bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relative Timing Of Inspiration And Expiration Affects Respiratory Sinus Arrhythmia
Authors: Strauss‐Blasche G , Moser M , Voica M , McLeod Dr , Klammer N , Marktl W 
Published: March 2003

SUMMARY1. The effect of a variation in inspiration and expiration times on heart rate variability was studied in 12 healthy subjects (mean age 30±6 years; five females).2. Two 2 min trials of controlled breathing, with either short inspiration followed by long expiration or long inspiration followed by short expiration, were compared. Average expiration/inspiration time ratios were 1.0 and 3.4, respectively. The respiration rate in both trials was approximately 10 cycles/min.3. In trials with short inspiration followed by long expiration, respiratory sinus arrhythmia (RSA; as measured by mean absolute differences and by the high frequency band) was significantly larger than in trials with long inspiration followed by short expiration. This effect could not be accounted for by differences in respiration rate or respiratory amplitude. The higher RSA during fast/slow respiration is primarily due to a more pronounced phasic heart rate increase during inspiration, indicating that inspiratory vagal blockade is sensitive to the steepness of inspiration.4. Respiration rate and tidal volume are respiratory variables known to modulate RSA. The results of the present study indicate that RSA can also be modulated by a third respiratory variable, the expiratory/inspiratory time ratio.
Role Of Voltage‐Gated Na+ Channels In Hypoxia‐Induced Neuronal Injuries
Authors: Fung Man‐Lung 
Published: March 2003

SUMMARY1. Mammalian neurons in the central nervous system are vulnerable to oxygen deprivation. In clinical conditions, such as stroke or apnoea, permanent loss of neuronal functions can occur within minutes of severe hypoxia.2. Recent studies have focused on the role of Na+ in acute neuronal responses to hypoxia. These studies have shown that the influx of extracellular Na+ is an important factor in hypoxia‐induced injury and that blockade of voltage‐gated Na+ channels reduces hypoxic responses and injury of neurons. Yet, the mechanism underlying the effect of blockade of Na+ channels on hypoxic injury is unclear.3. The aim of the present review is to discuss the above topics given the current understanding of the role of Na+ channels in hypoxia and its implications on therapeutic strategy for preventing hypoxia‐induced neurological damage.4. It has been known that the maintenance of ionic homeostasis and membrane properties in neurons are improved by reducing the activity of voltaged‐gated Na+ channels during acute hypoxia.5. Recent studies suggest that persistent Na+ current and Na+‐dependent exchangers may play a role in Na+ influx and neuronal injury during hypoxia.6. The neuroprotective action of blockers of the Na+ channel may also be via the improved maintainence of intracellular energy levels because the action is dependent on cellular energy levels and extracellular glucose during hypoxia.7. Hence, the blockade of voltage‐gated Na+ channels reduces the excitability of neurons, Na+ influx and the accumulation of intracellular Na+. These improve the ionic homeostasis and cellular energy levels and, thus, prevent hypoxia‐induced neuronal injury and neuronal damage mediated by Ca2+ overload.
Impaired Heart Function And Noradrenaline Release After Ischaemia In Stroke‐Prone Spontaneously Hypertensive Rats
Authors: Chen Hong , Azuma Makiko , Maeda Kana , Kajimoto Noriyoshi , Higashino Hideaki 
Published: March 2003

