bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECTS OF ANF PROHORMONE PEPTIDES IN CONSCIOUS PRIMATES
Authors: Benjamin Bruce A. 
Published: June 2007

SUMMARY1. Recent studies suggest that amino‐terminal peptides from the atrial natriuretic factor (ANF) prohormone are natriuretic.2. The effects of pro ANF 31–67 and ANF 99–126 on renal function were studied in conscious non‐human primates (Macaca fuscicularis).3. Results show that pro ANF 31–67 and ANF 99–126 are diuretic and natriuretic and that when the two peptides are given in combination sodium excretion increases in an additive fashion.4. These results indicate that multiple peptides from the ANF prohormone are natriuretic. Furthermore, these findings suggest that the combined action of these peptides causes the natriuresis that occurs after the release of endogenous atrial peptides.
REFLEX REGULATION OF HORMONAL RESPONSES DURING PREGNANCY
Authors: Keller‐Wood Maureen 
Published: June 2007

SUMMARY1. During pregnancy in most species, the resting levels of plasma angiotensin II, plasma ACTH (corticotropin) are increased. The concentration of vasopressin is also increased relatively to the osmolality in rats and in humans.2. In the pregnant state mean arterial pressure is decreased, despite an increase in blood volume. Vasopressin and ACTH responses to hypotension are altered in pregnant ewes; the relationship between mean arterial pressure and vasopressin or ACTH response is shifted to the left, consistent with a change in set‐point for regulation of mean arterial pressure. The vasopressin and cortisol responses to hypotensive haemorrhage are also altered in the pregnant dog; in this case the slope of the relation between mean arterial pressure and hormone response is decreased.3. The decrease in hormone responses to hypotension is stimulus‐specific; ACTH responses to hypoglycaemia are increased in the pregnant ewe and AVP responses to hyperosmolality are not altered in the pregnant ewe.4. The heart rate responses to hypotension are also decreased in pregnant ewes, consistent with the observation that baro‐reflex responses are decreased in the pregnant rat.5. The data suggest that a change in regulation of arterial pressure alters the hormonal responses to hypotension in the pregnant state.
LEFT VENTRICULAR FUNCTION FOLLOWING THROMBOLYTIC THERAPY FOR MYOCARDIAL INFARCTION
Authors: French John K. , White Harvey D. 
Published: June 2007

SUMMARY1.The aim of this study was to evaluate the utility of measurement of left ventricular function in assessing the efficacy of thrombolytic agents.2.All published studies were reviewed.3.The major effect of the introduction of thrombolytic therapy on mortality after myocardial infarction has been a dramatic decrease in the number of patients dying from cardiac failure. In the thrombolytic era, left ventricular function has remained the most important prognostic factor after recovery from acute myocardial infarction. There are three trials with the statistical power to evaluate left ventricular function, where both left ventricular function and survival were improved compared to placebo or control treatment. The recent Global Utility of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) Trial supports these findings, with left ventricular function being strongly correlated with mortality reduction. Left ventricular function, measured at 90 min either as ejection fraction, end‐systolic volume or infarct zone contractility, closely correlated with 30 day mortality, P< 0.01.4. Left ventricular function remains an important factor in the evaluation of the efficacy of different thrombolytic and adjuvant regimens.
CENTRAL NERVOUS SYSTEM ACTIVITY OF RHAZYA STRICTA (DECNE) IN MICE
Authors: Ali B. H. , Bashir A. K. , Banna N. R. , Tanira M. O. M. 
Published: June 2007

