摘要:

To explore the role of dopaminergic mechanisms in orthostatic hypotension we compared the postural responses of 20 such patients to those of a control group by radioenzymatic determination of free and sulfated catecholamines and related indices. Patients with orthostatic hypotension, unlike control subjects, experienced an increase in total plasma dopamine (DA) (free + sulfate) in response to upright posture (p < 0.01). Of the 20 patients with orthostatic hypotension, 16 were normo- or hyperadrenergic with normal basal and posture-responsive or hyperresponsive plasma free and total norepinephrine (NE). The other 4 were hypoadrenergic with low basal and posture-unresponsive NE. Hypoadrenergic patients had, in the upright position, no increase in pulse rate and more severe hypotension, less diuresis and natriuresis, lower urinary free and total DA, lower total NE excretion, and higher plasma and urinary total DA:total NE ratio than normo- or hyperadrenergic patients or control subjects. Normo- or hyperadrenergic patients had higher PRA and plasma aldosterone in the upright position than hypoadrenergic patients or control subjects (all p < 0.05).We suggest that an excessive increase in free DA occurs in response to upright posture, perhaps representing a compensatory reaction of the remaining autonomic nervous system to an excessive fall in blood pressure. The free dopamine may be biologically active but it is so rapidly sulfoconjugated that it can be detected only as DA sulfate. These findings, combined with reports of orthostatic hypotension precipitated by administration of dopaminomimetic drugs and relieved by administration of dopaminergic antagonists, are consistent with the interpretation that excessive DA release may perpetuate, by its vasodilating and natriuretic action, the orthostatic hypotension.

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Glucose is used in peritoneal dialysate to produce the gradient for ultrafiltration. The peritoneal membrane's low reflection coefficient for glucose imposes a demand for high transmembrane concentrations, perhaps adding unwanted body burden of glucose. A polymer with a lower permeation rate used as an osmotic agent would circumvent this. We evaluated the mass transfer coefficient (mtc), T1/2disappearance from the peritoneal cavity and ultrafiltration capabilities of a 900 dalton (Mn) starch derived polymer. We compared an 8% (455 mOsm/L) and a 10% (484 mOsm/L) polymer (Pol) solution to available dialysate solutions containing 2.5% (399 mOsm/L) and 4.25% (491 mOsm/L) × glucose (Glc). The dialysate compositions were otherwise similar. Using a randomized complete block design, 5 anephric dogs maintained on chronic peritoneal dialysis were studied. The mtc (ml/min) was greater for the glucose than the polymer solutions (p<0.05): 2.5%-13 and 4.25%-14 vs 8%-5 and 10%-6. The T1/2disappearance (min) was also greater (p<0.05): 2.5% Glc-112 and 4.25% Glc-111 vs 8% Pol-281 and 10% Pol-252. Over a 180 min. period the 2.5% glucose solution generated the least volume of ultrafiltrate (ml, p<0.05):2.5% Glc-113 and 4.25% Glc-589 vs 8% Pol-640; 10% Pol-912. We conclude that the lower permeation rate of the polymer yields ultrafiltration at a lower dialysate osmolality. A polymer solution may be a feasible alternative to glucose.

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Amyloid fibrils in familial amyloid polyneuropathy, the familial (AF) form of systemic amyloidosis, are composed of the monomeric unit (14,000 MW) of prealbumin molecules. By radioimmunoassay, the serum level of prealbumin was measured in 25 patients from 12 different kinships with this dominantly inherited form of amyloidosis and 56 unaffected, but at risk, relatives from two of the kinships. Results were compared to prealbumin levels in normal individuals and patients with primary (AL) and secondary (AA) forms of systemic amyloidosis. Significantly lowered prealbumin levels were found in the AF patients (149.2 ug/ ml) and their at risk relatives (169.0 ug/ml) when compared to normal individuals (232.9 ug/ml), AL patients (221.9 ug/ml) and AA patients (211.7 ug/ml). No abnormality was found in levels of retinol binding protein (RBP), which is carried by prealbumin, in the serum of either the AF patients or their relatives. The depressed prealbumin levels may indicate a structural variant molecular form, an extra hepatic synthesis or an abnormality in catabolism of this protein that is present prior to the clinical or histopathologic onset of the AF disease.

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The deleterious effects of ethanol on a variety of tissues may result largely from altered ion permeabilities and transport. Clinically relevant ethanol concentrations in blood increase the sodium permeability of the plasma membrane and depress active sodium transport by suppressing Na, K-ATPase activity. As a result, intracellular sodium concentration increases. The total tissue content of calcium increases. Important transport mechanisms deranged by ethanol probably include those regulating calcium-sodium and hydrogen-sodium exchange at the plasma membrane and calcium uptake by the sarcoplasmic reticulum. A modest decline in magnesium content of muscle occurs after chronic exposure to ethanol. This also has been associated with accumulation of calcium.After days to weeks of sustained ethanol intake, sodium pump activity, active sodium transport and tissue oxygen consumption increase. The cell membrane potential, initially lowered by alcohol, increases to supraphysiological levels. This is likely an electrogenic effect of increased sodium transport in response to a sodium leak. Eventually the earlier derangements in tissue composition, including retention of sodium, chloride, and calcium, and reductions in magnesium, potassium, and phosphate, slowly undergo correction. This biphasic response of injury and adaptation appears to depend upon adequate nutrition and the absence of other factors that can adversely affect cell function. That the Na, K-ATPase activity and oxygen consumption remain elevated suggests an ongoing sodium leak of the sacrolemmal membrane.Chronic ethanol-induced cell necrosis may be related to the increased intracellular calcium that accompanies the increase in sodium permeability. Conceivably, critically elevated concentrations of calcium in the cytoplasm may activate autolytic enzymes that in turn may be responsible for structural damage to the cell. [Am J Med Sci 1985; 289(1):22–26.]

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

A hypothalamic metastasis was demonstrated by computed tomography in a 71-year-old patient, with previously unknown small cell lung cancer, who presented with diabetes insipidus and biological signs of hypothyroidism and hypogonadism. Brain irradiation resulted in resolution of polyuria, elevation of thyroid hormones, improvement of pituitary responsiveness to hypothalamic releasing hormones, and complete disappearance of contrast-enhanced suprasellar metastasis.

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

A four-year-old girl with growth failure and clinical and laboratory evidence of Bartter's syndrome responded to indomethacin treatment with decreased urinary prostaglandin excretion, symptomatic and chemical improvement, and accelerated growth. Large doses of aspirin produced a comparable decrease in prostaglandin excretion but no improvement in any other metabolic abnormality thus suggesting that abnormalities in prostaglandins were the result rather than the cause of the electrolyte abnormalities. Progressive renal insufficiency while on indomethacin prompted a renal biopsy, which revealed morphological changes of focal, segmental glomerular sclerosis. Subsequently, the child underwent renal transplantation with complete resolution of symptoms and abnormal metabolic findings. This observation suggests that extrarenal factors were not responsible for the development of Bartter's syndrome in this child.

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID