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Biomedical subjects

E Maher

Publications and source records attributed to E Maher.

47 records · Page 3Linked to original sources
PubMed1987

Diuretic-induced growth failure in rats and its reversal by sodium repletion.

The aim of diuretic therapy is the prevention of excessive sodium accumulation. However, sodium retention is necessary for growth. Inasmuch as many of the clinical conditions for which diuretics are used are associated with growth retardation, we investigated the influence of diuretic therapy on growth in an animal model. In Part I, 32 weanling Sprague-Dawley rats were fed a diet adequate for growth which contained 0.08% sodium and 0.17% potassium. Daily i.p. injections of saline (0.4 ml) containing furosemide in doses of 0, 50, 100 or 200 mg/M2 were given for 9 days. There was a dose-related reduction in weight gain which could not be explained by lower food intake. The highest dose group gained only 58% as much as the control group. Balance studies and muscle, bone and carcass analysis demonstrated that this was accounted for by decreases in protoplasmic, bone, fat and extracellular fluid volume accretion. In Part II, 32 weanling rats, all treated daily with furosemide (100 mg/M2 i.p.) received replacement of NaCl, KCl, both or neither in their drinking water. Sodium replacement resulted in increased growth rates whereas potassium replacement alone had no effect on growth. Sodium replacement also increased the balance of all measured minerals. We conclude that diuretic therapy causes growth retardation by preventing retention of sodium needed for growth.

Animals↗
PubMed1977

Functioning and nonfunctioning cysts of the adrenal cortex and medulla.

Adrenal cysts are rare clinical and pathologic entities. The vast majority are minute in size, unilateral, and found in females at autopsy. They come to the physician's attention when they produce symptoms or are identified on x-ray studies. When symptomatic, they generally produce lumbar discomfort and gastrointestinal symptoms, and occasionally are palpable by abdominal examination. There is no significant agreement as to cause and pathogenesis of the disease. The most common histologic types are lymphangiomatous endothelial cysts, secondary to lymphangiectasis, and the fibrous wall or hemorrhagic pseudocysts. In many patients preoperative diagnosis is now possible with high quality nephrotomography, ultrasonography, and adrenal arteriography. The presence of a suprarenal mass with peripheral or laminar calcification strongly suggests the presence of an adrenal pseudocyst. Selective biochemical studies are mandatory to rule out the presence of an occult cystic pheochromocytoma, and adrenal cortical tumor. Adrenal cysts must be differentiated from all space-occupying lesions of the upper abdomen. Surgical exploration is recommended in almost all patients for accurate diagnosis and to rule out malignant disease or occult pheochromocytoma. The choice of the surgical approach should be planned to provide for safe and adequate exposure, depending on the size and location of the lesion. Careful dissection with preservation of the adjacent kidney, liver, and pancreas should be performed.

Adrenal Cortex↗
PubMedDate not supplied

Response to atrial natriuretic peptide in dogs with acute selective intrahepatic hypertension.

Acute selective intrahepatic hypertension (IHH) is associated with the renal tubular retention of sodium in volume expanded dogs. To determine if acute selective IHH per se, without volume loading or ascites sequestration, would blunt the natriuretic response to i.v. infusions of atrial natriuretic peptide (ANP), 175 ng/kg/min of the 1-28 rat peptide was infused into 6 hydropaenic dogs where intrahepatic hydrostatic pressures were normal, and again, following the portal infusion of histamine, a maneuver known to selectively increase postsinusoidal resistance, within the hepatic microcirculation and so raise intrahepatic sinusoidal pressure. In 6 healthy dogs, while histamine 4.0 micrograms/min free base on average was being infused into a femoral vein, the infusion of ANP increased sodium excretion by 168 microEq/min, compared to 160 microEq/min when the same dose of histamine was being infused into the portal vein (portal pressure increased by 46% or 6 cm H2O). These changes in sodium excretion were not significantly different. Urine flow rate increased by 1.5 ml/min in the control phase and by 1.4 ml/min during intrahepatic hypertension (NS). Although the ANP infusion did not alter GFR or CPAH during the control phase, during IHH, ANP caused GFR to rise significantly by 20%, while there was no change to CPAH. Despite the increment in GFR, the natriuretic response during IHH was not different from that observed during the control phase of the study. We conclude that acute IHH per se does not blunt the renal tubular natriuretic response to ANP.

Animals↗