SUMMARY1. The effects of orally administered aqueous lyophilized extract of the leaves of Rhazya stricta (2, 4 & 8 g/kg) on aspects of nervous system function were investigated in mice.2. In three antinociceptive tests (hot plate, abdominal constriction, and warm water tail flick tests), the extract exhibited dose‐dependent and significant antinociceptive activity. Naloxone was ineffective in antagonizing the analgesic effect of Rhazya stricta on tail‐flick and abdominal constriction tests, possibly indicating that this effect occurs via non‐opiate pathways.3. Pretreatment of mice with the xenobiotic metabolizing enzymes inhibitor cimetidine (50 mg/kg) did not significantly alter the antinociceptive action of the extract, indicating that the effect is probably due to the parent compound(s) present in the extract and not to metabolites thereof.4. R hazy a stricta produced dose‐dependent sedation, decreased motor activity, and impaired motor control. Time spent on a rotarod treadmill was significantly decreased after treatment with the extract.5. R hazy a stricta extract (8 g/kg) produced a degree of sedation comparable to that produced by diazepam (5–10 mg/kg), and also significantly increased the reaction time of the tail‐flick test, an action which was not produced by diazepam.6. Administration of R. stricta extract potentiated pento‐barbitone sleeping time in a dose dependent manner. The extract did not significantly antagonize picrotoxin induced convulsions. The extract (4 and 8 g/kg) significantly decreased the rectal temperature of normothermic and hyperthermic mice.7. Pretreatment with R. stricta extract (8 g/kg) completely prevented the occurrence of aggressive behaviour in male mice.8. It is concluded that the crude extract of R. stricta has central nervous system depressant properties.
EVIDENCE OF AN ADENOSINE‐DEPENDENT MECHANISM IN THE HYPOTENSIVE EFFECT OF l‐ARGININE IN MAN
Authors: Pasini Franco Laghi , Frigerio Carlo , Blardi Patrizia , Domini Lorenzo , Giorgi Laura De , Borgogni Giovanna , Pecchi Silvio , Cati Graziella , Franchi Massimo , Volpi Luciana , Perri Tullio Di 
Published: June 2007

SUMMARY1. The hypothesis that endogenous adenosine could play a role in the haemodynamic response to l‐arginine is investigated.2. The study has been divided into two parts. The first part was a single blind, randomized, placebo‐controlled study in which L‐arginine i.v. infusion (0.07 mmol/kg per min) in five healthy volunteers caused a significant fall in systolic (‐14.2%, from 129.0 ± 8.2 to 110.6 ± 8.5 mmHg; F= 62.89, P<0.0l), diastolic (‐16%, from 80.0 ± 7.9 to 67.2 ± 7.0 mmHg; F= 18.97, P < 0.0l) and mean (‐15.5%, from 96.4 ± 6.7 to 81.4 ± 6.5 mmHg; F= 28.78, P< 0.01) arterial blood pressure, with a concomitant increase of plasma adenosine concentration (from 244.0 ± 32.2 to 637.0 ± 43.4 nmol/L; F= 79.3 P<10.01). Maximal effects were obtained at the end of L‐arginine infusion: haemodynamic parameters returned to basal values in about 30 min while adenosine concentrations normalized in about 15 min. Saline infusion had no effect on these parameters.3. In the second study the effect of L‐arginine i.v. infusion on arterial blood pressure, lower limb blood flow and plasma adenosine, before and after theophylline treatment (1000 mg/day for 3 days, p.o.) was examined. In 10 healthy volunteers the i.v. infusion of l‐arginine (0.07 mmol/kg per min) was followed by the same haemodynamic changes as reported above and by a Significant increase in lower limb blood flow (+ 36.7%, from 2.18 ± 0.40 to 2.98 ± 0.71mL/min/lOOmL;t = 4.61, P< 0.01). Pretreatment with theophylline, an adenosine‐receptor antagonist, did not affect basal values of arterial pressure, lower limb blood flow and adenosine concentration. The pretreatment with theophylline reduced maximal decrease in systolic pressure (‐ 8.2 vs ‐15%), in mean pressure (‐ 9.9 vs ‐13.7%) and maximal increase in lower limb blood flow (+19 vs + 37%) caused by i.v. infusion of l‐arginine (0.07 mmol/kg per rnin). Such a treatment allowed a progressive restoration of basal blood pressure values and of blood flow, during the second half of l‐arginine infusion. This observation was confirmed by the analysis of the area under the curves (AUC). A significant difference in AUC values before and after treatment was obtained for systolic pressure (t = 8.25, P< O.Ol), mean pressure (t= 6.67, P<0.0l) and blood flow (t= 2.31, P<0.05).4. Theophylline study suggested that the endogenous adenosine increase is sufficient to participate at least in part in the haemodynamic changes caused by l‐arginine and that it is involved in a secondary response to l‐arginine.
CYCLOSPORINE A HEPATOTOXICITY: EFFECT OF PROLONGED TREATMENT WITH CYCLOSPORINE ON BILIARY LIPID SECRETION IN THE RAT
Authors: Galán Ana I. , Fernández Emilio , Morán Dominica , Muñoz Maria E. , Jiménez Rafael 
Published: June 2007

