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)

11 patients with histories of clinical bleeding were selected as examples of platelet release abnormality. Mean bleeding time was 18 +/- 2.6 min (normal +/- SEM; 6 +/- 0.44); mean platelet adhesiveness was 9.9 +/- 4.3% (normal +/- SEM; 30 +/- 2.2). Clot retraction and platelet factor 3 were normal. Platelet aggregation with adenosine diphosphate (ADP), epinephrine and collagen was decreased, as was 14C-serotonin release. Electron microscopic studies of platelets exposed to epinephrine showed 2 subgroups: one which failed to aggregate or have centralization of organelles and a second which developed pseudopodia and centralization of organelles, but rarely aggregated or degranulated. Measurements of activity of adenylate cyclase and phosphodiesterase under basal conditions were performed on platelets from patients and control subjects. Adenylate cyclase activity was significantly lower and phosphodiesterase activity significantly higher in the patient group. Prostaglandin E1 was a potent stimulator of adenylate cyclase in both groups, as was NaF. It was concluded that the causative defects with "platelt release abnormality" do not reside in either the activity of adenylate cyclase or of phosphodiesterase. Changes in formation and destruction of cyclic adenosinemonophosphate (AMP) may instead be regarded as a compensatory response to a defect in another effector system.
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PMID:Adenylate cyclase and phosphodiesterase activity in the platelet release abnormality. 20 56

Two dogs were prepared with Pavlov pouches of the fundic area of the stomach using standard techniques. During treatment periods of 14 days, 200 mg acetylsalicylic acid (ASA) was introduced into the pouch twice daily by insufflation. One hour after each drug administration the pouch was washed with saline and the fluid assayed for blood. Bleeding from the pouch increased to a maximum on the 3rd or 4th day of the treatment period and subsequently declined such that by the 8th day blood loss was minimal and approximated that found during control periods. Platelet aggregation (in vitro) responses to adenosine diphosphate were significantly (p less than 0.01) inhibited on day 3 when aggregation curve heights were reduced by 66.2 +/- 13.11% (mean +/- SEM) from control values. On day 7 and during the ensuing 7-day period when ASA was given twice daily, the heights of aggregation responses were reduced by only 20-30% from controls. These responses were significantly (p less than 0.001) greater than those found on day 3. Similar changes in platelet reactivity were found in plasma from rats given ASA twice daily for 7 days. Aggregation responses to collagen were depressed by 95.5 +/- 4.49% on day 1 following two doses of ASA. As the treatment period continued, the aggregation responses increased in magnitude until the 7th day they were similar in height to those from control animals. The mechanism involved in this adaptation to ASA treatment seen with these platelets is not known.
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PMID:Changes in platelet function and gastrointestinal bleeding following repeated administration of acetylsalicylic acid in the rat and the dog. 31 83

Platelets eluted from nylon fiber filters after filtration leukapheresis have been studied. The platelet yield from 61 routine donations was 1.25 +/- 0.18 x 10(11), (mean +/- SEM) corresponding to 1.78 x 10(10) per 500 ml blood processed. Filtered platelets labeled with radiochromate demonstrated reduced recovery in vivo 15 minutes after infusion (38.5 +/- 1.7%) when compared to the control value (68.5 +/- 6.8, p less than 0.001). The survival of those platelets remaining in the circulation after 15 minutes did not however differ from the control value. ADP (10 micrometer, 1 mM), adrenaline (100 micrometer) and collagen (7.25 mg/ml) added in vitro induced less aggregation of filtered platelets than normal control platelets and electron microscopy revealed structural abnormalities. It is concluded that recipients of granulocyte transfusions obtained by filtration leukapheresis are unlikely to be benefited by the platelets contained in these transfusions.
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PMID:Studies on platelets contained in eluates following filtration leukapheresis. 43 22

The authors had previously found an inverse correlation between per sperm creatine phosphokinase activity and sperm concentrations in men. Because creatine phosphokinase is a key enzyme in sperm energy transport, the possible relationship of sperm creatine phosphokinase activity, sperm adenosine triphosphate (ATP) concentrations, sperm ATP/ADP (adenosine diphosphate) ratios, and computer-aided semen analysis sperm motility parameters were then studied. The ATP concentrations and ATP/ADP ratios, measured by high-pressure liquid chromatography in washed sperm, were similar in normospermic and oligospermic specimens (ATP: 123.1 +/- 21.6 vs. 90.0 +/- 24.5 pmol/10(6) sperm; ATP/ADP: 2.8 +/- 0.4 vs. 2.1 +/- 0.4, N = 32 and 17, mean +/- SEM), and in samples with normal and less than 40% sperm motility (ATP: 96.8 +/- 27.2 vs. 122.2 +/- 19.6 pmol/10(6) sperm; ATP/ADP: 2.4 +/- 0.5 vs. 2.8 +/- 0.4, n = 26 and 23). In the swim-up sperm fractions, which showed improved motility, the ATP concentrations, but not the ATP/ADP ratios, were lower than in the initial semen samples (ATP: 152.9 +/- 28.4 vs. 90.3 +/- 10.6 pmol/10(6) sperm, P less than 0.05; ATP/ADP: 3.3 +/- 0.5 vs. 3.9 +/- 0.7, N = 18 pairs of samples). This is consistent with our previous finding of a lower cytoplasmic content in sperm in swim-up fractions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adenosine triphosphate (ATP) concentrations and ATP/adenosine diphosphate ratios in human sperm of normospermic, oligospermic, and asthenospermic specimens and in their swim-up fractions: lack of correlation between ATP parameters and sperm creatine kinase concentrations. 139 31

