bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECTS OF CHANGING HAEMATOCRIT, VENTRICULAR RATE AND MYOCARDIAL INOTROPY ON THE ACCURACY OF IMPEDANCE CARDIOGRAPHY
Authors: Quail A. W. , Traugott F. M. 
Published: June 2007

SUMMARY1. The accuracy and limitations of the non‐invasive impedance cardiograph technique were examined in dogs with electromagnetic flow‐transducers mounted on the aortic root over a wide range of physiological conditions of anaemia, heart rate, stroke volume and myocardial inotropy.2. The in vivo blood resistivity (ρ)‐haematocrit relationship is linear and slightly inverse, and is thus opposite to the curvilinear, direct relationship of the bench‐derived p‐haematocrit relationship. At haematocrit 41%, in vivoρ is 135 ohm. cm (s.e.m. = 1.0, n ‐ 134) and rises only to 143 ohm. cm (s.e.m. = 1.6, n= 134) as haematocrit falls to 26%.3. When in vivoρ is used in the Kubicek formula for stroke volume (SV) calculation, the instrument is linear and accurate for heart rates over 38–156 min‐1. Thus 82% of all points fall within ±20% of the line of equal value over stroke volumes ranging from 8–46 ml (N = 3, n= 105). The standard error of the estimate for pooled data is ±2% of the mean impedance stroke volume value of 22.2 ml. The instrument tends to overread at heart rates lower than 60 min‐1.
INCREASED CONVERSION OF ARACHIDONIC ACID TO VASODILATOR PROSTANOIDS IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Dusting G. J. , Davies W. , Drysdale T. , Doyle A. E. 
Published: June 2007

SUMMARY1. Vasodepressor responses to intravenous injection of prostacyclin, arachidonic acid, and nitroprusside were examined in anaesthetized, spontaneously hypertensive rats (SHR) of the Okamoto strain, and in their normotensive Wistar– Kyoto (WKY) controls.2. Depressor responses to prostacyclin and nitroprusside did not differ significantly between the two strains.3. The vasodepressor effects of arachidonic acid were greater and much more prolonged in SHR than in WKY. In rats treated with indomethacin (2 mg/kg) arachidonic acid induced only transient depressor responses which did not differ significantly between these strains.4. It is concluded that SHR do not differ from WKY in their sensitivity to prostacyclin but they have enhanced ability to transform exogenous arachidonic acid into vasodilator prostanoids.
IMMUNOREACTIVE β‐ENDORPHIN LEVELS IN PLASMA AND PITUITARY TISSUE FROM GENETICALLY HYPERTENSIVE AND NORMOTENSIVE RATS
Authors: Hutchinson J. S. , Lim A. , DiNicolantonio R. , Clements J. A. , Funder J. W. 
Published: June 2007

SUMMARY1. Levels of immunoreactive β‐endorphin were measured in neurointermediate lobes, anterior lobes and plasma from the Japanese and New Zealand strains of genetically hypertensive rats and their normotensive controls.2. No significant differences were observed in β‐endorphin between the hypertensive and normotensive rats of the New Zealand strain.3. The hypertensive rats of the Japanese strain showed significantly higher levels of β‐endorphin in neurointermediate lobe and lower levels in plasma than their normotensive controls.4. These results suggest that the differences in β‐endorphin levels in the Japanese strain reflect a genetic difference not necessarily related to elevated blood pressure.
ON THE RELATIONSHIP BETWEEN CARDIAC OUTPUT AND PERIPHERAL ARTERIAL RESISTANCE
Authors: Boyd G.W. , Yong A.C. 
Published: June 2007

SUMMARYThe concept of ‘whole body auto‐regulation’ is a somewhat unsatisfactory explanation of the increased peripheral arterial resistance which follows a rise in cardiac output in ‘volume’ forms of hypertension. This analysis suggests that the resistance change may be due to the sodium retention and increased cardiac output having a direct effect to alter haemodynamics of flow through the arterioles in such a way as to damage their walls, and so lead to the gradual development of structural arteriolar narrowing. Studies are presented in the DOCA/salt hypertensive rat consistent with this proposal.
CENTRAL AMINERGIC MECHANISMS ASSOCIATED WITH THE CLONIDINE WITHDRAWAL SYNDROME
Authors: Lewis S.J. , Fennessy M. R. , Taylor D. A. 
Published: June 2007