SUMMARY1. Stroke‐prone spontaneously hypertensive rats (SHRSP) are a strain of rat that exhibit severely high blood pressure and stroke attacks at an early age, but their heart function in vitro has seldom been studied in detail. Although the activity of the sympathetic nervous system is known to increase after myocardial ischaemia, there is little information about the cardiac release of noradrenaline (NA) associated with heart function after ischaemia in SHRSP. The aim of the present study was to examine heart function and cardiac NA release after ischaemia in SHRSP.2. Isolated hearts of 4‐ and 8‐month‐old SHRSP and age‐matched Wistar‐Kyoto (WKY) rats were perfused in a working heart preparation and were subjected to 30 min ischaemia followed by 30 min reperfusion. Heart function and coronary flow were monitored throughout the experiment. Coronary effluent was collected for determination of NA using high‐ performance liquid chromatography coupled with electrochemical detection.3. Under baseline conditions, cardiac output of 4‐month‐old SHRSP was slightly but significantly decreased compared with that of WKY rats (P < 0.05), although coronary flow was maintained normally at this age. Eight‐month‐old SHRSP showed a further impairment of systolic heart function, with lower coronary flow and higher coronary vascular resistance under baseline conditions. Elevated left ventricular end‐diastolic pressure was evident in SHRSP at both ages before ischaemia. Heart function was severely damaged after 30 min global ischaemia in SHRSP from both age groups. Stroke‐prone spontaneously hypertensive rats also showed lower coronary flow and higher coronary vascular resistance during reperfusion.4. Coronary NA was not detectable in WKY rats or SHRSP at 4 months of age under baseline conditions. In 8‐month‐old SHRSP, pre‐ischaemic NA release was significantly higher than that in age‐matched WKY rat controls. The concentration of NA in the coronary effluent of SHRSP during reperfusion was also significantly higher than that of WKY rats at both ages.5. These data demonstrate that SHRSP have early impairment of both systolic and diastolic heart function compared with WKY rats. Severe damage of heart function and coronary flow after ischaemia in SHRSP was accompanied with an increased release of NA, which may play a harmful role in heart function impairment in SHRSP after ischaemia.
Introduction: A Brief History Of Capillaries And Some Examples Of Their Apparently Strange Behaviour
Authors: Baldwin Ann L 
Published: March 2003

SUMMARY1. Over the past decade, evidence has accumulated challenging the notion that the smallest blood vessels, the capillaries, are static, uniform, semipermeable pipes with no function except as a passive barrier marking the boundary between the vascular compartments from the tissue compartment.2. Instead, capillaries are dynamic structures that participate in the active regulation of water, waste and nutrient exchange, the formation and destruction of exchange vessels and the sites for initiation of signals to regulate the flow of blood into the exchange vascular network.3. The following papers will provide insight into the expanded appreciation of the varied nature of capillaries and how their functions are co‐ordinated to achieve ‘whole organ’ exchange.
Diversity Within Pericytes
Authors: Sims David E 
Published: March 2003

SUMMARY1. Pericytes are cells of microvessels (arterioles, capillaries and venules) that wrap around endothelial cells. They are most abundant on venules and are common on capillaries.2. The pericyte population is highly variable between different tissues and organs, probably in a manner reflecting postarteriolar hydrostatic pressures. Pericytes are more abundant in the distal legs and feet, again suggesting a hydrostatic pressure‐driven mechanical role for pericytes as protectors of microvessel wall integrity.3. Pericyte alteration or degeneration is linked directly with microangiopathy in diabetes, scleroderma, hypertension, dementias and, possibly, inappropriate calcification of blood vessels.4. Pericytes are functionally codependent on endothelial cells. Each cell type influences each others’ mitotic rate and probably phenotypic expression.5. Pericytes are not randomly located around microvessels. Instead, they are located adjacent to or over endothelial cell junctions of venules and especially over gaps between endothelial cells during inflammation. Pericytes are emerging as essential components of the microvessel wall, with metabolic, signalling and mechanical roles to support the endothelial cell.
Circular Muscle Contraction, Messenger Signalling And Localization Of Binding Sites For Neurokinin A In Human Sigmoid Colon
Authors: Warner Fiona J , Liu Lu , Lubowski David Z , Burcher Elizabeth 
Published: March 2003

SUMMARY1. Neurokinin (NK)A is the endogenous ligand for the tachykinin NK2 receptor. In the present study, tachykinins and selective receptor agonists were tested as contractile agonists in human colon circular muscle and [125I]‐NKA was used to localize binding sites in human colon.2. In strips of circular muscle, removal of mucosa and submucosa significantly (P < 0.05) increased the potency and the maximum response achieved by NKA.3. The rank order of potency of tachykinin and selective receptor agonists in contracting circular muscle strips was NKA ≥ [Lys 5,MeLeu
9,Nle
10]NKA(4–10) ≥ neuropeptide (NP)γ≥ [βAla
8]NKA(4–10) » NKB > substance P (SP) » senktide ≈ [Pro
9]SP.4. Specific binding sites for [125I]‐NKA were densely localized over circular muscle and muscularis mucosae. Weak specific binding was seen on longitudinal muscle and taenia coli, whereas no binding sites were seen on mucosa, ganglia or blood vessels.5. In circular muscle, the selective NK2 receptor agonist [Lys
5,MeLeu
9,Nle
10]NKA(4–10) produced weak increases (maximum 37%) in inositol monophosphate formation with a pD2 of 6.8±0.51 (n = 3). Carbachol (100 μmol/L) was also a weak stimulant (maximum 45%). These agonists were over 10‐fold more efficacious in stimulation of inositol monophosphate in rat urinary bladder.6. In conclusion, [125I]‐NKA binding sites localized on human colon circular muscle were characterized as NK2 receptors. Functionally, the tachykinin NK2 receptor is mediating circular smooth muscle contraction. Although the human NK2 receptor is coupled to the phosphatidylinositol pathway, other second messenger mechanisms may also operate in this tissue.
Proceedings of the Australian Neuroscience Society Symposium: Schizophrenia MOLECULAR GENETICS OF SCHIZOPHRENIA
Authors: Mowry Bj , Nancarrow Dj 
Published: March 2003

