bluuebunny/crossref_metadata_2025_split huggingface dataset:
The distance from the Amplatzer septal occluder to the mitral valve in patients undergoing interventional closure of defects in the oval fossa increases with growth of the patient
Authors: English Robert F. , Ettedgui Jose A. 
Published: January 2005

The Amplatzer septal occluder is an alternative to operative closure of atrial septal defects within the oval fossa. An issue when deploying the device is its distance from the mitral valve. The purpose of this study is to determine how this distance changes with growth of the patient. We identified, through a review of charts, all patients undergoing closure of defects within the oval fossa by insertion of an Amplatzer septal occluder. Data were obtained from the echocardiogram 24 hours after closure, and at most recent follow-up, including left ventricular end-diastolic diameter, left atrial diameter, degree of mitral valvar regurgitation, body surface area, and distance from the device to the mitral valve. We divided the patients into 2 groups based upon change in body surface area. The first group had an increase in body surface area of at least 10%. All others were in the second group.We inserted 55 Amplatzer septal occluders in 54 patients. Of these we excluded 17 patients, 1 because quality of images was inadequate, 1 who underwent placement of 2 devices, 1 in whom the device embolised to the left ventricle the day after deployment, and 14 who have not yet had a follow-up echocardiogram.The group which exhibited an increase in body surface area of greater than 10% demonstrated an increase in distance from the device to the mitral valve, left ventricular end-diastolic, and left atrial diameters. Those who did not undergo significant growth had no increase in distance from the device to the mitral valve, but did have an increase in left atrial and left ventricular end-diastolic diameters. No patient developed mitral regurgitation. We conclude that, when deploying an Amplatzer septal occluder close to the mitral valve in children, the distance from the device to the mitral valve can be expected to increase with growth of the patient.
Molecular characterisation of neonatal cardiac hypertrophy and its regression
Authors: Gopinath Bamini , Trent Ronald J. , Yu Bing 
Published: January 2005

Neonatal cardiac hypertrophy associated with diabetic pregnancy is transient and regresses naturally, but is associated with increased morbidity and mortality.This study was undertaken to analyse the changes in expression of 5 cardiac genes, including atrial natriuretic peptide, α- and β-myosin heavy chain, and cardiac and skeletal α-actin genes, using a rat neonatal model, in which cardiac hypertrophy was induced via maternal diabetes.In the hypertrophied left ventricle of neonates from diabetic mothers, the levels of mRNA from all the above genes except skeletal α-actin were increased by between 1.8- and 12-fold compared with the controls at birth (p < 0.05). In the first 28 days, the level of mRNA for α-myosin heavy chain increased slightly, while that for atrial natriuretic peptide and β-myosin heavy chain decreased continuously similar to the controls, but at a significantly faster rate. No significant difference between the two groups of neonates was observed in all 5 genes after 1 month, indicating complete regression.Expression of 5 cardiac genes in the neonatal cardiac hypertrophy was characterised in both hypertrophic and regressive phases. Hypertrophic regression provides a unique model for the testing of new drugs or genetic modifying factors in cardiac hypertrophy.
Diagnosis, management, and results of treatment for aortopulmonary window
Authors: Mert Murat , Paker Tufan , Akcevin Atif , Cetin Gurkan , Ozkara Ahmet , Saltik Levent , Bakir Ihsan , Yildiz Cenk Eray 
Published: January 2005

