bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dynamic Aspects Of Platelet Adhesion Under Flow
Authors: Dopheide Sacha M , Yap Cindy L , Jackson Shaun P 
Published: March 2003

SUMMARY1. Cell–cell and cell–matrix adhesive interactions are critical for a wide range of physiological processes, including embryogenesis, inflammation, immunity and haemostasis.2. The ability of circulating blood cells, such as platelets and leucocytes, to adhere to sites of vascular injury is complicated by the presence of blood flow, which imposes hydrodynamic forces on adhesion contacts.3. To overcome this problem, platelets and leucocytes have evolved specific adhesion receptors with unique biomechanical properties that enable these cells to adhere to the vessel wall under flow conditions.4. Platelet adhesion in the normal circulation appears to be a multiple‐step process involving an initial reversible interaction between the platelet adhesion receptor glycoprotein Ib‐IX‐V and the vascular adhesion protein von Willebrand factor. Once tethered to the vessel wall, platelets form irreversible adhesion contacts through the binding of one or more platelet integrins to specific subendothelial matrix proteins.5. There is now a wealth of evidence demonstrating that these receptors not only mediate platelet adhesion, but also transduce signals leading to platelet activation.6. In the present review, we will briefly discuss the current understanding of the specific roles of individual platelet receptors in supporting the haemostatic function of platelets and discuss mechanisms by which these receptors induce platelet activation.
Prophylactic Effects Of Pilocarpine Hydrochloride On Xerostomia Models Induced By X‐Ray Irradiation In Rats
Authors: Asari Tetsuya , Komatsu Yoshimitsu , Misawa Keiko , Hara Kiyoto , Akahane Masuo 
Published: March 2003

SUMMARY1. In the present study, we investigated the prophylactic effects of pilocarpine hydrochloride on xerostomia models induced by either single (15 Gy) or repeated (8.6 Gy ×3 days) X‐ray irradiation in rats. Pilocarpine hydrochloride was administered orally 90 min before each irradiation session. Then, 7 days later, salivary volume, amylase activity and protein concentration in the saliva secreted from the right parotid gland were measured before and after a subsequent administration of pilocarpine hydrochloride (intraduodenal).2. In irradiated no‐pretreatment rats, irradiation induced a significant reduction in both spontaneous and pilocarpine hydrochloride‐stimulated secretion (both total salivary volume and flow rate), regardless of the protocol used for X‐ray exposure. In irradiated, pilocarpine hydrochloride‐pretreated rats, salivary secretion was increased after stimulation by pilocarpine hydrochloride (intraduodenal) to a degree that depended on the pretreatment dose of pilocarpine hydrochloride (p.o.) in both xerostomia models.3. There were no differences in amylase or protein concentrations between irradiated rats pretreated with pilocarpine hydrochloride and irradiated no‐pretreatment control rats.4. A decrease in the weight of the parotid gland was observed in rats exposed to either the single dose or repeated irradiation protocols. Changes in the submandibular gland were less marked than those in the parotid gland. These changes in gland weight were not affected by pilocarpine hydrochloride pretreatment.5. The responsiveness of the parotid gland to subsequent stimulation with pilocarpine hydrochloride was apparently preserved in both xerostomia models by pretreatment with pilocarpine hydrochloride, which itself increased salivary secretion. This suggests that pilocarpine hydrochloride may exert functional protective effects against xerostomia that occurs following irradiation therapy through a stimulation of salivary secretion.
Ongoing Nicotinic And Non‐Nicotinic Inputs To Inhibitory Neurons In The Mouse Colon
Authors: Powell Andrew K , Fida Rosa , Bywater Robert AR 
Published: March 2003