SUMMARY1. Schizophrenia is a chronic, disabling brain disease that affects approximately 1% of the world’s population. It is characterized by delusions, hallucinations and formal thought disorder, together with a decline in socio‐occupational functioning. While the causes for schizophrenia remain unknown, evidence from family, twin and adoption studies clearly demonstrates that it aggregates in families, with this clustering largely attributable to genetic rather than cultural or environmental factors. Identifying the genes involved, however, has proven to be a difficult task because schizophrenia is a complex trait characterized by an imprecise phenotype, the existence of phenocopies and the presence of low disease penetrance.2. The current working hypothesis for schizophrenia causation is that multiple genes of small to moderate effect confer compounding risk through interactions with each other and with non‐genetic risk factors. The same genes may be commonly involved in conferring risk across populations or they may vary in number and strength between different populations. To search for evidence of such genetic loci, both candidate gene and genome‐wide linkage studies have been used in clinical cohorts collected from a variety of populations. Collectively, these works provide some evidence for the involvement of a number of specific genes (e.g. the 5‐hydroxytryptamine (5‐HT) type 2a receptor (5‐HT2a) gene and the dopamine D3 receptor gene) and as yet unidentified factors localized to specific chromosomal regions, including 6p, 6q, 8p, 13q and 22q. These data provide suggestive, but no conclusive, evidence for causative genes.3. To enable further progress there is a need to: (i) collect fine‐grained clinical datasets while searching the schizophrenia phenotype for subgroups or dimensions that may provide a more direct route to causative genes; and (ii) integrate recent refinements in molecular genetic technology, including modern composite marker maps, DNA expression assays and relevant animal models, while using the latest analytical techniques to extract maximum information in order to help distinguish a true result from a false‐positive finding.
Annual Scientific Meeting of ASCEPT, 1999 Immune‐Derived Opioids And Peripheral Antinociception
Authors: Cabot Pj 
Published: March 2003

SUMMARY1. Recent findings have suggested a significant involvement of the immune system in the control of pain. Immune cells contain opioid peptides that are released within inflamed tissue and act at opioid receptors on peripheral sensory nerve endings. It is also apparent that different types of lymphocytes contain β‐endorphin, memory T cells containing more β‐endorphin than naïve cells.2. These findings highlight an integral link between immune cell migration and inflammatory pain. The present review highlights immune system involvement in the site‐directed control of inflammatory pain.3. Full‐length mRNA transcripts for opioid precursor proteins are expressed in immune cells. Increased expression of pro‐opiomelanocortin mRNA and β‐endorphin has been demonstrated in stimulated lymphocytes and lymphocytes from animals with inflammation.4. Cytokines and corticotropin‐releasing factor (CRF) release opioids from immune cells. Potent peripheral analgesia due to direct injection of CRF can be blocked by antagonists to CRF, antibodies to opioid peptides, antisense to CRF and opioid receptor‐specific antagonists. The release of opioid peptides from lymphocytes is calcium dependent and opioid receptor specific. Furthermore, endogenous sources of opioid peptides produce potent analgesia when implanted into the spinal cord.5. Activated immune cells migrate directly to inflamed tissue using cell adhesion molecules to adhere to the epithelial surface of the vasculature in inflamed tissue. Lymphocytes that have been activated can express opioid peptides. Memory type T cells that contain opioid peptides are present within inflamed tissue; naïve cells are not present in inflamed tissue and do not contain opioid peptides. Inhibiting the migration of memory type T cells into inflamed tissue by blocking selectins results in reduced numbers of β‐endorphin‐containing cells, a reduced quantity of β‐endorphin in inflamed paws and reduced stress‐ and CRF‐induced peripheral analgesia.6. Immunosuppression is associated with increased pain in patients. Moreover, immunosuppression results in decreased lymphocyte numbers as well as decreased analgesia in animal models.
Annual Scientific Meeting of ASCEPT, 1999 Role Of Human Airway Smooth Muscle In Altered Extracellular Matrix Production In Asthma
Authors: Johnson Peter Robert Arundel 
Published: March 2003