The potential reversal of platelet aggregation in vitro by nitroglycerin in low concentrations was explored using both optical aggregometry and electron microscopy. Venous blood was collected from a cohort of normal volunteers (20 men and 10 women) aged 21 to 65 years. Aggregation in platelet-rich plasma was induced by adenosine diphosphate in concentrations just sufficient to maintain a steady state of aggregation, without a spontaneous disaggregation phase (3.5 to 5 microM). Administration of nitroglycerin after the induction of aggregation caused both inhibition of the primary wave of developing aggregation and marked disaggregation. This combined effect was maximal when nitroglycerin was added at 0.5 minute after the beginning of aggregation. The observed reversal of platelet aggregation by nitroglycerin was concentration-dependent. Significant effects occurred with nitroglycerin concentrations greater than or equal to 10(-8) M. Concentration associated with 50% reversal of aggregation was 1.52 +/- 0.24 (SEM) x 10(-6) M. Electron microscopy revealed that 10(-6) M nitroglycerin induced a significant reduction in both platelet clumping and morphologic changes associated with aggregation. The results of the current study suggest a beneficial antiplatelet effect of nitroglycerin in restoring homeostasis in the face of incipient platelet aggregation. The clinical use of nitroglycerin in patients with acute ischemic syndromes may rest on this action.
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PMID:Reversal of human platelet aggregation by low concentrations of nitroglycerin in vitro in normal subjects. 151 34

Changes in energy metabolism after 70% partial hepatectomy were investigated in normal and carbon-tetrachloride-(CCl4)-induced-cirrhotic rats by evaluating hepatic mitochondrial ATP synthesizing activity as well as liver tissue levels of adenine nucleotides and lipid peroxide. Preoperative concentrations of ATP and total adenine nucleotides (TAN: ATP + ADP + AMP) in mumol/g dry weight (dw) and the energy charge potential (ECP) in the cirrhotic livers were 8.53 SEM 0.25, 14.73 SEM 0.54, and 0.74 SEM 0.01, respectively, and were significantly lower than those of normal livers (12.04 SEM 0.34, 15.75 SEM 0.12, and 0.86 SEM 0.01, P less than 0.01 in TAN). There was no difference in the preoperative mitochondrial phosphorylation rate (PR = x 10(-10) mol ATP/sec per mg mitochondrial protein) between normal and cirrhotic livers (21.01 SEM 0.95 and 21.55 SEM 1.03, respectively). After hepatectomy, in the normal livers these values decreased slightly after 12 h, remained low until 48 h, and returned to the preoperative value at 72 h. PR was remarkably enhanced and reached the maximum level of 32.54 SEM 2.07 at 24 h (P less than 0.001, compared to the sham-operated rats) and gradually returned to the preoperative value at 72 h. In the cirrhotic livers, ATP and ECP levels were drastically decreased at 12 h and recovered to the preoperative levels within 24 h, while TAN level remained unchanged. Enhancement of PR was not observed in any of the cirrhotic livers during the experiment. Lipid peroxidation was transiently increased postoperatively with no difference between normal and cirrhotic livers both in the sham-operated and the hepatectomized rats. These findings suggest that the energy status was more depressed in the cirrhotic livers than in normal livers both before and after hepatectomy. This depressed energy status might be attributed to the low preoperative tissue levels of adenine nucleotides and ECP level in the cirrhotic livers as well as to the absence of the enhancement of PR in the remnant livers.
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PMID:Absence of mitochondrial enhancement in the remnant liver after partial hepatectomy in cirrhotic rats. 152 68

Cytosolic free adenosine diphosphate (ADP) concentration in remnant rabbit liver 24 hours after 70% hepatectomy was calculated from the measured components of the glyceraldehyde-3-phosphate dehydrogenase:3-phosphoglycerate kinase/lactate dehydrogenase reaction. The concentration of free cytoplasmic ADP of the remnant liver increased from the control value of 76.9 +/- 6.0 mumol/L to 208.8 +/- 31.9 mumol/L (mean +/- SEM) at 24 hours after hepatectomy. The calculated free ADP provides the following three interpretations with respect to mitochondrial respiration acceleration as a result of liver regeneration. First, the Michaelis-Menten equation for physiologic respiration relative to maximal respiration gave 1.16 as the value of acceleration. Next, the classical thermodynamic theory showed that the logarithm of [adenosine triphosphate]/[free ADP] [free inorganic phosphate], which is reciprocally correlated with mitochondrial respiration, was decreased by a factor of 0.78 after hepatectomy. Finally, the irreversible thermodynamic theory indicated that chemical affinity, which is linearly correlated to mitochondrial respiration, was increased 1.36 times. These interpretations suggest that the rate of mitochondrial respiration is accelerated after major hepatectomy.
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PMID:A role of cytoplasmic free adenosine diphosphate in regenerating rabbit liver. 158 84