The aortopulmonary window is a communication between the ascending aorta and the pulmonary trunk in the presence of two separate arterial valves. This uncommon congenital anomaly is reported rarely in the literature. We present here our experience with 16 patients, emphasizing the importance of early closure of the defect by a transaortic approach.We performed surgery on 16 patients over a period of 13 years using a transaortic approach under cardiopulmonary bypass. The median age of the patients at the time of operation was 6.5 months, with a range from 1 month to 11 years. Preoperative pulmonary arterial systolic pressure ranged from 30 to 100 mmHg. Associated cardiac anomalies were present in 7 of the patients, and were repaired at the same stage. The defect was between the ascending aorta and the proximal pulmonary trunk in 13 patients, and between the ascending aorta and the distal pulmonary trunk, with overriding of the orifice of the right pulmonary artery, in 3 patients. For closure, we used a patch of 0.4 mm Gore-Tex in 11, and gluteraldehyde-treated autologous pericardium in 5 of the patients.One patient died during surgery. The mean follow-up period for the surviving 15 patients was 52.2 months, with a range from 12 to 130 months. All the patients were in good condition during the follow-up, and no residual defects have been detected.Aortopulmonary window is a rare congenital cardiac anomaly, which can be repaired with very good operative results if surgery is performed before the development of irreversible pulmonary hypertension. We advise early correction of the defect with a transaortic patch, repairing all associated cardiac anomalies at the time of diagnosis.
Time‐course of deactivation of rat stomach ECL cells following cholecystokininB/gastrin receptor blockade
Authors: Ding X.‐Q. , Lindström E. , Håkanson R. 
Published: January 2005

The so‐called enterochromaffin‐like (ECL) cells constitute 65–75% of the endocrine cells in the acid‐producing part of the rat stomach. They produce and secrete histamine and pancreastatin, a chromogranin A (CGA)‐derived peptide, in response to gastrin. Cholecystokinin (CCK)B/gastrin receptor blockade is known to suppress their activity.
We have examined the time course of the deactivation of the ECL cells following treatment with the selective CCKB receptor antagonists RP73870 and YM022. The drugs were given by continuous subcutaneous infusion for a time span of 1 h to 3 weeks and the serum gastrin concentration and various ECL cell parameters were measured (oxyntic mucosal histidine decarboxylase (HDC) activity, histamine and pancreastatin concentrations, HDC mRNA and CGA mRNA levels, and circulating pancreastatin concentration).
The two antagonists caused a prompt and dramatic decline in the oxyntic mucosal HDC activity and HDC mRNA level. The HDC activity started to decline after 1–2 h, was reduced by 60–70% after 6 h and was maximally suppressed (80–90%) after 24–48 h. The HDC mRNA level was reduced after 12 h and was at about 20% of the pretreatment level after 2–4 days of infusion. The ECL cell histamine concentration was lowered by about 50% after 7–10 days.
RP73870 and YM022 lowered the serum pancreastatin concentration and the oxyntic mucosal CGA mRNA level. The serum pancreastatin concentration was reduced by 40% after 6 h and the reduction was maximal after 2–3 days. A decline in the oxyntic mucosal CGA mRNA level was noted after 12 h with a maximal reduction after 2–4 days of infusion. The ECL cell pancreastatin concentration was reduced by 30–40% after 3 weeks.
The infusion of RP73870 and YM022 induced hypergastrinaemia. The serum gastrin concentration started to rise after 2–4 h, there was a 2 fold increase after 6 h and maximal increase (3–4 fold) after 2–3 days of treatment.
In conclusion, CCKB/gastrin receptor blockade promptly deactivates the ECL cells. Deactivation, manifested in a greatly reduced HDC activity, was apparent after 1–2 h of the infusion. The serum pancreastatin concentration and the oxyntic mucosal HDC mRNA and CGA mRNA levels were greatly reduced after 1–2 days. The ECL cell concentrations of histamine and pancreastatin declined quite slowly by comparison.

British Journal of Pharmacology (1997) 122, 1–6; doi:10.1038/sj.bjp.0701316
Prominent role of intracellular Ca2+ release in hypoxic vasoconstriction of canine pulmonary artery
Authors: Jabr Rita I. , Toland Helen , Gelband Craig H. , Xia Wang Xiao , Hume Joseph R. 
Published: January 2005

