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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six subjects cycled on two occasions for 10 min at power output of 188 +/- 11 W (means +/- SEM), which corresponded to 70 +/- 2% of their maximal oxygen uptake (VO2 max). The exercise intensity was either increased gradually in a stepwise manner over about 15 min (slow transition-S), or increased directly (direct transition-D) to the predetermined power output. Muscle samples from the quadriceps femoris muscle were taken at rest and immediately after exercise in both trials. During exercise with both D and S muscle lactate increased approximately 10 times (P less than 0.01), phosphocreatine decreased about 50% (P less than 0.01) and ADP increased about 20% (P less than 0.05). There were no significant differences between S and D (P greater than 0.05). Furthermore, blood lactate, O2 deficit, O2 debt, and the calculated increase in muscle content of inorganic phosphate (Pi) were all similar between D and S (P greater than 0.05). It is concluded that the O2 deficit and the anaerobic energy utilization is not affected by the rate of transition from rest to exercise. Consequently, the O2 deficit at the onset of exercise is not due to a delay in O2 transport, but may be due to a limited peripheral O2 utilization as a result of metabolic adjustments at the cellular level. Increases in ADP and Pi are suggested to be primary metabolic regulators which activate both aerobic and anaerobic energy production resulting in the O2 deficit.
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PMID:Oxygen deficit at the onset of submaximal exercise is not due to a delayed oxygen transport. 322 42

The effects of PGI2 and PGE1 on the ultrastructure of human platelets were studied by scanning (SEM) and transmission (TEM) electron microscopy in relation to the record of an optical aggregometer. Addition of PGI2 or PGE1 to citrated platelet-rich plasma (C-PRP) resulted in a permanent slight decrease in percent light transmission (%T) recorded by the aggregometer. SEM investigation of the platelets showed marginal pseudopods and occasional large stomata after application of prostaglandins. These alterations occurred within the initial 30 s and remained constant during the subsequent 20 min of incubation. TEM studies revealed morphological changes of alpha granules and moderately electron-dense material in the dilated profiles of the surface-connected canalicular system (SCCS). Addition of 10 microM ADP to C-PRP preincubated for 30 s with either 2 ng/ml (5 nmol/liter) PGI2 or 30 ng/ml (85 nmol/liter) PGE1 resulted in a further decrease of %T followed by a slight increase. The alterations of the aggregometer tracing were characterized in SEM by platelet shape change and the generation of primary aggregates. C-PRP samples preincubated with 3 and 9 ng/ml (8 nmol/liter and 24 nmol/liter) PGI2 or 40 and 120 ng/ml (113 nmol/liter and 338 nmol/liter) PGE1 did not produce additional changes in the aggregometer curves or in the ultrastructure of platelets in response to ADP. Our morphological study indicates that antiaggregatory prostaglandins induce an early phase of platelet activation but inhibit "shape change" and the formation of aggregates.
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PMID:PGI2 and PGE1 induce morphological alterations in human platelets similar to those of the initial phase of activation. 330 81

Thirteen men, age 60 +/- 2 years (mean +/- SEM) with mild hypertension, 151 +/- 4/95 +/- 3 mm Hg, completed a randomized, double-blind, placebo-controlled crossover trial of ketanserin therapy. In comparison to placebo, ketanserin treatment at 40 mg bid for 6 weeks lowered systolic and diastolic blood pressure, 148 +/- 4/92 +/- 3 vs. 140 +/- 6/86 +/- 3 mm Hg, P = 0.19/0.02. The rate of platelet aggregation in response to ADP and epinephrine was unchanged while the response to serotonin was greatly diminished. Neither the systemic pressor response nor the pupillary mydriatic response to phenylephrine was significantly altered. Plasma norepinephrine concentration declined significantly. Ketanserin reduced blood pressure, particularly the diastolic component, in elderly men with mild hypertension. While antagonism of serotonin's effects on platelet aggregation was evident, blockade of alpha 1-receptor-mediated events was not apparent. The results suggest that during chronic therapy the antihypertensive effects of ketanserin were mediated by serotonergic blockade and a possible lytic effect on sympathetic drive. The dual effects of ketanserin on blood pressure and platelet aggregation may be beneficial in reducing cardiovascular complications in hypertensive patients.
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PMID:Effects of ketanserin on blood pressure and platelet aggregation in elderly men with mild hypertension. 341 5