SUMMARY1. Intracellular microelectrodes were used to record spontaneous and evoked inhibitory junction potentials (IJP) from the circular muscle layer of the mid‐distal region of the mouse isolated colon in the presence of nifedipine (1 μmol/L) and hyoscine (1 μmol/L).2. The length of the tissue preparation (> 1 cm) or the presence of the mucosa had no effect on the frequency of spontaneous IJP.3. Hexamethonium (500 μmol/L) reduced the frequency of spontaneous IJP to approximately 70% of the control frequency, whereas D‐tubocurarine (280 μmol/L) reduced the frequency to approximately 17% of control. Apamin (250 nmol/L) abolished all spontaneous IJP activity.4. The greater inhibition of spontaneous IJP in the presence of D‐tubocurarine compared with hexamethonium is discussed as a possible ‘apamin‐like’ effect.5. Although electrically evoked IJP (single pulse at 15 V, 0.6 msec) were not significantly affected by hexamethonium, D‐tubocurarine and apamin reduced the amplitude of evoked IJP to approximately 65 and 50% of control, respectively.6. These results suggest that the properties of spontaneous IJP cannot be inferred by a study of evoked IJP alone.
Participation Of Atp In Cell Volume Regulation In The Endothelium After Hypotonic Stress
Authors: Shinozuka Kazumasa , Tanaka Naoko , Kawasaki Kumiko , Mizuno Hideya , Kubota Yoko , Nakamura Kazuki , Hashimoto Michio , Kunitomo Masaru 
Published: March 2003

SUMMARY1. The role of ATP in the regulatory volume decrease (RVD) after hypotonic cell swelling was examined in cultured endothelial cells isolated from the rat caudal artery.2. Hypotonic stress increased [Ca2+]i in addition to increasing the overflow of ATP and cell volume. The hypotonicity induced increase in [Ca2+]i was prevented by pyridoxalphosphate‐6‐azophenyl‐1‐2′,4′‐disulphonic acid (PPADS; a P2 purinoceptor antagonist), U‐73122 (a phospholipase C inhibitor) and thapsigargin (a Ca2+ pump inhibitor). However, the hypotonicity induced increase in cell volume was potentiated by PPADS, U‐73122 and thapsigargin.3. Similar changes were observed in cells treated with 2‐methylthioATP, a P2Y purinoceptor agonist, but not by α,β‐methylene ATP, a P2X purinoceptor agonist. Thus, it appears that the responses observed following hypotonic stress are mediated by activation of P2Y purinoceptors.4. On the basis of these findings, it is suggested that ATP, which is released by hypotonicity, may participate in the RVD as a substantial regulator or initiator via P2 purinoceptor‐induced increases in [Ca2+]i.
Taurine Inhibits Development Of Atherosclerotic Lesions In apolipoprotein E‐Deficient Mice‡
Authors: Kondo Yukiko , Toda Yoshihisa , Kitajima Hideaki , Oda Hiroaki , Nagate Takatoshi , Kameo Kazuya , Murakami Shigeru 
Published: March 2003

SUMMARY1. The effects of taurine on the development of atherosclerotic lesions were investigated in apolipoprotein (apo) E‐deficient mice, an animal model with severe hypercholesterolaemia and extensive atherosclerosis. These mice were fed a normal laboratory chow containing 2% taurine for 12 weeks.2. Serum total cholesterol was significantly elevated after 12 weeks treatment with taurine. This elevation was due to increases in very low‐density lipoprotein‐ and low‐density lipoprotein–cholesterol.3. Despite such effects on serum lipoproteins, analysis using en face oil red O staining revealed that taurine reduced the area of arterial lipid accumulation by 28%, as measured quantitatively as an index of atherosclerosis. Histological examination also demonstrated a decrease in the size of aortic lesions in taurine‐treated mice.4. Serum levels of thiobarbituric acid reactive substances (TBARS) in apoE‐deficent mice were higher than in normolipidaemic C57BL/6J mice. Serum TBARS levels were significantly decreased by 12 weeks treatment of apoE‐deficient mice with taurine.5. Thus, taurine prevents the formation of atherosclerotic lesions, independently of serum cholesterol levels, and the results suggest that the anti‐oxidative effects of tauirne are related to its anti‐atherosclerotic actions.
Nociceptin/Orphanin Fq Modulates The Cardiovascular, But Not Renal, Responses To Stress In Spontaneously Hypertensive Rats
Authors: Kapusta Daniel R , Dayan Lisa A , Kenigs Velga A 
Published: March 2003