The possible role of sarcoplasmic reticulum (SR) Ca2+ stores in hypoxic pulmonary vasoconstriction (HPV) is not well understood. In order to assess the possible role of intracellular Ca2+ release from SR Ca2+ stores in HPV, we examined the effects of: (1) ryanodine (10 μM) depletion of intracellular Ca2+ stores, and (2) thapsigargin (THAPS, 2 μM) or cyclopiazonic acid (CPA, 10 μM) depletion of intracellular Ca2+ stores on HPV in canine pulmonary artery.
Isometric tension was measured from arterial ring suspended in Krebs‐Henseliet solution (K‐H) bubbled with 95%O2/5%CO2. Hypoxia was induced by bubbling phenylephrine (PE, 1 μM) precontracted rings with 95%N2/5%CO2. HPV was observed in both intact and endothelial‐denuded arteries and expressed as % of maximal KCl contraction (%Tkmax)=21.3±3.2%; n=13 and 21.7±4%; n=4, respectively.
When SR caffeine sensitive Ca2+ stores were depleted by pretreatment with ryanodine and brief caffeine (15 mM) exposure, the hypoxic response was signifcantly reduced to 19.1±9.2% of the control hypoxic contraction (n=7; P<0.001) with little or no effect on PE or KCl contractions. On the other hand, in normoxic rings pretreated with THAPS or CPA, the PE responses were significantly reduced (%Tkmax=18.2±3.1% compared to 39.0±3.9% in control; n=16; P<0.001; %Tkmax=3.4±1.6% compared to 49.9±7.9% in control; n=6; P<0.001; respectively) with no significant effect on caffeine‐induced contractions, suggesting that both THAPS and CPA preferentially deplete InsP3‐sensitive Ca2+ stores, without affecting the caffeine‐sensitive Ca2+ store; consistent with the existence of separate and independent InsP3 and caffeine‐sensitive Ca2+ stores in this preparation.
When hypoxia was induced in the presence of THAPS or CPA, developed tension was significantly larger than control (%Tkmax=64.5±6.0%; n=16; P<0.05%; %Tkmax=78.2±15%; n=6; P<0.05; respectively), was partially blocked by nisoldipine (10 μM) and ryanodine (%Tkmax=20.3±3.7%; n=6), and nearly completely blocked by SK&F 96365 (50 μM). However, the actions of SK&F 96365 appeared to be nonselective since this compound also significantly reduced contractions elicited by KCl, PE and caffeine.
Finally, evidence was obtained suggesting: (a) that at least some of the Ca2+ released from the caffeine‐ and ryanodine‐sensitive Ca2+ stores by hypoxia may be taken up and buffered by the InsP3‐sensitive Ca2+ stores, and (b) the apparent dependence of HPV on extracellular Ca2+ entry pathways may be partially due to the dependence of the Ca2+ content of intracellular SR Ca2+ stores on sarcolemmal Ca2+ entry pathways.
These data suggest that caffeine‐ and ryanodine‐sensitive SR Ca2+ stores contribute significantly to HPV under normal conditions and, in the presence of THAPS or CPA, an additional nisoldipine‐ and ryanodine‐insensitive Ca2+ entry pathway is evoked by hypoxia.

British Journal of Pharmacology (1997) 122, 21–30; doi:10.1038/sj.bjp.0701326
Action of ryanodine on neurogenic responses in rat isolated mesenteric small arteries
Authors: Garcha Robinder S. , Hughes Alun D. 
Published: January 2005