SUMMARY1. The effects of cyclosporine A (CyA) treatment on liver morphology, bile flow and biliary secretion of bile acid, cholesterol and phospholipid and some plasma biochemical indicators of liver function were examined.2. Wistar rats were treated i.p. with 10 or 20 mg of CyA/kg per day for 1, 2, 3 or 4 weeks.3. Treatment increased bile acid and bilirubin plasma concentration. Bile flow and biliary secretion of bile acid, cholesterol and phospholipid were reduced in CyA‐treated animals.4. All these effecs of the drug appeared at 1 week after the start of treatment and were enhanced during prolonged treatment. Cyclosporine A‐induced cholestasis was due to a decrease in both the bile acid‐dependent and ‐independent fractions of bile flow.5. The reduction in cholesterol and phospholipid biliary output may be secondary to the inhibition of the hepatobiliary flux of bile acid; however, perturbations in the removal of lipids from the canalicular membrane as well as intracanalicular interaction between CyA and lipid vesicles/micelles could also be involved.
NITRIC OXIDE: ROLE IN NEUROTOXICITY
Authors: Dawson Valina L. 
Published: June 2007

SUMMARY1. Nitric oxide (NO) is a novel neuronal messenger molecule which interacts with surrounding neurones, not by synaptic transmission but by diffusion between cells.2. No is produced following stimulation of the enzyme, NO synthase (NOS). After synthesis, NO exerts its biological actions by diffusion to the site of action. Therefore, the way to regulate the physiological actions of NO is to regulate NOS.3. NOS is activated by the influx of calcium from glutamate‐activated N‐methyl‐D‐aspartate receptors. Overactivation of these receptors leads to overproduction of NO and neuronal cell death.4. NOS can be regulated at the catalytic site, at the flavoproteins, at the calmodulin site and by phosphorylation.5. In excess, NO is toxic to neurones. This toxicity is mediated largely by an interaction with the superoxide anion, presumably through the generation of the oxidant, peroxynitrite.6. NO or peroxynitrite‐mediated neuronal injury involves the activation of the nuclear protein, poly(ADP‐ribose)synthetase.
EFFECTS OF GLYCERYL TRINITRATE TOLERANCE ON VASCULAR RESPONSIVENESS TO CONSTRICTOR AGENTS IN BOVINE ISOLATED CORONARY ARTERY
Authors: Zhang C. L. , de la Lande I. S. , Horowitz J. D. 
Published: June 2007

