bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sex Differences in Correlates of Steady State and Pulsatile Component of Blood Pressure
Authors: Scuteri A. , Cacciafesta A. M. , Di Bernardo M. G. , De Propris A. M. , Recchi D. , Celli V. , Idone G. , Nocco M. L. , Marigliano V. 
Published: August 2015

1. The aim of the present study was to evaluate whether metabolic factors are linked to the steady component and the pulsatile component of blood pressure, evaluated as mean arterial pressure and pulse pressure respectively, in a sex-specific manner. 2. A cohort of 299 subjects (152 males, 147 females; 25–80 years of age) was studied. Patients presenting congestive heart failure, coronary insufficiency, severe valvular heart disease, neurological accident in the last 6 months, renal or respiratory failure, cancer, diabetes mellitus or acute infectious disease were excluded. None of the women was taking oral contraceptives or oestrogen supplementation. All cardioactive drugs were withdrawn at least 2 weeks before the subjects entered the study.
3. Men presented higher mean arterial pressure (120 ± 15 compared with 115 ± 16 mmHg, P &lt; 0.01) and lower pulse pressure values (63 ± 16 compared with 67 ± 18 mmHg, P &lt; 0.05) than women. In men, no significant relation between mean arterial pressure and the tested variables was detected; multiple regression analysis demonstrated that age contributed independently to the model for pulse pressure with a multiple r2 of 0.10 (P &lt; 0.01). In women, body mass index contributed independently to the model for mean arterial pressure, with a multiple of 0.12 (P &lt; 0.005); age and, to a lesser extent, body mass index, glycaemia and triglyceridaemia persisted as independent determinants of pulse pressure at the multiple regression analysis, with a multiple r2 of 0.20 (P &lt; 0.001).
4. Our findings suggest that metabolic risk factors are associated differently with pulse pressure and mean arterial pressure values in the two sexes.
Augmented Thermic Effect of Amino Acids under General Anaesthesia Occurs Predominantly in Extra-Splanchnic Tissues
Authors: Selldén Eva , Bränstróam Robert , Brundin Tomas 
Published: August 2015

1. Intravenous infusion of amino acid mixtures stimulates human oxidative heat production more effectively under general anaesthesia than in the unanaesthetized state. To analyse the splanchnic and extra-splanchnic regional distribution of this stimulation, whole body and splanchnic oxygen uptake, blood flow and blood temperatures were measured by a catheterization technique in 14 patients undergoing isoflurane anaesthesia for abdominal surgery. During the anaesthesia period, a mixture of 19 amino acids (240 kJ/h) was infused intravenously into seven of the patients while the others served as controls, receiving isovolumic infusions of a nutrient-free saline solution.
2. Whole body oxygen consumption fell by ≈ 40% during anaesthesia and surgery in the controls. Approximately 80–95% of the reduction occurred in the extra-splanchnic tissues. The splanchnic oxygen uptake fell by 31 ± 6% in the controls during the initial phase of anaesthesia, after which it returned to the pre-anaesthesia level. The initial reduction of the controls' splanchnic oxygen consumption accounted for only ≈23% of the simultaneous anaesthesia-induced reduction in pulmonary oxygen uptake. No initial reduction of the splanchnic oxygen uptake was observed in the patients treated with amino acid.
3. The amino acid infusion stimulated the whole body oxidative heat production by ≈18 W during anaesthesia and surgery and by ≈70 W at the emergence from anaesthesia. Approximately 74% of the stimulation occurred in the extra-splanchnic tissues. At awakening, the splanchnic oxygen uptake rose to ≈64% above the pre-anaesthesia level in the amino acid group.
4. During the entire period of anaesthesia, the whole body heat content fell by 282 ± 68 kJ in the controls and by 57 ± 25 kJ in the amino acid group. Amino acid treatment thus prevented ≈80% of the anaesthesia-induced reduction in whole body heat content.
5. During anaesthesia and surgery, cardiac output was ≈25% and ≈6% below the baseline, pre-anaesthesia levels in the control and amino acid groups, respectively. At awakening, it rose to ≈44% above baseline in the amino acid group while in the controls it remained unchanged. In both groups the splanchnic blood flow was unaffected by anaesthesia or by amino acid infusions.
Time Course Study of Oxidative Stress in Aorta and Heart of Diabetic Rat
Authors: Kakkar Rakesh , Mantha Subrahmanyam V. , Kalra Jawahar , Prasad Kailash 
Published: August 2015