Surgical preparation of human saphenous vein for coronary artery bypass grafting involving distension and storage in iso-osmotic sodium chloride solution reduced tissue adenosine triphosphate (ATP) (mean(SEM] concentration from 280(20) nmol.g-1 wet wt (n = 25) to 140(30) nmol.g-1 wet wt (n = 12) and the adenosine triphosphate to adenosine diphosphate (ATP:ADP) concentration ratio from 2.4(0.1) to 1.2(0.2). Since removal of endothelium from freshly isolated vein did not affect ATP concentration or ATP:ADP ratio, these changes quantified medial damage. Distension of the vein at a pressure of 150 mmHg caused no change in ATP concentration or ATP:ADP ratio, but these values were reduced progressively by distension at 300 mmHg and 600 mmHg. Damage was not reversed but was exacerbated by subsequent incubation of the distended vein in blood. Distension of the vein at 600 mmHg caused release of tissue lactate dehydrogenase. The data show that acute medial damage can result from distension of the vein but that this does not occur at pressure equivalent to normal arterial pressure. Distension induced medial damage is unlikely to be rapidly reversible.
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PMID:Nature and pressure dependence of damage induced by distension of human saphenous vein coronary artery bypass grafts. 350 70

An isocratic HPLC system has been developed which allows for the rapid (single run of 20 min) measurement of creatine phosphate (PCr) and adenine nucleotides (ATP, ADP and AMP) in extracts from freeze-clamped and freeze-dried myocardial tissues. The separation was achieved at room temperature by using a RP18 column and a dual variable wavelength spectrophotometer, set at 210 and 254 nm. The solvent was 30 mM potassium dihydrogen phosphate, 15 mM tetrabutylammonium hydrogen sulfate, pH 6.7, 19% (v/v) acetonitrile. A distinct separation (confirmed with the retention time of standard sample) of these high energy compounds was achieved. Standard curves were linear. In isolated rat hearts the following values were obtained (mumol/g dry wt, mean +/- SEM): ATP 21.5 +/- 1.3, ADP 4.6 +/- 0.2, AMP 1.5 +/- 1.1 and PCr 32.5 +/- 1.3; which are consistent with previously published values for high energy compounds in this tissue.
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PMID:Simultaneous determination of myocardial creatine phosphate and adenine nucleotides by reversed-phase HPLC. 350 28

During exercise, ATP is converted to ADP and AMP to supply energy for muscular contraction. It is then regenerated via various pathways of intermediary metabolism. However, with high levels of exercise, net ATP degradation in muscle occurs. In exercise and other clinical situations, adenine nucleotide degradation leads to an accumulation of degradative purine products including hypoxanthine. In an effort to monitor events of energy metabolism, we examined plasma hypoxanthine levels at various exercise intensities. Peak plasma hypoxanthine levels after maximal exercise (18.9 +/- 2.6 microM, mean +/- SEM) were significantly greater than resting levels (1.1 +/- 0.1 microM; p less than 0.001). Hypoxanthine levels after steady state exercise at 52, 76, and 97% of ventilatory threshold did not exceed resting levels. However, plasma hypoxanthine rose significantly after exercise at 124% of ventilatory threshold (6.3 +/- 1.0 microM; p less than 0.01) and at 152% of ventilatory threshold (17.0 +/- 3.6 microM; p less than 0.001). Exercise at subventilatory threshold intensity (74% of ventilatory threshold) for a prolonged time period, such that total work equaled that performed at 152% of ventilatory threshold, did not elevate hypoxanthine levels (0.46 +/- 0.1 microM) above resting values. We conclude that elevation of plasma hypoxanthine levels occur during exercise at intensities that exceed the ventilatory threshold and indicate that net adenine nucleotide degradation has occurred.
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PMID:Plasma hypoxanthine and exercise. 360 51

The time course of ADP induced aggregation of human platelets was determined in aliquots of stored platelet rich plasma 3.5, 10, 30 and 100 minutes after venepuncture. The maximal rate of aggregation was found to increase throughout this entire period, even though pH (7.4), CO2 (7 volume per cent) and temperature (35 degrees C) of the samples were kept constant. The mean acceleration (+/- SEM) between 3.5 and 100 minutes was 41.7 +/- 6.9 per cent (n = 67) at an ADP-concentration of 1 mumol/l and 18.3 +/- 6.2 per cent (n = 23) at 2 mumol/l ADP. The effect did not result from changes of any platelet regulatory factors putatively present alone in the plasma. Acceleration of aggregability was only found when the platelets themselves underwent storage, but not when freshly prepared plasma was given to prestored platelets. The change in aggregability was not diminished after inhibition of platelet cyclooxygenase by oral administration of acetylsalicylic acid.
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PMID:Increasing platelet aggregability after venepuncture is platelet, not plasma derived. 371 16