SUMMARY1. Recent clinical studies have raised the possibility that intermittent nitrate dose regimens, while limiting the extent of nitrate tolerance development, may trigger rebound aggravation of ischaemia after abrupt withdrawal of nitrate. To date, only limited studies have been performed to examine the mechanism of this phenomenon.2. In a bovine isolated coronary artery model, we tested the hypothesis that induction of glyceryl trinitrate (GTN) tolerance might affect large coronary artery responsiveness to a variety of non‐catecholamine constrictor agents. Glyceryl trinitrate tolerance was induced by pre‐exposure to GTN (10 μmol/L) for 60 min followed by 15 min washout. In some experiments, the effect of prior endothelial removal on putative interactions was also examined.3. Our results showed that GTN tolerance did not affect responses to KCI, the thromboxane A2 mimetic U46619, endo‐thelin‐1 and 5‐HT, irrespective of presence or absence of endothelium. None of the constrictor agents tested induced endothelium‐dependent constriction.4. We conclude that in this model of GTN tolerance induction, there is no evidence of ‘rebound’ vasoconstriction to this group of non‐catecholamine vasoconstrictors with GTN withdrawal.
SPECTRAL ANALYSIS OF SYSTOLIC BLOOD PRESSURE AND HEART RATE OSCILLATIONS RELATED TO RESPIRATION
Authors: Laude Dominique , Weise Frank , Girard Arlette , Elghozi Jean‐Luc 
Published: June 2007

SUMMARY1. Non‐invasive assessment of short‐term systolic blood pressure (SBP) and heart rate (HR) variability was obtained with the plethysmographic finger blood pressure measurement device. Respiration was measured with a respiratory inductive plethysmograph, which was calibrated prior to each study.2. The effects of breathing pattern on the respiratory (high frequency, HF) component of the SBP or HR spectrum were analysed by Fourier transform.3. Our quantification of the changes in the HF (respiratory) peak of the HR or SBP spectrum with changes in tidal volume (Vt) and breathing frequency (BF) indicates that the modulus of this component may be predicted for any combination of depth and frequency of breathing.4. The modulus of this HF component for the HR or SBP spectrum was linearly related to the respiratory sinus arrhythmia (RSA) or to the SBP oscillation related to respiration.
ENDOTHELIAL DYSFUNCTION IN CORONARY VESSELS AND THORACIC AORTA OF RATS EXPOSED TO CIGARETTE SMOKE
Authors: Jorge P. A. Ribeiro , Ozaki M. R. , Almeida E. A. 
Published: June 2007

SUMMARY1. The aim of this study was to evaluate the role of endothelium in mediating the response to acetylcholine in the thoracic aorta and coronary vessels of rats exposed to cigarette smoking. Total serum cholesterol was measured at the beginning and end of the experiment.2. The relaxation response to acetylcholine was significantly impaired in the aortae of rats exposed to cigarette smoking (P < 0.05); and the coronary flow during the administration of acetylcholine (0.02 μg/min.) was significantly reduced (P < 0.05). The total cholesterol plasma levels increased 31.13% in those exposed to smoke when compared to the controls (P < 0.05).3. It is concluded that exposure to cigarette smoking increases total serum cholesterol levels, and also produces primary endothelial dysfunction in aorta rings and coronary vessels.
EFFECTS OF GARLIC EXTRACT ON PLATELET AGGREGATION: A RANDOMIZED PLACEBO‐CONTROLLED DOUBLE‐BLIND STUDY
Authors: Morris Jenny , Burke Valerie , Mori Trevor A. , Vandongen Robert , Beilin Lawrie J. 
Published: June 2007

SUMMARY1. Studies of the effects of garlic on platelet aggregation have produced inconsistent results possibly related to variations in study design and in the garlic preparations used.2. The present study examined the effects on platelet aggregation and serum thromboxane and lyso‐platelet activating factor, of feeding garlic extract to healthy men using a placebo‐controlled, double‐blind design. The effects of the same garlic preparation on platelet aggregation in vitro were also investigated.3. There were no significant differences in platelet aggregation with adenosine diphosphate, platelet activating factor (PAF) or collagen according to treatment group. Serum thromboxane and IysoPAF also showed no change related to garlic supplements.4. In vitro aggregation with collagen decreased linearly with increasing amounts of garlic extract, but concentrations were higher than those attainable in vivo. Gastrointestinal side effects prevented the use of higher doses of garlic which must be considered to be pharmacological as they exceed changes achievable by dietary modification.
A CONTROLLED TRIAL OF NURSE COUNSELLING ON LIFESTYLE CHANGE FOR HYPERTENSIVES TREATED IN GENERAL PRACTICE: PRELIMINARY RESULTS
Authors: Woollard J. , Beilin L. , Lord T. , Puddey I. , MacAdam D. , Rouse I. 
Published: June 2007