1. Oxygen free radicals have been suggested to be a contributory factor in complications of diabetes mellitus. In the present study, we investigated the lipid peroxide level [thiobarbituric acid-reactive substances (TBARS)] and activities of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) in aorta, heart and blood of control and streptozotocin-induced diabetic rats at various stages of development of diabetes (0 to 6 weeks).
2. There was no change in the TBARS levels of aorta, heart and blood in the control group. A significant (P &lt; 0.05) increase in TBARS levels of aorta, heart and blood was observed in the diabetic group.
3. There were no significant changes in the activities of superoxide dismutase, catalase and glutathione peroxidase in the aorta, heart and blood of control rats at all time intervals. In the diabetic group, there was a significant (P &lt; 0.05) increase in the activity of superoxide dismutase and glutathione peroxidase in aorta from the fourth week onwards while the activity of catalase increased at all time intervals. In the heart of diabetic rats, the activity of total superoxide dismutase and Cu—Zn-superoxide dismutase increased significantly (P &lt; 0.05) from the second week onwards while activity of Mn-superoxide dismutase decreased at the fourth week and increased at the sixth week. The activity of catalase and glutathione peroxidase increased significantly (P &lt; 0.05) at all time intervals. In the blood, the activity of superoxide dismutase and glutathione peroxidase increased from the third week while catalase activity increased from the fourth week.
4. The present findings suggest that oxidative stress starts at early onset of diabetes mellitus and increases progressively.
Validation of the Supine Venous Pump Function Test: A New Non-Invasive Tool in the Assessment of Deep Venous Insufficiency
Authors: Janssen M. C. H. , Claassen J. A. H. R. , Van Asten W. N. J. C. , Wollersheim H. , De Rooij M. J. M. , Thien TH. 
Published: August 2015

1. A new non-invasive test was developed to assess calf muscle pump function: the supine venous pump function test. The technique uses strain-gauge plethysmography and is performed in the supine position. The method is superior to other non-invasive methods because basically the most essential haemodynamic parameter, venous pressure decrease, is used by properly converting venous volume measurements into venous pressure. The validity of this test was established by comparison with invasive venous pressure measurements and by determining the reproducibility. Additionally, normal values were determined.
2. In 28 extremities the supine venous pump function test was performed simultaneously with invasive venous pressure measurements. The reproducibility of the test was assessed in 10 randomly chosen volunteers. In 34 volunteers normal values were obtained and 26 patients with clinical venous insufficiency were examined.
3. Comparison of the two methods revealed a correlation coefficient of r = 0.98 (P &lt; 0.001). A mean difference of 3.9%pf between both methods was found with limits of agreement of − 6.3%pf to 14.1%pf. The coefficient of repeatability was 13%pf and the coefficient of variation was 9%. The normal range was found to be &gt;60%pf. The mean pump function in the patient group was 45%pf.
4. The limits of agreement are small enough to be confident that the supine venous pump function test can be used instead of invasive venous pressure measurements to assess calf muscle pump function in clinical practice. The reproducibility of the test is good.
Cerebral Oxidative Metabolism in Hypertension
Authors: Dickinson C. John 
Published: August 2015