SUMMARY1.Rats were injected twice daily, at 12.00 and 24.00 hours, with clonidine hydrochloride (50 μg/kg, i‐P‐) until they had received seven injections. Two hours after the 7th injection, their blood pressures, heart rates and body temperatures were decreased (P<0.05) when compared to saline‐treated controls.2. In rats which received six injections of clonidine hydrochloride (50 μg/kg, i.p.) and an injection of saline when the 7th injection of clonidine was due, the blood pressure, heart rate and body temperature were all significantly (P<0.05) increased 2 h after the saline injection, which was 14 h after the 6th injection of clonidine.3. Chronic treatment with clonidine hydrochloride significantly (P<0.05) increased the concentrations of noradrenaline and decreased those of histamine in the medulla oblongata/pons. In the hypothalamus the concentrations of noradrenaline and serotonin were significantly (P<0.05) increased.4. During the withdrawal phase the concentrations of dopamine and histamine were significantly (P<0.05) increased in the medulla oblongata/pons, while those of noradrenaline had returned to the control values. In the hypothalamus the concentrations of histamine and noradrenaline were significantly (P<0.05) increased while those of serotonin had returned to the control value.5. Methysergide (2 mg/kg, i.p.) when injected during the withdrawal phase produced significant (P<0.05) reductions in the hypertension, tachycardia and hyperthermia which are displayed at this time.6. It is concluded that chronic clonidine treatment may decrease the release of noradrenaline from the medulla oblongata/pons and that of serotonin from the hypothalamus. However, on cessation of treatment, increases in the release of these amines appear to be associated with the increases in blood pressure, heart rate and body temperature.
THE CARDIOVASCULAR EFFECTS OF INTRA VERTEBRAL ANGIOTENSIN II BEFORE AND AFTER TREATMENT WITH CLONIDINE
Authors: Lumbers Eugenie R. , Reid I. A. 
Published: June 2007

SUMMARY1. In anaesthetized mongrel dogs it was shown that intravertebral infusions of angiotensin II (2–4 ng/kg per min) increased mean arterial pressure by causing an increase in cardiac output, while infusions of 10 ng/kg per min increased mean arterial pressure through an effect on peripheral resistance. After intravenous clonidine, intravertebral angiotensin no longer had any stimulatory effect on cardiac output, but arterial pressure still increased to the same extent.2. It is concluded that intravertebral angiotensin can increase arterial pressure by increasing either cardiac output or peripheral resistance. The effects of intravertebral angiotensin on cardiac output can be reduced by concomitant stimulation of baroreflex pathways but its effects on peripheral resistance are not so readily antagonized.
β‐ADRENOCEPTORS IN THE HYPERTROPHIED RIGHT VENTRICLE OF THE DOG WITH PULMONARY STENOSIS
Authors: Sturm M. , Taylor R. R. 
Published: June 2007

SUMMARY1.Right ventricular hypertrophy was produced in dogs by banding of the pulmonary artery for 28 days (n= 7) and results were compared with those in sham‐operated dogs (n= 5).2. Myocardial noradrenaline and adrenaline levels were depressed in both the hypertrophied right ventricle and the non‐hypertrophied left ventricle and plasma levels were increased compared to the control dogs.3. Myocardial β‐adrenoceptors were assessed in membrane preparations of both ventricles by 3H‐dihydroalprenolol binding. No change in binding site concentration (pmol/mg membrane protein) or in binding affinity was found in either the hypertrophied right ventricle or in the left ventricle.4. Divergent results of studies on β‐adrenoceptors in ventricular hypertrophy are difficult to reconcile.
EFFECTS OF α‐ AND β‐ADRENOCEPTOR AGONISTS AND A PHOSPHODIESTERASE INHIBITOR (ICI 63 197) ON CYCLIC AMP AND GMP LEVELS IN BOVINE SPLENIC NERVE
Authors: Merican Zainuddin , Nott M. W. 
Published: June 2007