SUMMARY1. The central administration of the endogenous opioid‐like peptide nociceptin/orphanin FQ (N/OFQ) produces marked cardiovascular depressor and renal sympathoinhibitory responses in conscious animals. These findings are evidence that central N/OFQ may modulate the cardiovascular and renal responses to acute environmental stress.2. The changes in cardiovascular and renal function produced by intracerebroventricular (i.c.v.) N/OFQ were measured in conscious spontaneously hypertensive rats (SHR) under basal conditions and during the acute environmental stimulus of air jet stress.3. In SHR, central N/OFQ produced profound hypotensive, bradycardic, renal sympathoinhibitory (delayed) and water‐diuretic effects by a pathway that does not involve activation of central α2‐adrenoceptors or classical opioid receptors.4. Intracerebroventricular injection of N/OFQ prevented the pressor response and blunted the tachycardia to air jet stress. A similar renal sympathoexcitatory and antinatriuretic response was observed in conscious SHR during air stress, before and after i.c.v. N/OFQ.5. These findings are evidence that, in conscious SHR, i.c.v. N/OFQ selectively inhibited the neural responses to air jet stress by attenuating sympathetic outflow to the heart and, potentially, vasculature, but not to the kidneys. Central endogenous N/OFQ systems may be activated and contribute to regional changes in sympathetic outflow during acute stress.
Central Mechanisms Underlying Short‐ And Long‐Term Regulation Of The Cardiovascular System
Authors: Dampney RAL , Coleman MJ , Fontes MAP , Hirooka Y , Horiuchi J , Li Y‐W , Polson JW , Potts PD , Tagawa T 
Published: March 2003

SUMMARY1. Sympathetic vasomotor nerves play a major role in determining the level of arterial blood pressure and the distribution of cardiac output. The present review will discuss briefly the central regulatory mechanisms that control the sympathetic outflow to the cardiovascular system in the short and long term.2. In the short term, the sympathetic vasomotor outflow is regulated by: (i) homeostatic feedback mechanisms, such as the baroreceptor or chemoreceptor reflexes; or (ii) feed‐forward mechanisms that evoke cardiovascular changes as part of more complex behavioural responses.3. The essential central pathways that subserve the baroreceptor reflex and, to a lesser extent, other cardiovascular reflexes, have been identified by studies in both anaesthetized and conscious animals. A critical component of these pathways is a group of neurons in the rostral ventrolateral medulla that project directly to the spinal sympathetic outflow and that receive inputs from both peripheral receptors and higher centres in the brain.4. Much less is known about the central pathways subserving feed‐forward or ‘central command’ responses, such as the cardiovascular changes that occur during exercise or that are evoked by a threatening or alerting stimulus. However, recent evidence indicates that the dorsomedial hypothalamic nucleus is a critical component of the pathways mediating the cardiovascular response to an acute alerting stimulus.5. Long‐term sustained changes in sympathetic vasomotor activity occur under both physiological conditions (e.g. a change in salt intake) and pathophysiological conditions (e.g. heart failure). There is evidence that the paraventricular nucleus in the hypothalamus is a critical component of the pathways mediating these changes.6. Understanding the central mechanisms involved in the long‐term regulation of sympathetic activity and blood pressure is a major challenge for the future. As a working hypothesis, a model is presented of the postulated central mechanisms that result in sustained changes in sympathetic vasomotor activity that are evoked by different types of chronic stimulation.
Chronic Hypoxia Preconditioning Increases Survival In Rats Suffering From Heatstroke
Authors: Wen Hsiao‐Chuan , Lee Chin‐Cheng , Lee Wen‐Chuan , Huang Kuo‐Sheng , Lin Mao‐Tsun 
Published: March 2003