1. The evidence is now overwhelming that so-called ‘essential’ hypertension in man, i.e. high systemic arterial pressure for no apparent cause, is commonly initiated by increased efferent sympathetic activity directed to the cardiovascular system. Eventually structural and other changes take place in the heart, kidneys and blood vessels. These may reinforce, augment and even conceal the initially neurogenic background. The cause of the increased sympathetic activity remains in dispute, but it is probably not psychological in most cases.
2. The brain has a high requirement for energy — twice that of the heart, at rest. In the normotensive adult, the brain's needs are met almost exclusively by the oxidation of glucose. This results in a cerebral respiratory quotient for the brain of approximately unity. The brain can utilize other materials, notably ketones, as it does to a considerable extent in the fetus. It retains this capability in adult life, even though normal adults do not make use of it.
3. In human hypertension the cerebral respiratory quotient falls in proportion to the rise of arterial pressure, indicating the consumption of other fuels in addition to glucose. β-Hydroxybutyrate is certainly one of these, but fatty acids may also be utilized.
4. A similar or greater reduction of cerebral respiratory quotient than in essential hypertension is seen in chronic cerebrovascular disease and in chronic heart failure in man. This raises the possibility that although cerebral blood flow is only slightly reduced in hypertensive patients at rest, the cerebral circulation is potentially under threat. The change in the pattern of oxidative metabolism may be looked upon as an adaptation to the threat. This would fit in with strong epidemiological and pathological evidence linking hypertension with cerebral, especially vertebrobasilar, atheroma.
5. Many of the pathophysiological changes in essential hypertension have parallels in the spontaneous hypertensive rat and its stroke-prone variant. Such rats have an impaired cerebral blood supply. Infarctions are easily produced by arterial occlusions which have little adverse effect on Wistar—Kyoto rats. Spontaneous hypertensive rats and stroke-prone spontaneous hypertensive rats also have reduced cerebral glucose utilization, which mirrors the situation in essential hypertension.
6. The Cushing response — threatened medullary ischaemia activating sympathetic vasomotor efferent nerves — could provide the mechanism by which chronic borderline or intermittent cerebral circulatory inadequacy passed a signal to activate sympathetic efferent nerves, either directly or through altered brain metabolism.
7. Other interpretations are possible, but the evidence of this review suggests that further investigation of cerebral oxidative metabolism in hypertension and in related conditions may shed light on the still elusive aetiology of essential hypertension.
Impaired Endothelium-Dependent and Independent Dilatation of Forearm Resistance Arteries in Men with Diet-Treated Non-Insulin-Dependent Diabetes: Role of Dyslipidaemia
Authors: Watts G. F. , O'brien S. F. , Silvester W. , Millar J. A. 
Published: August 2015

1. We measured endothelium-dependent and independent dilatation of forearm resistance arteries in 29 men with diet-treated non-insulin-dependent diabetes mellitus and 18 age- and sex-matched control subjects. None of the diabetic patients had hypercholesterolaemia, overt hypertension or microproteinuria.
2. We examined endogenous and exogenous nitric oxide-mediated vasodilatation by measuring forearm blood flow with venous occlusive plethysmography after administration of acetylcholine (7.5 and 15 μg/min) and sodium nitroprusside (3 and 10 μg/min), respectively, into the brachial artery. NG-monomethyl-l-arginine was also infused to study the inhibition of basal and stimulated release of nitric oxide.
3. The vasodilatory response to acetylcholine, expressed as area under curve, was significantly decreased in the diabetic patients compared with the control subjects (P = 0.019). NG-monomethyl-l-arginine significantly reduced basal (P &lt; 0.001) and acetylcholine-stimulated blood flow (P &lt; 0.02) in both groups. The vasodilatory response (also expressed as area under curve) to sodium nitroprusside was significantly less (P = 0.044) in the diabetic patients than in the control subjects.
4. In the diabetic patients, impaired vasodilatory responses to acetylcholine were significantly correlated with higher serum triacylglycerols (P = 0.048) and lower high-density lipoprotein-cholesterol concentrations (P = 0.007); the association with high-density lipoprotein was independent of age, glycated haemoglobin and blood pressure. Sodium nitroprusside responses were not correlated with lipid and lipoprotein concentrations.
5. We conclude that there is impaired endothelial and smooth muscle cell function in men with diet-treated non-insulin-dependent diabetes mellitus uncomplicated by overt hypertension or microproteinuria. Endothelial dysfunction may be related to diabetic dyslipidaemia and associated metabolic disturbances.
Effects of Limb Immobilization on Cytochrome C Oxidase Activity and GLUT4 and GLUT5 Protein Expression in Human Skeletal Muscle
Authors: Blakemore Stephen J. , Rickhuss Peter K. , Watt Peter W. , Rennie Michael J. , Hundal Harinder S. 
Published: August 2015

