Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenaline was infused in incremental doses of 0.05 up to 0.1 microgram/kg/min over a 60-min period in nine patients with mild essential hypertension and six age-matched normotensive controls. Blood samples were drawn at preset time intervals and plasma adrenaline, platelet count, serum thromboxane B2 (TxB2) and plasma beta-thromboglobulin (beta-TG) were measured. Adrenaline levels (m +/- SEM) rose significantly, from 0.078 +/- 0.01 (baseline) to 0.902 +/- 0.03 ng/ml (60 min), in the hypertensive group; a similar increase was observed in the control group (from 0.049 +/- 0.007 to 0.877 +/- 0.03 ng/ml). Platelet count increased significantly at early time points and remained high throughout infusion in both groups (hypertensive from 250 +/- 25 to 305 +/- 24 x 10(3)/microliters, control from 219 +/- 16 to 260 +/- 18 x 10(3)/microliters). TxB2 levels likewise increased significantly from 15 minutes after initiation of infusion. In hypertensive subjects the mean resting value of 186 +/- 17 ng/ml rose to 312 +/- 42 ng/ml, while in control subjects the resting value of 174 +/- 29 ng/ml rose to 286 +/- 32 ng/ml. Baseline levels of TxB2 were found to be higher in the hypertensive patients but not significantly. beta-TG levels increased from an initial value of 43.84 +/- 3.69 ng/ml to 59.5 +/- 4.69 ng/ml at 60 min in the hypertensive group, while a similar change from 28.7 +/- 19.2 ng/ml to 40.36 +/- 3.16 ng/ml was observed in the control group. These changes were significant, as was the difference between basal values in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of adrenaline infusion on serum thromboxane B2 and plasma beta-thromboglobulin levels in hypertensive and normotensive subjects. 138 33

The goal of this study was to test the hypothesis that atherosclerosis alters responses of cerebral arteries and the ocular circulation to the activation in vivo of leukocytes and platelets. We measured blood flow to the brain and eye using microspheres and pressure in the cerebral microvessels of normal and atherosclerotic monkeys. The intracarotid injection of 10(-7) M N-formyl-L-methionyl-L-leucyl-L-phenylalanine to activate leukocytes did not alter cerebral blood flow in 11 normal or 10 atherosclerotic monkeys but increased the resistance of large cerebral arteries by 46 +/- 11% (mean +/- SEM) in the atherosclerotic animals. The injection of N-formyl-L-methionyl-L-leucyl-L-phenylalanine did not alter blood flow to the eye in 10 normal monkeys but decreased blood flow to the choroid by 38 +/- 9% in 11 atherosclerotic monkeys. The intracarotid injection of 3 x 10(-9) M prostaglandin E2, a leukocyte product, produced an increase in the resistance of large cerebral arteries in five atherosclerotic but not in six normal monkeys. Prostaglandin E2 reduced blood flow to the retina and choroid in the atherosclerotic monkeys by 62 +/- 22% and 65 +/- 17%, respectively. The intracarotid infusion of 25 micrograms/min collagen to activate platelets increased cerebral blood flow by 21 +/- 5% in 10 normal monkeys but did not alter it in 11 atherosclerotic monkeys. Collagen did not alter blood flow to the choroid in 10 normal monkeys but decreased it by 29 +/- 8% in 11 atherosclerotic monkeys.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of atherosclerosis on cerebral vascular responses to activation of leukocytes and platelets in monkeys. 205 80

The reticuloendothelial system, including the spleen, subserves important immunologic functions. Loss of splenic function results in an increased incidence of severe bacterial infections and is accompanied by thrombocytosis. Several nephrotic children were noted to have remarkably high platelet counts and predisposition to bacterial infection with encapsulated organisms. We, therefore, investigated the splenic function of nine children with primary nephrotic syndrome and measured the phagocytic function of the spleen by sequestration of Technetium-99-labelled heat-treated autologous RBC, administered intravenously. Four children had decreased splenic function. Repeat studies performed in two of these children after remission of the nephrotic syndrome gave normal results. There were six episodes of bacterial infection (3 peritonitis, 1 septic arthritis, 1 cellulitis, and 1 Escherichia coli urinary tract infection) among the four patients with decreased splenic function. There were no episodes of bacterial infection among the five nephrotic children with normal splenic function. Nephrotic patients with decreased splenic function had significantly increased platelet counts (921,000 +/- 196,000; mean +/- SEM) compared to those with normal function (435,000 +/- 46,000; P less than 0.001). Our findings suggest the possibility that some nephrotic children may have decreased splenic function in association with increased susceptibility to bacterial infections.
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PMID:Splenic hypofunction in the nephrotic syndrome of childhood. 370 96

Intracellular free (cytosolic) calcium has been reported to be increased in the platelets of patients with essential hypertension. We investigated the possibility that the high cytosolic calcium concentration may be caused by a circulating plasma factor, by incubating platelets from normotensive subjects with plasma ultrafiltrates from patients with essential hypertension. The cytosolic calcium concentration in normal platelets increased after incubation with plasma from patients with untreated hypertension (80 +/- 15 percent [+/- SEM]) or from patients in whom hypertension was well controlled by calcium-influx blockers (129 +/- 33 percent). In contrast, the cytosolic calcium concentration was unchanged after incubation with plasma from normotensive subjects. When platelets from the patients were incubated with plasma from the controls, cytosolic calcium in platelets decreased by more than 30 percent, into the normal range (P less than 0.01). These data demonstrate that plasma from patients with essential hypertension contains a substance that increases the cytosolic calcium concentration in platelets. Cytosolic calcium is a trigger for vascular smooth-muscle-cell contraction, and if the plasma factor acts on these cells as it acts on platelets, it may be responsible for the increased peripheral vascular resistance associated with hypertension.
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PMID:Effects of a circulating factor in patients with essential hypertension on intracellular free calcium in normal platelets. 380 94