SUMMARY1. In the present study, we assessed the protective effects of chronic hypoxia preconditioning against heatstroke‐induced injury in urethane‐anaesthetized rats. Heatstroke was induced by exposing the animals to an ambient temperature of 42°C. The time at which both the mean arterial pressure (MAP) and local cerebral blood flow (CBF) in the striatum began to decrease from peak levels was taken as the onset of heatstroke. Control rats were exposed to a temperature of 24°C.2. Mean arterial pressure, CBF, blood pH, PaO2, PaCO2 and survival time (the interval between onset of heatstroke and cardiac arrest) after heat stress were all lower than in control rats (in which ‘survival time’ was defined as > 360 min). However, blood lactate concentrations were greater in rats exposed to heat. Rats placed at high altitude (HA), when exposed to the same heat stress (42°C) survived much longer (113 ± 26 min; n = 8) than rats maintained at sea level (SL; 20 ± 2 min; n = 8).3. After the onset of heatstroke, blood pH and lactate concentrations were found to be significantly higher and lower, respectively, in HA rats than in SL rats.4. Western blot assay revealed that chronic hypoxia preconditioning induced heat shock protein (HSP) 72 expression in both the kidneys and lungs.5. Thus, it appears that the observed benefit of chronic hypoxia preconditioning is related to attenuation of tissue acidification and elevations of HSP72 expression in both kidneys and lungs during heatstroke.
Involvement Of α‐Calcitonin Gene‐Related Peptide In Heat Stress‐Induced Delayed Preconditioning In Rat Hearts
Authors: Peng Jun , Lu Rong , Xiao Liang , Deng Han‐Wu , Li Yuan‐Jian 
Published: March 2003

SUMMARY1. Previous studies have shown that hyperthermia is capable of activating capsaicin‐sensitive sensory nerves and stimulating the release of neurotransmitters from their peripheral terminals. Calcitonin gene‐related peptide (CGRP) has recently been found to participate in delayed cardioprotection in rat isolated hearts.2. The purpose of the present study was to explore whether the delayed cardioprotection by heat stress in vivo involves the expression and release of CGRP.3. Sprague‐Dawley rats were pretreated with whole‐body hyperthermia (rectal 42°C) for 15 min, 24 h before the experiments and then the left main coronary artery of rat hearts was subjected to a 45 min occlusion followed by 3 h reperfusion. The degree of myocardial injury was evaluated by measurement of infarct size and plasma creatine kinase (CK) activity. The plasma levels of CGRP and expression of CGRP (α
and β isoforms) mRNA in lumbar dorsal root ganglia at 4, 8, 16 or 24 h after heat stress treatment were measured.4. Pretreatment with hyperthermia significantly reduced infarct size and CK release. Heat stress also significantly increased plasma concentrations of CGRP and the expression of α‐CGRP mRNA, but not β‐CGRP mRNA. The effect of heat stress was completely abolished by pretreatment with capsaicin (50 mg/kg, s.c.), which selectively depletes transmitters in capsaicin‐sensitive sensory nerves.5. In summary, the results suggest that the delayed cardioprotection by heat stress involves the synthesis and release of CGRP and that the protection is mainly mediated by the α‐CGRP isoform.
Effects Of Endotoxin‐Induced Shock On Withdrawal Contractions In The Guinea‐Pig Isolated Ileum
Authors: Fatehi M , Tanomand A , Fatehi‐Hassanabad Z 
Published: March 2003