1. We investigated the effects of limb immobilization (for 1 or 6 weeks) in a long leg cast after a closed tibial fracture (n = 11). Biopsies of vastus lateralis were taken on admission and after either 1 week (n = 5) or 6 weeks (n = 6) and analysed for muscle fibre type characteristics, cytochrome c oxidase activity and the abundance of GLUT4 and GLUT5 hexose transporters.
2. After 1 week of immobilization there was a significant decrease (8%) in the cross-sectional area of type I, but not type II, muscle fibres and in the protein—DNA ratio (16%) compared with the initial biopsy. Six weeks of immobilization led to further muscle atrophy compared with the initial biopsy and a further reduction in the cross-sectional area of both type I and II fibres (29% and 36% decrease respectively) and in the protein—DNA ratio (25%). No changes were observed in the free leg after 1 week. However, at the end of the 6 week study period, the cross-sectional area of both type I and II fibres of the free leg were increased (7% and 5%) and there was significant increase in the protein—DNA ratio (14%), indicating a net increase in muscle protein content.
3. Assay for cytochrome c oxidase activity showed significant reduction after 1 (30%) or 6 weeks (36%) of immobilization, reflecting a reduced capacity for oxidative metabolism. No significant changes in activity were observed in muscle from the free leg after 1 or 6 weeks of study.
4. The concentrations of GLUT4 and GLUT5 protein were determined by Western blot analysis. Limb immobilization induced a marked (50%) reduction in muscle GLUT4 protein concentration after 1 week that persisted for 6 weeks. A transient but significant increase (approximately twofold) in GLUT4 concentration was detected in muscle from the free leg after 1 week, but this returned to preimmobilization values at 6 weeks. Unlike GLUT4, no significant changes in the abundance of the GLUT5 protein were detected in either the immobilized or free leg at the end of the 1 or 6 week periods.
5. The present findings indicate that disuse rapidly induces a selective loss of activity and abundance of some non-myofibrillar proteins in humans. The decrease in GLUT4 protein abundance and cytochrome c oxidase activity during muscle disuse is consistent with a decreased capacity for glucose uptake and with a lower oxidative potential of inactive muscle. The lack of any major changes in GLUT5 protein abundance during limb immobilization indicates that the expression of some non-myofibrillar proteins is differentially regulated in response to muscle disuse.
Chronic Administration of Octreotide Increases Vascular Responsiveness in Rats with Portal Hypertension
Authors: Huang Yi-Tsau , Tsai Ju-Fen , Liu Tsun-Bin , Hong Chuang-Ye , Yang May C.-M. , Lin Han-Chieh 
Published: August 2015

1. It has been reported that octreotide partially corrects the hyperdynamic state in patients and animals with portal hypertension. The aim of the present study was to investigate whether chronic administration of octreotide can increase vascular responsiveness in rats with portal hypertension.
2. Portal hypertension was induced by partial portal vein ligation. Octreotide was given for 9 days subcutaneously (100 μg/kg every 12 h) starting 1 day before ligation. The aorta and mesenteric artery were then removed to study contraction after pressure recording.
3. Octreotide treatment significantly reduced portal pressure and plasma glucagon concentrations compared with the vehicle-treated group. Both phenylephrine and vasopressin induced concentration-dependent contractile responses in the aorta and mesenteric artery from both groups. The maximum contractile responses to phenylephrine and vasopressin in aorta and mesenteric artery were significantly greater in the octreotide-treated group than in the vehicle-treated group. The EC50 values for phenylephrine and vasopressin were significantly different in the aorta, but not in the mesenteric artery, between the two groups. In contrast, octreotide treatment did not alter the contractile responsiveness of arteries from sham-operated rats.
4. These results show that, in rats with portal vein stenosis, octreotide increases arterial contractile responsiveness and reduces portal pressure.
No Relation between Angiotensin-Converting Enzyme Gene Polymorphism and Dermal Responses to Bradykinin in Healthy Subjects
Authors: Chadwick I. G. , Kraskiewicz M. , Yeo W. W. , Higgins K. S. , Jackson P. R. , Ramsay L. E. 
Published: August 2015

1. The dermal wheal response to bradykinin is increased by drugs which inhibit angiotensin-converting enzyme, and thus provides a measure of angiotensin-converting enzyme activity at the tissue level. An insertion/deletion polymorphism of the angiotensin-converting enzyme gene predicts serum angiotensin-converting enzyme activity, but its relation to angiotensin-converting enzyme activity in tissue is unclear.
2. The relations between angiotensin-converting enzyme genotype and wheal responses to intradermal bradykinin were studied in 105 healthy subjects: 30 of genotype DD, 51 of genotype ID and 24 of genotype II. Dermal wheal area was measured by digitized planimetry and the angiotensin-converting enzyme genotype by polymerase chain reaction.
3. Bradykinin produced significant linear log dose—wheal area responses. The potency of bradykinin by parallel line bioassay did not differ significantly between the genotypes; the potency in the II subjects relative to DD subjects was 1.25 (95% confidence interval: 0.83–1.88).
4. Although the angiotensin-converting enzyme gene polymorphism is a consistent and powerful predictor of serum angiotensin-converting enzyme activity, it does not appear to predict tissue angiotensin-converting enzyme activity as measured by dermal responses to bradykinin.
Integrins and Disease
Authors: Hillis Graham S. , MacLeod Alison M. 
Published: August 2015