SUMMARY1. We assessed whether a lifestyle modification programme implemented by nurse counsellors in a general practice setting would improve blood pressure (BP) control in treated hypertensive patients.2. Patients were randomized into a control group or one of two intervention groups who received either a high or low level of counselling.3. Patients in the intervention groups had appointments every 4th week for 18 weeks. The low intervention group had one practice appointment and five telephone counselling appointments while the high intervention group had six appointments in their general practice. The patients were counselled using a stage of change behavioural model and motivational interviewing to: reduce alcohol consumption, dietary fat and salt intake and weight; cease smoking; and increase leisure time physical activity.4. Compared with controls the low intervention group showed signifcant decreases in alcohol and salt intake while the high intervention resulted in significant decreases in both weight and BP.5. We conclude that nurse counselling targeted to specific aspects of lifestyle can improve BP control and weight in treated hypertensive patients over 18 weeks. Its longer term effectiveness in the management of hypertension warrants further evaluation.
SYMPATHETIC REGULATION IN RABBITS WITH HEART FAILURE: EXPERIENCE USING POWER SPECTRAL ANALYSIS OF HEART RATE VARIABILITY
Authors: Moguilevski V. , Oliver J. , McGrath B. P. 
Published: June 2007

SUMMARY1. In five intact rabbits β‐adrenoreceptor blockade (i.v. propranolol), and combined cardiac blockade (i.v. propranolol plus i.v. methscopolamine sulphate) revealed that spectral power of heart rate (HR) variability at low frequencies (LF: 0.0625–0.1875 Hz) was modulated predominantly by the sympathetic nervous system and power at high frequencies (HF: 0.4373–0.5625 Hz) by vagal influences.2. In 16 rabbits resting power of HR at LF and changes in LF power in response to maximal treadmill exercise were examined prior to and after 4 and 6 weeks of doxorubicin treatment (1 mg/kg twice weekly).3. The development of doxorubicin‐induced congestive heart failure (CHF) was accompanied by a progressive increase in resting LF power [control, 8.5 ± 2.1; 4 weeks, 13.4 ± 1.8; 6 weeks, 21.9 ± 3.5 (beats/min)2, P < 0.005].4. Power spectral analysis (PSA) of HR variability in the immediate post‐exercise period showed no change from resting values in normal rabbits [5.3 ± 1.4 vs 8.5 ± 2.1 (beats/min)2, P>0.05] whereas CHF rabbits showed falls in LF power after 4 weeks [4.6 ± 1.0 vs 13.4 ± 1.8 (beats/min)2, P < 0.005] and 6 weeks [6.5 ± 2.4 vs 21.9 ± 3.5 (bents/min)2, P < 0.005] of doxorubicin treatment.5. It was concluded that PSA of HR variability reflects the autonomic regulation of sinus node function in conscious rabbits. In doxorubicin‐treated animals, the rise in LF power reflects increased sympathetic activity as CHF develops. However, the apparent paradoxical fall in LF power with exercise in these animals underscores the need for caution in interpretation of PSA profiles.
INFLUENCE OF BODY TEMPERATURE ON RESPONSES TO HYPOXIA AND HYPERCAPNIA: IMPLICATIONS FOR SIDS
Authors: Maskrey Michael 
Published: June 2007