Rat mesenteric arteries (∼250 μm) were set up in a single‐channel isometric myograph designed to allow fluorescence measurements concurrent with field stimulation of intramural nerves. Vessels were loaded with 6 μM fura‐2AM for 2 h and simultaneous recordings of neurogenic contraction (force) and intracellular calcium [Ca2+]i were obtained. In other experiments, arteries were loaded with 1 μCi ml−1 [3H]‐noradrenaline (NA) for 30 min in order to measure release of [3H]‐NA in response to field stimulation to examine whether ryanodine directly inhibited neuronal release of NA.
Arteries were activated by single intermittent field stimulation or continuously to excite intrinsic sympathetic nerves, or by cumulative addition of noradrenaline (1 nM–10 μM) to the bathing solution.
Pre‐incubation with ryanodine markedly inhibited the contraction and [Ca2+]i release in response to single‐pulse nerve stimulation. Ryanodine also inhibited an early phasic component of the response to continuous field stimulation and reduced the rate of rise in force in response to continuous field stimulation. However, stable maximal contraction and [Ca2+]i in response to continuous field stimulation as well as maximal responses to exogenous NA were unaffected. Release of [3H]‐NA in response to single intermittent field stimulation was not affected by ryanodine when compared to vehicle.
Our results suggest that brief intermittent activation of intramural sympathetic nerves increases [Ca2+]i and contracts small arteries primarily by releasing Ca2+ from a ryanodine‐sensitive intracellular store. In contrast, the stable rise in tone and [Ca2+]i resulting from continuous nerve stimulation may largely depend on sources of Ca2+ other than the ryanodine‐sensitive intracellular store.

British Journal of Pharmacology (1997) 122, 142–148; doi:10.1038/sj.bjp.0701337
Inhibition by ATP of calcium oscillations in rat cultured hippocampal neurones
Authors: Koizumi Schuichi , Inoue Kazuhide 
Published: January 2005

The effect of adenosine 5′‐triphosphate (ATP) on glutamatergic synaptic transmission in hippocampus was examined by an indicator of intracellular Ca2+ oscillations. These oscillations were postsynaptic responses by glutamate released from presynaptic sites. ATP completely inhibited the oscillations in a concentration‐dependent manner.
The ATP‐induced inhibition was mediated via P2‐purinoceptors since ATP exhibited the inhibitory action even in the presence of P1‐purinoceptor antagonists. Also non‐hydrolysable ATP analogues and uridine 5′‐triphosphate (UTP) inhibited the oscillation.
The rank order of agonist potency of ATP analogues for inhibition of the Ca2+ oscillation was as follows: 2‐methyl‐thio‐adenosine 5′‐triphosphateATP>adenosine 5′‐O‐(3‐thiotriphosphate)>UTP>α,β‐methylene‐adenosine 5′‐triphosphate. These inhibitory effects were insensitive to suramin. Judging from this rank order of potency, the inhibitory P2‐purinoceptor could be assigned to a subclass of GTP‐binding protein coupled‐type receptors.
The site of action of ATP was thought to be presynaptic since ATP did not affect the postsynaptic Ca2+ responses by glutamate. These results suggest the existence of a presynaptic inhibitory P2‐receptor that inhibits glutamate release in the hippocampus.

British Journal of Pharmacology (1997) 122, 51–58; doi:10.1038/sj.bjp.0701344
Selective inhibition of adenylyl cyclase by octopamine via a human cloned α2A‐adrenoceptor
Authors: Airriess Chris N. , Rudling Jane E. , Midgley John M. , Evans Peter D. 
Published: January 2005

In this study we have compared the abilities of the enantiomers of the structural isomers of the phenolamines, octopamine and synephrine, and the catecholamines, noradrenaline and adrenaline, to couple selectively a human cloned α2A‐adrenoceptor, stably expressed in a Chinese hamster ovary (CHO) cell line, to G‐protein linked second messenger pathways mediating an increase and a decrease in cyclic AMP production.
The catecholamines couple the α2A‐adrenoceptor to both an increase and a decrease in the rate of cyclic AMP production. In the absence of pertussis toxin pretreatment both catecholamines tested showed a dose‐dependent decrease with a maximum at 100 nM. After pertussis toxin pretreatment they both produced a dose‐dependent increase in cyclic AMP production with a maximum at 10 μM.
The phenolamines, octopamine and synephrine were only able to couple the α2A‐adrenoceptor to a dose‐dependent decrease in cyclic AMP production at concentrations up to 1 mM, with the synephrine isomers being more potent than the corresponding octopamine isomers. The meta‐isomers of both phenolamines were more potent than the corresponding para‐isomers and the (−)‐enantiomers were more potent than the (+)‐enantiomers. Thus, (−)‐meta‐synephrine [(−)‐phenylephrine] was the most effective isomer tested with an observable decrease occurring between 100 nM and 1 μM.
The effects of octopamine and the catecholamines on the decrease in cyclic AMP production were additive at submaximal concentrations, whilst octopamine reduced the stimulant effect of submaximal concentrations of noradrenaline on cyclic AMP production after pertussis toxin pretreatment.
The time courses of the inhibitory effects of both meta‐octopamine and noradrenaline were parallel and peaked after a 1 min exposure to the agonist. In contrast, the stimulant effects of noradrenaline after pertussis toxin pretreatment were of a much slower time course with a maximum effect occurring after a 5 min incubation period.
Since octopamine and synephrine occur naturally in, and are co‐released with catecholamines from, mammalian tissues, the results of the present study suggest that the human cloned α2A‐adrenoceptor can be coupled selectively by different endogenous agonists to G‐protein pathways mediating the regulation of adenylyl cyclase activity.

