blood pressure.

When sodium intake was increased from 70-200 mmol/day in normotensive volunteers, their blood pressure rose by 6/4 mmHg. In most people over 50 years, blood pressure rose and it also rose in about 15% of younger people. Those who had a rise in blood pressure had a creatinine clearance lower than others when on a reduced sodium intake. In the sodium sensitive group creatinine clearance rose when sodium intake was increased. In the people with a rise in blood pressure there was a fall in plasma volume. Increased sodium intake altered a number of factors that control sodium transport across cell membranes. The changes are complex but suggest that genetically inherited and environmentally caused defects are necessary to allow hypertension to be expressed. Reduction of sodium intake reduced blood pressure in people with mild hypertension. Potassium interacted with sodium to reduce the rise in blood pressure caused by sodium. Sodium intake and blood pressure are linked by many mechanisms. If the intake is excessive for that individual or if there are defective control mechanisms, hypertension will result.

Age Factors↗
PubMed1984

The role of potassium in control of blood pressure.

Extra potassium intake has been found to be a determinant of blood pressure for epidemiological and experimental reasons. People with hypertension have a small fall in blood pressure with added potassium. Potassium chloride (48 mmol/day) was given to 36 male patients with high blood pressure; 5 did not comply with therapy. In the entire group of patients, potassium chloride had no significant effect on blood pressure, but prevented the rise in blood pressure and pulse rate produced by posture. In patients with a urinary Na+ excretion less than 75 mmol per 10 mmol creatinine, potassium chloride had no effect on supine blood pressure, but prevented the rise in blood pressure and pulse rate with standing. In those on a high sodium intake, potassium chloride lowered both the systolic and diastolic pressures. In sodium-responsive subjects, potassium chloride prevented the rise in blood pressure induced by sodium chloride but had no significant effect on blood pressure when on a low sodium intake. These results indicate that potassium reduces the rise in blood pressure caused by sodium chloride and reduces the increased sympathetic postural response seen in people on a low sodium intake.

Aged↗
PubMed1984

Lithium administration and urinary electrolyte excretion in the rat.

The effect of lithium administration on urine eletrolyte excretion is controversial with reports of increased, unaltered and reduced excretion rates of sodium, potassium, calcium, magnesium and inorganic phosphate. Therefore rats treated with daily intraperitoneal lithium chloride for 3 weeks were studied and were found to have marked fluctuations in electrolyte excretion when compared to untreated rats. Although lithium-treated rats were always polyuric, urinary sodium, potassium and calcium excretion was significantly elevated immediately following intraperitoneal lithium but their excretion rates then returned towards normal. Magnesium excretion was initially unaltered by lithium administration (6.8 +/- 1.3 compared with 7.3 +/- 1.7 mumol/100 g/8 h) but then decreased (2.5 +/- 0.5 with 7.8 +/- 1.1 mumol of magnesium/100 g/8 h; p less than 0.01) during the final collection period. A persistent phosphaturia also occurred with lithium treatment (122 +/- 5 compared with 92 +/- 6 mumol/100 g body weight/24 h). Despite these significant changes in renal electrolyte transport with lithium administration, similar changes were also noted in rats similarly treated with equimolar doses of sodium chloride although polyuria did not occur. Thus it is postulated that lithium ions exert their effect on renal electrolyte transport in a similar manner to that of sodium.

Animals↗
PubMed1984

Diuretics 1984.

Diuretics increase water excretion by inhibiting sodium transport in the nephron. They can be grouped according to their chemical class or (more practically) their site of action in the nephron. The site determines certain features of their effect, an important one being their effect on potassium excretion. Diuretics which act late in the nephron inhibit sodium transport in the region in which potassium is secreted, causing retention of potassium and hydrogen ions. These diuretics produce a hyperkalaemic acidosis; most others cause loss of potassium and hydrogen and a hypokalaemic alkalosis.

Anesthetics↗
PubMed1984

Renal colic.

The most common and overt manifestation of a ureteric calculus is renal colic. This paper discusses its clinical presentation and diagnostic difficulties and follows the management of the patient until the stone is passed or retrieved surgically; it does not address the overall picture of renal calculous disease. The role of subsequent metabolic investigation is outlined.

Aged↗
PubMed1983

Effect of calcitonin on urine concentration in the rat.

Because mammalian distal nephron segments with both calcitonin- and antidiuretic hormone- (ADH) sensitive adenylate cyclase activity have been described, in vivo and in vitro experiments were performed to study the effect of calcitonin on rat distal nephron water permeability. Calcitonin 1 and 0.1 U/ml, but not 0.01 U/ml, significantly increased the diffusional water permeability in the isolated papillary collecting duct by 15 and 11%, respectively. However, this effect was small when compared with a 68% increase with a supramaximal concentration of ADH (from 4.0 +/- 0.3 to 6.7 +/- 0.9 microns/s; n = 6, P less than 0.01). The normal increase in water permeability with increasing concentration of ADH (0.02 and 0.2 mU/ml) was depressed by the previous addition of calcitonin (1 U/ml) to the bath but was unaltered with the supramaximal ADH concentration (2 mU/ml). Verapamil, a compound that antagonizes cellular calcium entry, did not alter the effect of calcitonin on diffusional water permeability. Calcitonin in concentrations of 0.05, 0.5, and 5 U/ml produced a significant reduction in urine flow and free water clearance. Pretreatment with calcitonin in these concentrations inhibited the antidiuretic action of ADH. These studies suggest that calcitonin acts as a partial agonist to ADH within the distal nephron. It is unclear whether such an action represents a physiological or a pharmacological effect.

Animals↗
PubMed1983

The use of centrally acting antihypertensive drugs in patients with renal disease.

Clonidine was given to patients with essential hypertension, renovascular hypertension, and hypertension with parenchymal renal disease. The drug was effective in all groups but was more effective in patients with high plasma renin concentration. Renal function did not deteriorate when the drug was used, and there was an increase in renal blood flow and a small increase in glomerular filtration rate in those with renovascular or essential hypertension. These changes may have been due to falls in plasma renin. Clonidine can be used in patients with renal disease and does not cause worsening of renal function.

Clonidine↗