SUMMARY1. Taking into consideration the effect of septic shock on releasing various mediators, the present study was undertaken in an attempt to elucidate the effect of endotoxin on naloxone‐induced withdrawal contractions in the guinea‐pig isolated ileum.2. To induce withdrawal contractions, preparations removed either from saline‐ or endotoxin (2.5 mg/kg in 0.4 mL, i.p.)‐treated animals were incubated for 5 min with morphine (40 μmol/L) and naloxone (50 μmol/L) was then applied.3. In tissues removed from endotoxin‐treated animals, a significant reduction in withdrawal contractions was observed. In control preparations, indomethacin (1 μmol/L
for 15 min) significantly reduced naloxone‐induced contractions, whereas NG‐nitro‐L‐arginine
methyl ester (L‐NAME; 10 μmol/L for 15 min) had no effect.
However, indomethacin pretreatment of tissues removed from endotoxin‐treated animals
did not modify the withdrawal contractions, whereas L‐NAME pretreatment enhanced the amplitude of the withdrawal‐induced contractions.4. These results suggest that attenuation of the withdrawal contractions in guinea‐pig isolated ileum induced by endotoxin‐pretreatment may be due, in part, to the activation of an L‐arginine–nitric oxide pathway.
Insulin‐Enhanced Liposome‐Mediated Gene Transfer Into A Gastric Carcinoma Cell Line
Authors: Ohmiya Naoki , Emi Nobuhiko , Niwa Yasumasa , Goto Hidemi , Hayakawa Tetsuo 
Published: March 2003

SUMMARY1. Liposome‐mediated transfection is useful due to no DNA constraints, lower immunogenicity and easy preparation. However, it has the disadvantage of low transfection efficiency. We aimed to test whether lipofection efficiency could be enhanced in gastrointestinal cell lines by the growth‐promoting effect of insulin.2. To assess the effect of insulin on lipofection efficiency and the cell cycle, expression of green fluorescent protein (GFP) and DNA distribution in gastric (MKN1), colonic (HT29) and pancreatic (BxPC3) carcinoma cell lines was analysed using flow cytometry.3. The percentage of positive cells with GFP was significantly higher in MKN1 cells in culture medium with 5 mg/mL insulin than without insulin, whereas the percentage was the same in HT29 and BxPC3 cells with insulin as without insulin. The percentage of S phase fraction MKN1 cells with insulin was greater than without insulin, whereas the percentage of S phase fractions of HT29 and BxPC3 cells was the same with or without insulin. Lipofection efficiency correlated with the percentage of S phase fraction.4. Insulin has the potential to enhance efficiency of lipofection into a sensitive cell line by increasing cellular proliferation.
Effects of cytokines on contractile and dilator responses of airway smooth muscle
Authors: Shore Stephanie A , Moore Paul E 
Published: March 2003

Summary1. Increased bronchoconstrictor responses to contractile agonists and decreased dilator responses to β‐adrenoceptor agonists are characteristics of human asthma. One explanation for these features of asthma is that cytokines released in the asthmatic airway have direct effects on airway smooth muscle cells that alter their phenotype.2. The present review summarizes data indicating that inflammatory cytokines, such as interleukin (IL)‐1β and tumour necrosis factor‐α, T helper (h) 1 cytokines, such as interferon‐γ, and Th2 cytokines, such as IL‐13 and IL‐5, have the capacity to enhance contractile responses and/or decrease relaxant responses of airway smooth muscle. These effects are observed in smooth muscle from human airways and airway smooth muscle of other species.3. Understanding the mechanistic basis for the effects of these cytokines may prove to be an important step in improving the efficacy of β‐adrenoceptor agonists for the treatment of asthma.
Heat stress increases endothelium‐dependent relaxations and prevents reperfusion‐induced endothelial dysfunction
Authors: Richard Vincent , Laude Karine , Artigues Cecile , Kaeffer Nathalie , Henry Jean‐Paul , Thuillez Christian 
Published: March 2003