1. Adhesion is a vital property of cells. It provides a stable environment for cell growth and differentiation and allows cells to migrate.
2. The interaction between cells and their extracellular matrices is also an important factor in the regulation of further protein deposition. Likewise, matrix proteins can influence cellular function thus creating a complex feedback mechanism.
3. The adherence of cells to each other, their extracellular matrices and endothelial surfaces is mediated by a variety of membrane proteins collectively known as adhesion molecules.
4. Adhesion molecules can be further divided into four subfamilies: the integrins, the selectins, the cadherins and the immunoglobulin superfamily. This article will review our current knowledge of the integrin family of adhesion receptors, focusing principally on their role in the pathogenesis of human disease.
Is there a Therapeutic Future for ‘Potassium Channel Openers’?
Authors: Lawson Kim 
Published: August 2015

1. Potassium channels, which control cell electrical activity, are among the most regulated of all ion channels in biology. Promotion of activity in K+ channels by a wide range of physiological factors tends to stabilize cell function.
2. The discovery of synthetic molecules (e.g. cromakalim) that ‘directly’ open ATP-sensitive K+ channels has led to a new direction in pharmacology. ATP-sensitive K+ channel-opening properties have subsequently been demonstrated in a diverse range of chemical structures (synthetic and endogenous).
3. The existence of so many different subtypes of K+ channels has been an impetus in the search of new potassium channel openers with different channel selectivities and thus biological profiles.
4. The decrease in cell excitability following K+ channel opening implies a broad clinical potential in a number of pathological conditions for K+ channel openers. Preclinical and clinical evidence supports therapeutic roles of K+ channel openers in disorders of a wide range of biological cells.
5. Although lack of selectivity of current compounds remains a major hurdle, advances in K+ channel openers and K+ channel pharmacology are encouraging. Differences already observed in the pharmacology of K+ channel openers are important factors for the development of second-generation compounds, when tissue selectivity is sought.
6. The availability of subtype-selective K+ channel openers will facilitate detailed study, through a combined effort of electrophysiology, functional pharmacology and molecular biology, leading to focused therapeutic approaches for defined pathological conditions.
Increased Oxidative and Delayed Glycogenolytic ATP Synthesis in Exercising Skeletal Muscle of Obese (Insulin-Resistant) Zucker Rats
Authors: Sanderson A. L. , Kemp G. J. , Thompson C. H. , Radda G. K. 
Published: August 2015

1. To examine metabolic correlates of insulin resistance in skeletal muscle, we used 31P magnetic resonance spectroscopy to study glycogenolytic and oxidative ATP synthesis in leg muscle of lean and obese Zucker rats in vivo during 6 min sciatic nerve stimulation at 2 Hz.
2. The water content of resting muscle was reduced by 21 ± 7% in obese (insulin-resistant) animals compared with lean animals, whereas the lipid content was increased by 140 ± 70%. These results suggest that intracellular water content was reduced by 17% in obese animals.
3. During exercise, although twitch tensions were not significantly different in the two groups, rates of total ATP synthesis (expressed per litre of intracellular water) were 48 ± 20% higher in obese animals, suggesting a 50 ± 8% reduction in intrinsic ‘metabolic efficiency’. Changes in phosphocreatine and ADP concentration were significantly greater in obese animals than in lean animals, whereas changes in intracellular pH did not differ.
4. These results imply that oxidative ATP synthesis during exercise is activated earlier in obese animals than in lean animals. This difference was not fully accounted for by the greater increase in the concentration of the mitochondrial activating signal ADP. Neither the post-exercise recovery kinetics of phosphocreatine nor the muscle content of the mitochondrial marker enzyme citrate synthase was significantly different in the two groups. The increased oxidative ATP synthesis in exercise must therefore be due to altered kinetics of mitochondrial activation by signals other than ADP.
5. Thus, the insulin-resistant muscle of obese animals may compensate for its decreased efficiency (and consequent increased need for ATP) by increased reliance on oxidative ATP synthesis.