British Journal of Pharmacology (1997) 122, 191–198; doi:10.1038/sj.bjp.0701348
Anti‐thrombotic effects and bleeding risk of AJvW‐2, a monoclonal antibody against human von Willebrand factor
Authors: Kageyama Shunsuke , Yamamoto Hiroshi , Nagano Mitsuyo , Arisaka Harumi , Kayahara Takashi , Yoshimoto Ryota 
Published: January 2005

A murine anti‐human vWF monoclonal antibody, AJvW‐2, was developed that inhibited the interaction between platelet glycoprotein Ib (GPIb) and von Willebrand factor (vWF) during the ristocetin‐ (IC50=0.7±0.1 μg ml−1) and botrocetin‐ (IC50=1.8±0.3 μg ml−1) induced aggregation of human platelets.
AJvW‐2 inhibited the high shear stress (10.8 N m−2) induced aggregation of human platelets dose‐dependently with an IC50=2.4±0.3 μg ml−1, but had no effect on low shear stress induced platelet aggregation (1.2 N m−2) up to 100 μg ml−1.
AJvW‐2 also inhibited the high shear stress (5.0 N m−2) induced adhesion of human platelets to collagen I with the same efficacy (IC50=2.4±0.3 μg ml−1), but had no effect at low shear conditions (1.5 N m−2).
AJvW‐2 inhibited the botrocetin‐induced aggregation of platelets from guinea‐pig, rat, rabbit, dog and pig at the same concentration range as human platelets; it likewise also inhibited the high shear stress induced aggregation and adhesion to collagen I of guinea‐pig platelets.
AJvW‐2 prevented arterial thrombus formation in guinea‐pigs at a dose of 100 μg kg−1 without prolonging the template bleeding time, whereas the GPIIb/IIIa antagonist lamifiban mediated inhibition of thrombosis at 1000 μg kg−1 was accompanied by a significant prolongation of the bleeding time.
These results suggest that AJvW‐2 is a potent inhibitor of the GPIb‐vWF interaction and a potential novel antithrombotic agent with lower bleeding risk than GPIIb/IIIa antagonists.

British Journal of Pharmacology (1997) 122, 165–171; doi:10.1038/sj.bjp.0701354
Role of the purinergic and noradrenergic components in the potentiation by endothelin‐1 of the sympathetic contraction of the rabbit central ear artery during cooling
Authors: García‐Villalón A. L. , Padilla J. , Monge L. , Fernández N. , Gómez B. , Diéguez G. 
Published: January 2005