Summary1. Heat stress has been widely used to stimulate the expression of stress proteins and is associated with various cardiovascular changes, including anti‐ischaemic effects. However, the effect of heat stress on endothelial function is less clear.2. Heat stress was induced in anaesthetized rats by increasing body temperature to 42°C for 15 min. Twenty‐four hours later, segments of rat aorta and mesenteric and coronary arteries were mounted in organ chambers.3. Heat stress markedly increased relaxation to acetylcholine (ACh) in all three blood vessels studied, without affecting the response to the nitric oxide (NO) donor sydnonimine‐1.4. Heat stress also increased aortic relaxation to histamine and the calcium ionophore A23187.5. In the aorta, an inhibitor of NO synthesis abolished the response to ACh in both control and heat stressed‐rings, whereas a cyclo‐oxygenase inhibitor had no effect.6. Heat stress also prevented completely the impaired response to ACh in coronary arteries isolated from rats subjected to myocardial ischaemia and reperfusion.7. Thus, heat stress increases the stimulated release of NO the rat aorta and mesenteric and coronary arteries and prevents reperfusion‐induced injury at the level of the coronary endothelium.
Reduced [125I]‐Bolton Hunter substance P binding (NK1 receptors) in the basal forebrain nuclei of aged rats
Authors: Geraghty Dominic P , Maguire Christine M 
Published: March 2003

Summary1. Quantitative autoradiography and homogenate radioligand binding of [125I]‐Bolton Hunter substance P ([125I]‐BHSP) were used to compare brain NK1 receptors in young (2 months) and aged (18–20 months) rats.2. The autoradiographic distribution and density of [125I]‐BHSP binding sites was similar in all cortical regions of young and aged rats. In contrast, the density of [125I]‐BHSP binding sites was significantly (P < 0.05) lower in the basal forebrain nuclei (intermediate part of the lateral septal nuclei, medial septal nucleus and horizontal and vertical nuclei of the diagonal band) of aged rats. In all other brain regions examined, binding densities were almost identical in young and aged rats.3. Because a population of NK1 receptors ([125I]‐BHSP binding sites) in the basal forebrain nuclei is associated with cholinergic neurons, the decrease in NK1 receptors in aged rats may reflect degeneration of cholinergic neurons and contribute to the motor and cognitive deficiencies that occur with ageing.
Increased Renal Vascular Resistance In Zinc‐Deficient Rats: Role Of Nitric Oxide and Superoxide
Authors: Kurihara Nobutaka , Yanagisawa Hiroyuki , Sato Masamichi , Tien Chang‐Kuen , Wada Osamu 
Published: March 2003

Summary1. Zinc deficiency (ZD) induces many kinds of pathological states. However, the effects of ZD on haemodynamics remain unclear. In the present study, we measured mean blood pressure (BP) and renal blood flow (RBF) under anaesthesia and calculated renal vascular resistance (RVR) from these parameters in rats maintained on a ZD diet (0.5 p.p.m. zinc) for 4 weeks.2. Zinc deficiency did not change mean BP, but significantly reduced RBF and increased RVR (each P < 0.01). In addition, these effects of ZD were reversible.3. Because Cu/Zn superoxide dismutase (SOD) is a zinc‐containing enzyme and superoxide is a potent scavenger of nitric oxide (NO), a vasodilator, we hypothesized that one of the mechanisms by which ZD increases RVR is by decreasing NO bioavailability by the enhanced formation of superoxide due to low Cu/Zn SOD activity. To test this hypothesis, we observed the roles of NO and superoxide in the mechanism, after having confirmed the low activity of Cu/Zn SOD in the kidneys of ZD rats.4. Administration of the SOD mimetic tempol (5 mg/kg per min) decreased RVR to a significantly greater extent in ZD rats compared with control, suggesting that superoxide was responsible for the mechanism. Low doses of the NO donor sodium nitroprusside (SNP; 2.0 µg/kg per min, continuous) decreased RVR to a significantly smaller extent in ZD rats compared with control, whereas a high dose of SNP (0.75 mg/kg, bolus) decreased RVR to a significantly greater extent in ZD rats compared with control, suggesting that the mechanism includes an inhibition of NO activity in ZD, which is most likely to be a scavenging of NO by the activated superoxide.5. In summary, ZD may increase RVR. The mechanism probably includes changes in NO and superoxide activities.