SUMMARY1. The underlying abnormality in asthma is not fully understood; however, inflammation, airway remodelling and bronchial hyperresponsiveness are key factors. The plasma exudate from the microvascular leakage plays a significant role in remodelling, which includes extracellular matrix (ECM) protein deposition/ breakdown and airway smooth muscle (ASM) hyperplasia/ hypertrophy.2. The ECM is an intricate network of macromolecules that forms the ‘scaffolding’ of the airways. This scaffolding not only acts as mechanical support that plays a crucial role in the maintenance of airway function and structure, but it is also a dynamic and complex network that has the potential to influence cellular function, including migration, differentiation and proliferation of a number of cell types.3. In asthmatic airways, the profile of ECM proteins is altered. The deposition of collagen I, III, V, fibronectin, tenascin, hyaluronan, versican and lamininα2/β2 is increased, whereas the deposition of collagen IV and elastin is decreased.4. This imbalance in the ECM profile within the asthmatic airway could be due to: (i) increasedde novosynthesis of ECM proteins; (ii) decreased activity of its degrading enzymes, namely matrix metalloproteinases (MMP); or (iii) upregulation of the tissue‐specific inhibitors of metalloproteinases (TIMP).5. One of the characteristic features of asthma is an increase in the amount of ASM within the airways. The ECM proteins/MMP/TIMP in and around the smooth muscle may play a contributory role in this increased growth.6. The role of current asthma treatments in the prevention or reversal of airway ECM changes is an area that has only recently become of interest, with the majority of thein vivowork focusing on the effects of corticosteroids.7. The evidence presented in this review indicates that the ASM may influence its own environment/proliferation through the production of ECM proteins, MMP and TIMP. Further studies are needed to fully understand the role of the ASM in the production of ECM proteins, MMP and TIMP and their potential influence in the mechanisms underlying asthma.
Chronic Administration Of Docosahexaenoic Acid Improves The Performance Of Radial Arm Maze Task In Aged Rats
Authors: Gamoh Shuji , Hashimoto Michio , Hossain Shahdat , Masumura Sumio 
Published: March 2003

SUMMARY1. In the present study, we investigated the effect of docosahexaenoic acid (DHA) on spatial memory related learning ability in aged (100 weeks) male Wistar rats.2. Rats were fed a fish oil‐deficient diet through three generations and were then randomly divided into two groups. Over 10 weeks, one group was per orally administered 300 mg/kg per day DHA dissolved in 5% gum Arabic solution and the other group was administered the vehicle alone. Five weeks after the start of the administration, rats were tested with the partially baited eight‐arm radial maze to estimate two types of spatial memory related learning ability displayed by reference memory error and working memory error.3. Chronic administration of DHA significantly decreased the number of reference memory errors and working memory errors.4. The level of lipid peroxide (LPO) in the hippocampus tended to decrease with chronic DHA administration and demonstrated a positive correlation with the number of reference memory errors.5. These results suggest that the accumulation of hippocampal LPO reduces spatial memory related learning ability in aged rats. Moreover, chronic administration of DHA was effective in decreasing the level of hippocampal LPO, then improving learning ability.
New Perspectives On The Role Of Aldosterone Excess In Cardiovascular Disease
Authors: Stowasser Michael 
Published: March 2003