SUMMARY1. This paper reviews current knowledge regarding interactions between body temperature and the respiratory responses to hypoxia and/or hypercapnia, with special emphasis on how these interactions might predispose towards sudden infant death syndrome (SIDS).2. Use has been made of an adult rat model in which body core temperature is fixed by means of an intra‐abdominal heat exchanger. Initial studies indicated that hyperthermia (Tb∼ 41° C) enhanced the ventilatory response to hypercapnia, whereas hypothermia (Tb∼35°C) interacted with hypoxia to depress respiration.3. Studies involving hypothalamic lesions in urethane‐anaesthetized rats have implicated the posterior hypothalamic area in the hypoxia/hypothermia interaction. Further studies are directed towards examining the role played by more caudal areas, including the raphe nuclei.4. It has been shown that not only does the hypoxial hypothermia interaction depress breathing but it also reduces, or sometimes eliminates, the ventilatory response to hypercapnia, which under normal circumstances provides one of the most powerful excitatory inputs to the respiratory centres. This implies that an expected reversal of the respiratory depression by build up of CO2 levels may not occur, which in turn has important implications for SIDS.5. The literature dealing with the effects of hyperthermia on hypoxic and hypercapnic responses is also reviewed. It is concluded that environmental heat stress may only become a significant problem when it accompanies a febrile infection, under which circumstances it may seriously compromise thermo‐regulatory ability and alter breathing responses to chemical stimuli.
PHYSIOLOGICAL STUDIES OF GASTRO‐OESOPHAGEAL REFLUX AND AIRWAY PROTECTIVE RESPONSES IN THE YOUNG ANIMAL AND HUMAN INFANT
Authors: Jeffery Heather E. , Page Megan , Post Elizabeth J. , Wood Andrew K. W. 
Published: June 2007

SUMMARY1. The mechanisms that underlie the Sudden Infant Death Syndrome (SIDS) must explain its two unique features; age at death and death during apparent sleep.2. The occurrence of gastro‐oesophageal reflux (GOR) during active sleep in infants presenting with apparent life threatening episodes (ALTE) and their similar age distribution to SIDS infants, suggested that reflux could be a cause of asphyxia.3. Sleep related GOR was found to be a physiological and not a pathological event in normal, healthy term infants.4. In healthy term infants, those infants that were formula‐fed (who have a higher incidence of SIDS) had significantly longer oesophageal clearance times for acid reflux and significantly more active sleep compared with breast fed infants.5. In very preterm infants (who are at increased risk for SIDS), both the frequency and duration of reflux during active sleep was significantly less at term equivalent age compared with healthy term infants, suggesting additional factors must operate to promote an ALTE.6. One mechanism which may explain the pathogenesis of GOR could be that the reflux reaches the level of the pharynx and this, in turn, stimulates laryngeal receptors to produce apnoea.7. Simulated reflux to the level of the pharynx in the sleeping piglet evoked airway protective responses, namely swallow, arousal and occasionally expectoration, but neither apnoea nor oxygen desaturation.8. In the same piglets treated with pentobarbitone sodium, swallowing was impaired and arousal depressed. Simulated reflux to the pharynx produced significant apnoea and oxygen desaturation and death in two of five piglets.9. In the infant, the co‐existence of reflux to the level of the pharynx during sleep, together with impaired swallowing, depressed arousal or both, is one mechanism that may lead to an age‐limited, sudden and fatal apnoea.
GOOD VIBRATIONS? RESPIRATORY RHYTHMS IN THE CENTRAL CONTROL OF BLOOD PRESSURE
Authors: Pilowsky Paul 
Published: June 2007

SUMMARY1. Arterial blood pressure is maintained, and reflexly controlled, by the activity of neurons in the medulla and spinal cord.2. Rhythmic, automatic, respiratory activity is generated by neurons in the ventral medulla and transmitted to pre‐motoneurons and motoneurons in the medulla and spinal cord.3. Sympathetic nerve activity often has a respiratory rhythmicity.4. One site at which the interaction between respiratory and sympathetic neurons occurs is the ventrolateral medulla.5. Different types of sympathetic neurons, such as muscle vasoconstrictor, sudomotor and pilo‐erector, have different patterns of respiratory rhythmicity.6. Inputs from medullary respiratory neurons to medullary sympathetic premotor neurons may be the mechanism that co‐ordinates the activity of these two vital systems.