To examine the role of the purinergic and noradrenergic components in the potentiation of endothelin‐1 on the vascular response to sympathetic nerve stimulation, we recorded the isometric response of isolated segments, 2 mm long, from the rabbit central ear artery to electrical field stimulation (1–8 Hz) under different conditions, at 37°C and during cooling (30°C).
Electrical field stimulation produced frequency‐dependent contraction, which was reduced during cooling (about 60% for 8 Hz). Both at 37°C and 30°C, phentolamine (1 μM) or blockade of α1‐adrenoceptors with prazosin (1 μM) reduced, whereas blockade of α2‐adrenoceptors with yohimbine (1 μM) increased, the contraction to electrical field stimulation. This contraction was increased after desensitization of P2‐receptors with α,β‐methylene adenosine 5′‐triphosphate (α,β‐meATP, 3 μM) at 37°C but not at 30°C, and was not modified by blockade of P2‐receptors with pyridoxalphosphate‐6‐azophenyl‐2,4′‐disulphonic acid (PPADS, 30 μM) at either temperature.
Endothelin‐1 (1, 3 and 10 nM) at 37°C did not affect, but at 30°C it potentiated in a concentration‐dependent manner the contraction to electrical field stimulation (from 28±6 to 134±22%, for 8 Hz). At 37°C, endothelin‐1 in the presence of phentolamine or prazosin, but not in that of yohimbine, α,β‐meATP or PPADS, potentiated the contraction to electrical stimulation. At 30°C, phentolamine or yohimbine reduced, prazosin or PPADS did not modify and α,β‐meATP slightly increased the potentiation by endothelin‐1 of the response to electrical stimulation.
The arterial contraction to ATP (2 mM) and the α2‐adrenoceptor agonist BHT‐920 (10 μM), but not that to (−)‐noradrenaline (1 μM), was potentiated by endothelin‐1 at both 37°C and 30°C.
These results in the rabbit central ear artery suggest that the sympathetic response: (a) at 37°C, could be mediated mainly by activation of α1‐adrenoceptors, with low participation of P2‐receptors, (b) is diminished during cooling, probably by a reduction in the participation of α1‐adrenoceptors, and in this condition the response could be mediated in part by P2‐receptors, and (c) is potentiated by endothelin‐1 during cooling, probably by increasing the response of both postjunctional α2‐adrenoceptors and P2‐receptors.

British Journal of Pharmacology (1997) 122, 172–178; doi:10.1038/sj.bjp.0701359
Stretch‐induced contraction of rabbit isolated pulmonary artery and the involvement of endothelium‐derived thromboxane A2
Authors: Nakayama Koichi , Ueta Kiichiro , Tanaka Yoshio , Tanabe Yoshiyuki , Ishi Kunio 
Published: January 2005

The mechanism of stretch‐induced contraction of the intrapulmonary artery of rabbit was studied with special regard to the endothelium‐dependence and production of prostanoids.
Isolated intrapulmonary artery of rabbits in ring form produced contraction when stretched slowly up to 180% of its initial muscle length (=100%) at a rate of 0.44 mm s−1, with a stimulus period of 5 min.
The stretch‐induced contraction was attenuated by the mechanical removal of the endothelium, inhibitors of cyclo‐oxygenase such as aspirin and indomethacin, [1S‐[1α,2α(Z),3α,4α]]‐7‐[3‐[[2‐[(phenylamino) carbonyl] hydrazino]methyl]‐7‐oxabicyclo[2.2.1]hept‐2‐yl]‐5‐heptenoic acid (SQ 29,548), which is a thromboxane A2/prostaglandin H2 receptor antagonist, or by ozagrel, an inhibitor of thromboxane A2 synthase.
Biochemical assay indicated that the production of thromboxane B2, a stable metabolite of thromboxane A2, was increased 17 times in response to stretch only when the endothelium was intact. The production of thromboxane B2 was also inhibited by aspirin or ozagrel.
The production of 6‐keto prostaglandin F1α, a stable metabolite of prostacyclin, was also increased in response to stretch in the preparation with intact endothelium. However, ozagrel showed no apparent effect on the production of 6‐keto prostaglandin F1α.
These results suggest that a mechanical stimulus like stretch can act on endothelial cells of rabbit pulmonary artery to cause contraction by activation of arachidonic acid metabolism via the cyclo‐oxygenase pathway and subsequent release of thromboxane A2 and/or an increase in the ratio of thromboxane A2/prostacyclin.

British Journal of Pharmacology (1997) 122, 199–208; doi:10.1038/sj.bjp.0701362