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Biomedical subjects

L Shilo

Publications and source records attributed to L Shilo.

28 records · Page 2Linked to original sources
PubMed1988

Atrial natriuretic peptide administration to normal and salt depleted rats--effects on digoxin-like immunoreactive factor, aldosterone, ACTH, and renal function.

In view of the known interrelationships between renin, aldosterone, and atrial natriuretic peptide (ANP), we sought to examine whether there also exists an interaction between ANP and digoxin-like immunoreactive factor (DLIF). We therefore studied the effects of ANP administration on normal and salt-depleted rats, and measured the effects on blood pressure, urine output, glomerular filtration rate, sodium excretion, aldosterone, ACTH, and DLIF levels. ANP administration resulted in a significant elevation of sodium excretion and glomerular filtration rate and a fall in blood pressure. DLIF concentrations in plasma rose significantly, as did urinary DLIF excretion. ANP administration resulted in a fall in aldosterone as well as ACTH. These observations suggest that ANP has a direct inhibitory effect on ACTH secretion. Our findings support the concept of an interrelationship between ANP and DLIF.

Adrenocorticotropic Hormone↗
PubMed1988

Myalgias and muscle contractures as the presenting signs of Addison's disease.

Severe generalized myalgias and muscle contractures of the lower extremities were the major initial manifestations of adrenal insufficiency in a 26 year old black male. The intensity of increased skin pigmentation was not fully appreciated until the patient's skin colour was compared to that of his brother. Replacement with physiological doses of gluco- and mineralocorticoids was associated with complete amelioration of symptomatology.

Addison Disease↗
PubMed1987

Digoxin-like immunoreactivity: occurrence in three molecular forms and partial characterization.

Digoxin-like immunoreactivity (DLI) has been found in serum from subjects with a variety of physiological and pathological conditions, including uremia, liver disease, pregnancy, and the neonatal period. The physicochemical nature of this material is still not known. Using gel filtration chromatography, extraction with methylene chloride, and treatment with beta-glucuronidase, we determined that serum DLI exists in three forms: protein-bound, glucuronidated, and free, with respective mol wt of 5000, 400, and 230. In serum, DLI exists in the protein-bound and free forms, while in urine, DLI is found in the glucuronidated and free states.

Chemical Phenomena↗
PubMed1987

Hemorrhagic shock prevents lung microvascular permeability and hypoxemia associated with complement activation in the awake sheep.

The effect of hemorrhagic hypotension on pulmonary dysfunction induced by complement activation was studied in 43 awake sheep, divided into six groups: Group I (n = 6), pulmonary vascular pressure was increased by inflation of a left atrial balloon; group II (n = 9), the complement system was activated by infusion of zymosan activated plasma (ZAP); group III (n = 5), hemorrhagic shock of 50 torr was induced for 3 hr; group IV (n = 10), hemorrhagic shock was induced as in group III, and after 2 hr of shock, ZAP was infused; group V (n = 8), 5 mg/kg of indomethacin was administered before ZAP infusion; group VI (n = 5), pretreatment with indomethacin as in group V, hemorrhagic shock and ZAP as in group IV. ZAP infusion in group II led to a fall in WBC to 2,600/ml (P less than 0.001), and a rise in mean pulmonary artery pressure to 41.1 torr (P less than 0.001) and in pulmonary shunting (QS/QT) to 29.4% (P less than 0.001). Arterial oxygen tension (PaO2) fell to 62.0 torr (P less than 0.001), pulmonary lymph flow (QL) rose to 14.0 ml/hr (P less than 0.01), and lymph protein clearance (L/P.QL) to 8.9 ml/hr (P less than 0.01). Plasma thromboxane B2 (TxB2) increased to 2.43 ng/ml (P less than 0.025) and pulmonary lymph TxB2 to 3.02 ng/ml (P less than 0.005). Hemorrhagic shock was followed by a rise in PaO2 to 97.5 torr (P less than 0.01), a fall in QS/QT to 7.9% (P less than 0.005), QL to 5.0 ml/hr (P less than 0.05), and L/P QL to 2.9 ml/hr (P less than 0.05). During hemorrhage, plasma TxB2 rose to 2.18 ng/ml (P less than 0.005) and lymph TxB2 to 2.32 ng/ml (P less than 0.001). Infusion of ZAP during hemorrhagic shock was followed by a fall in WBC to 2,300/microliter (P less than 0.001); but QS/QT, PaO2, QL, and L/P.QL remained unchanged. After indomethacin and ZAP, WBC fell to 3,210/microliter (P less than 0.001), Ppa rose to 27.0 torr (P less than 0.05), QL rose to 8.3 ml/hr (P less than 0.05), and L/P.QL rose to 5.2 ml/hr (P less than 0.05). PaO2 fell to 75.0 torr (P less than 0.05) and QS/QT increased to 17.1% (P less than 0.005). The protective effect of hemorrhagic shock on ZAP-induced pulmonary dysfunction was not reversed by indomethacin. It is concluded that hemorrhagic shock prevents hypoxemia and increased pulmonary permeability induced by activation of the complement system by ZAP.

Animals↗