Thirteen patients suffering from acute malaria attack and thirteen apparently healthy human volunteers (control) were used for the study. Platelet aggregation was determined by platelet count ratio technique in which a reduction in platelet count ratio signified an increase in platelet aggregation. Platelet count ratio in acute malaria patients was 0.75 +/- 0.03 (SEM). Platelet count ratio in subjects used as control was 0.88 +/- 0.02. This value was significantly higher than the former (P less than 0.001). Platelet count ratio correlated negatively with the degree of parasitaemia (r = -0.71; P less than 0.01). ADP, a platelet aggregating drug, also reduced platelet count ratio in rats significantly. Acute malaria attack therefore enhances platelet aggregation in vivo.
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PMID:In vivo platelet aggregation in acute malaria. 168 3

This study compared new and traditional measures of platelet function in 16 patients with severe peripheral arterial occlusive disease and 15 age-matched controls. Circulating platelets were characterized by the use of fluorescence flow cytometry to assess platelet aggregate formation and expression of the secretion-dependent alpha granule membrane protein GMP-140, by measurement of plasma beta-thromboglobulin (beta-TG), and by performance of platelet-rich plasma aggregation studies. In addition, blood samples were treated with graded concentrations of adenosine diphosphate (ADP; 0 to 10 mumols/L) to characterize by fluorescence flow cytometry the secretory and aggregatory responses to mild stimulation. No differences were detected between the two groups with regard to platelet function in unstimulated circulating blood by use of these techniques. Values (mean +/- SEM) observed were: GMP-140-positive platelets, 11% +/- 3% versus 13% +/- 2%; platelet aggregates in circulating whole blood, 4% +/- 1% versus 9% +/- 3%; plasma beta-TG, 92 +/- 12 versus 94 +/- 22 ng/ml; and ED50 (concentration of ADP required to produce half maximal aggregation), 3.8 +/- 1.1 versus 3.1 +/- 0.5 mumol/L in the patients with peripheral arterial occlusive disease and controls, respectively. Treatment with ADP caused a dose-related increase in GMP-140 expression in both groups, without significant differences in this parameter between the groups at any given concentration. However, stimulation with ADP concentrations greater than 1 mumol/L resulted in more frequent aggregate formation in the control than in the peripheral arterial occlusive disease group (25% +/- 4% versus 11% +/- 2%, respectively at 5.0 mumols/L, p = 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Flow cytometric assessment of platelet function in patients with peripheral arterial occlusive disease. 172 Apr 68

The quantification of adenine nucleotides released from the heart is hampered by their rapid dephosphorylation to adenosine in the extracellular space catalyzed by highly active ectonucleotidases. To determine the total release of adenine nucleotides from isolated Langendorff-perfused guinea pig hearts, ecto 5'-nucleotidase was effectively blocked by infusion of alpha, beta-methylene-ADP (AOPCP, 50 microM). Adenine nucleotides were measured in the coronary venous effluent by the luciferin-luciferase method after enzymatic rephosphorylation to ATP. In hearts perfused at a constant flow rate (10 ml/min) with normoxic buffer (95% O2, 5% CO2) the release +/- SEM of adenine nucleotides and adenosine was 0.06 +/- 0.01 (n = 11) and 0.04 +/- 0.01 (n = 13) nmol/min. In the presence of AOPCP, the release of adenine nucleotides increased to 0.43 +/- 0.04 nmol/min (n = 9; p less than 0.05), whereas adenosine remained unchanged. Hypoxic perfusion (10% O2, 85% N2, 5% CO2) caused a threefold increase in adenine nucleotide release but a 40-fold increase in adenosine. In contrast, global ischemia (30 seconds) caused adenine nucleotide and adenosine release to rise to similar values of 1.06 +/- 0.10 and 0.80 +/- 0.14 nmol/min (n = 9). Stimulation of hearts with isoproterenol (4 nM) likewise increased the release of adenine nucleotides (0.50 +/- 0.04 nmol/min) and adenosine (0.87 +/- 0.21 nmol/min) (n = 6). To determine the cellular source of adenine nucleotides released from the heart, the coronary endothelial adenine nucleotide pool was selectively prelabeled by [3H]adenosine. Global ischemia increased the specific radioactivity of released adenine nucleotides by 57%. The findings indicate that 1) adenine nucleotides and adenosine are released at the same order of magnitude from the well-oxygenated heart; 2) beta-adrenergic stimulation and ischemia stimulate the release of adenine nucleotides and adenosine, both purines reaching vasoactive concentrations in the effluent perfusate; 3) during hypoxic perfusion only the release of adenosine is greatly enhanced; and 4) the coronary endothelium preferentially contributes to the ischemia-induced adenine nucleotide release.
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PMID:Adenine nucleotide release from isolated perfused guinea pig hearts and extracellular formation of adenosine. 174 67


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