SUMMARY1. Evidence from recent experimental and clinical studies suggests that excessive circulating levels of aldosterone can bring about adverse cardiovascular sequelae independent of the effects on blood pressure. Examples of these sequelae are the development of myocardial and vascular fibrosis in uninephrectomized, salt‐loaded rats infused with mineralocorticoids and, in humans, an association of aldosterone with left ventricular hypertrophy, impaired diastolic and systolic function, salt and water retention causing aggravation of congestion in patients with established congestive cardiac failure (CCF), reduced vascular compliance and an increased risk of arrhythmias (resulting from intracardiac fibrosis, hypokalaemia, hypomagnesaemia, reduced baroreceptor sensitivity and potentiation of catecholamine effects).2. These sequelae of aldosterone excess may contribute to the pathogenesis and worsen the prognosis of CCF and hypertension.3. The heart and blood vessels may be capable of extra‐adrenal aldosterone biosynthesis, raising the possibility that aldosterone may have paracrine or autocrine (and not just endocrine) effects on cardiovascular tissues.4. The high prevalence of CCF, which is associated with secondary aldosteronism, and primary aldosteronism (PAL; recently recognized to be a much more common cause of hypertension than was previously thought) argue for an important role for aldosterone excess as a cause of cardiovascular injury.5. The recognition of non‐blood pressure‐dependent adverse sequelae of aldosterone excess raises the question as to whether normotensive individuals with PAL, who have been detected as a result of genetic or biochemical screening among families with inherited forms of PAL, are at excess risk of cardiovascular events.6. Provided that patients are carefully investigated in order to permit the appropriate selection of specific surgical (laparoscopic adrenalectomy for PAL that lateralizes on adrenal venous sampling) or medical (treatment with aldosterone antagonist medications) management and safety considerations for the use of aldosterone antagonists are kept in mind, the appreciation of a widening role for aldosterone in cardiovascular disease should provide a substantially better outlook for many patients with CCF and hypertension.
Comparison Of Telemetric And Tail‐Cuff Blood Pressure Monitoring In Adrenocorticotrophic Hormone‐Treated Rats
Authors: Fraser Tafline B , Turner Steven W , Mangos George J , Ludbrook John , Whitworth Judith A 
Published: March 2003

SUMMARY1. The aim of the present study was to validate a telemetric blood pressure (BP) monitoring system against tail‐cuff blood pressure in both adrenocorticotrophic hormone (ACTH)‐ and sham‐treated rats. In the statistical analyses, we first tested whether there was a detectable effect on systolic blood pressure (SBP) of 10 days treatment with ACTH compared with saline. Second, we compared results of telemetered and tail‐cuff measurements and, third, we developed a novel method for estimating the relative power of the two techniques.2. Twenty‐three male Sprague‐Dawley rats were randomly divided into two groups: (i) ACTH (100 μg/kg per day, s.c.; n = 12) treated; or (ii) sham treated (0.9% saline, s.c.; n = 11). Systolic BP was measured by the telemetric system (sampled for 10 s every 2 min) continuously for 4 h (n = 16) or for 30 min (n = 23) and also by the indirect tail‐cuff method daily (n = 23). Data were compared within and between groups; ordinary least products (OLP) regression analysis was then performed to test for bias between the two methods. Sample size/power estimations were also performed.3. Adrenocorticotrophic hormone treatment raised telemetered SBP by 11 mmHg (P < 0.001) compared with 14 mmHg (P < 0.001) using the tail‐cuff method. There was no fixed or proportional bias between the two methods of measurement, as shown by regression analysis. Power calculations indicate that a minimum sample size of six gives a power of telemetered to tail‐cuff of 0.84/0.86 = 0.98. The power of 4 h versus 30 min BP measurements was 0.99/0.82 = 1.2.4. Telemetry gave very similar results to the tail‐cuff method. Telemetry allows for a longer period of measurement, giving greater power to the study so that fewer animals are needed.
Increased Cerebral Blood Flow And Cardiac Output Following Cerebral Arterial Air Embolism In Sheep
Authors: Williams David J , Doolette David J , Upton Richard N 
Published: March 2003

SUMMARY1. The effects of cerebral arterial gas embolism on cerebral blood flow and systemic cardiovascular parameters were assessed in anaesthetized sheep.2. Six sheep received a 2.5 mL injection of air simultaneously into each common carotid artery over 5 s. Mean arterial blood pressure, heart rate, end‐tidal carbon dioxide and an ultrasonic Doppler index of cerebral blood flow were monitored continuously. Cardiac output was determined by periodic thermodilution.3. Intracarotid injection of air produced an immediate drop in mean cerebral blood flow. This drop was transient and mean cerebral blood flow subsequently increased to 151% before declining slowly to baseline. Coincident with the increased cerebral blood flow was a sustained increase in mean cardiac output to 161% of baseline. Mean arterial blood pressure, heart rate and end‐tidal carbon dioxide were not significantly altered by the intracarotid injection of air.4. The increased cardiac output is a pathological response to impact of arterial air bubbles on the brain, possibly the brainstem. The increased cerebral blood flow is probably the result of the increased cardiac output and dilation of cerebral resistance vessels caused by the passage of air bubbles.