The scanning (SEM) and transmission (TEM) electron microscopic appearance of blood cells was studied in correlation with the aggregometer tracing recorded after activation of whole blood samples by collagen or ADP. Early morphologic alterations of platelets characterized by the formation of marginal pseudopods and bulbous protrusions were not indicated by the aggregometer. The initial increase in impedance was caused by the attachment of platelets displaying typical shape change morphology at the surface of the electrode wires joint with collagenous fibrils in collagen activated specimens. During further increase in impedance, aggregates were detectable in the blood suspension and at the electrode, the number and size of which increased up to the maximal extension of the aggregometer tracing. Using low doses of ADP (2-3 microM), dissociation of aggregates in the blood suspension was detectable by SEM, which was not recorded by the aggregometer tracing indicating further limitation of the impedance aggregometer. In collagen activated samples, platelet aggregates were covered by PMN and monocytes that in TEM displayed distinct phagocytosis of platelet fragments and fibrin masses. In ADP specimens, activation of leukocytes was only rarely detectable. The detection of mixed aggregates may be important for further employment of the impedance aggregometer in the diagnosis of hematologic diseases.
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PMID:Morphologic alterations of blood cells in the impedance aggregometer. 383 70

Rat reticulocytes contain a cytosol activator protein (RCAP) that augments hormone-sensitive adenylate cyclase activity in the rat reticulocyte and other systems. In a previous publication, using a highly purified preparation of RCAP, we reported that the stimulatory guanine nucleotide-binding protein (Ns) was required for the actions of RCAP. We investigated this possibility by studying the actions of RCAP on cholera toxin-dependent ADP ribosylation of Ns. RCAP decreased cholera toxin-dependent ADP ribosylation of the 42,000-dalton subunit of Ns of reticulocyte [40.2 +/- 3.7 (+/-SEM) to 26.5 +/- 3.8 fmol/mg; n = 10; P less than 0.001], S49 wild-type (33.9 +/- 2.4 to 24.9 +/- 2.8 fmol/mg; n = 9; P less than 0.01), and UNC (25.3 +/- 3.5 vs. 17.6 +/- 3.1; n = 5; P less than 0.02) membranes. In contrast, pertussis toxin-dependent ADP-ribosylation of the inhibitory guanine nucleotide binding protein, Ni in reticulocyte, S49 wild-type lymphoma, and its UNC and cyc- variant membranes were all significantly augmented by RCAP. Moreover, when reticulocyte Ni was functionally ablated by exposure to pertussis toxin, RCAP no longer enhanced isoproterenol-responsive adenylate cyclase activity in reticulocyte membranes. These results suggest that RCAP stimulates adenylate cyclase activity by inhibiting Ni function, thus permitting enhanced Ns coupling to the adenylate cyclase enzyme (C).
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PMID:Reticulocyte cytosol activator protein: effects on the stimulatory and inhibitory regulatory proteins of adenylate cyclase. 392 80

The release of vasodilating substances from the vascular endothelium has been postulated to depend on a rise in the level of intracellular free calcium (Cai++). We measured Cai++ in intact monolayers of calf endothelial cells, grown in culture, that were loaded with the fluorescent calcium indicator quin 2. Fluorescence (excitation wavelength 340 nm, emission wavelength 492 nm) was calibrated by raising Cai++ to a maximum with the calcium ionophore ionomycin (0.1 microM) and by lowering it to a minimum with ionomycin plus manganese (0.4 mM), which quenches quin 2 fluorescence completely. Loss of fluorescent dye from the cells was calculated from fluorescence at the isosbestic excitation wavelength (365 nm). Resting Cai++ was 71 +/- 3 (SEM) nM. ATP (adenosine-5'-triphosphate) raised Cai++ dose-dependently and reversibly to 458 +/- 60 nM at a concentration of 10 microM, and at 0.1 mM to values close to those that occurred under ionomycin. ADP (A-5'-PP) and AMP (A-5'-P) had smaller effects with a maximal Cai++ of 287 +/- 72 nM at 30 microM ADP and 176 +/- 17 nM at 0.1 mM AMP. At these concentrations, ADP and AMP attenuated significantly the increase of Cai++ under ATP (10 microM). Adenosine (0.1 or 0.3 mM) and acetylcholine (0.1 to 30 microM) enhanced Cai++ inconsistently, by a maximum of 50 nM. These effects were abolished by theophylline and atropine, respectively. In the absence of extracellular calcium, ATP still raised Cai++, although endothelial responsiveness declined after repetitive stimulations. We conclude that activation of purinergic receptors increases intracellular free calcium in endothelial cells, and that this increase is probably an essential trigger for synthesis of prostacyclin and the labile endothelium-derived relaxant factor.
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PMID:Increased free calcium in endothelial cells under stimulation with adenine nucleotides. 394 90


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