SUMMARY1. Cyclic AMP and cyclic GMP levels were determined in bovine splenic nerve segments in the absence and presence of (±) ‐ isoprenaline, (‐)‐phenylephrine, clonidine and ICI 63 197 (a phosphodiesterase inhibitor). The chosen concentrations of adrenoceptor agonists were those which are known to affect stimulation‐induced overflow of noradrenaline from nerve terminals.2. The mean levels of cyclic AMP ranged from 229 to 555 pmol/g of microwave irradiated tissue. Mean cyclic GMP levels ranged from 27.9 to 42.2 pmol/g.3.Isoprenaline enhanced cyclic AMP levels but did not affect cyclic GMP levels. The effect was blocked with (±)‐propranolol. ICI 63 197 increased cyclic AMP levels but did not change cyclic GMP. Phenylephrine and clonidine caused no consistent changes in cyclic AMP or cyclic GMP levels or in the concentration ratio between these two nucleotides.4.The results support the involvement of cyclic AMP in the enhancing effect of β‐adrenoceptor agonists and phosphodiesterase inhibitors on stimulation‐induced release of noradrenaline from sympathetic nerves.
KCL CONTRACTIONS IN THE RAT INTACT AND BISECTED VAS DEFERENS: CONTRIBUTION OF ENDOGENOUS NORADRENALINE RELEASE
Authors: Hay D. W. P. , Wadsworth R. M. 
Published: June 2007

SUMMARY1 KCl produced a biphasic contraction in the intact rat vas deferens. Both components were larger and the initial rapid phasic component was faster in the prostatic portion than the epididymal portion. In some experiments the epididymal phasic response was a single slow contraction, while in others it had a mixture of fast and slow responses.2 Phentolamine reduced the phasic response but not the tonic response of the intact vas deferens. This effect was not observed after denervation produced by chronic guanethidine treatment.3 Both phases of the response to KC1 160 mmol/1 were substantially reduced by phentolamine in the epididymal portion. In the prostatic portion phentolamine produced only slight inhibition of the phasic component and had no effect on the tonic component.4 Isoprenaline had no effect on the response to KC1160 mmol/1 but reduced both phases of the response to KC150 mmol/1. This effect was antagonized by propranolol.5 It is concluded that part of the phasic component of the response to KC1 in the rat vas deferens is due to the release of noradrenaline from intramural nerves.
CEREBROVASCULAR AND METABOLIC EFFECTS OF BRADYKININ, ATP AND HYPERCAPNIA IN THE GOAT
Authors: Hoffman William E. , Miletich David J. , Volkman Paul H. , Albrecht Ronald F. 
Published: June 2007

SUMMARY1. Cerebral blood flow (CBF) and cerebral O2 metabolism (CMRO2) changes were measured in these studies during treatment with three reputed cerebral vasodilators: bradykinin, adenosine triphosphate (ATP) and increased arterial Pco2.2. Intracerebrovascular bradykinin infusions increased CMRO2 and CBF to a similar degree. Intramaxillary ATP infusions increased CBF to an extent greater than that required for increases seen in CMRO2. Hypercapnia increased CBF without a significant change in CMRO2.3. Results suggest that increases in cerebral metabolism may mediate most, some and none of the cerebrovascular changes produced by bradykinin, ATP or hypercapnia, respectively.
MODIFICATION BY GABA‐ERGIC AGENTS AND CLONIDINE OF MORPHINE‐INDUCED CONVULSIONS AND TOXICITY IN RATS
Authors: Kulkarni S. K. , Nagrath Alka 
Published: June 2007

SUMMARY1. Intracerebroventricular (i.c.v.) administration of morphine produced dose‐dependent behavioural changes in rats, the highest dose producing violent tonic convulsions.2. Naloxone (up to 10 mg/kg i.p., or 100 μg i.c.v.) failed to reverse morphine‐induced toxicity.3. The conventional anticonvulsant drugs also failed to offer protection to morphine‐induced seizures.4. GABA‐ergic substances, GABA, piracetam and diazepam, on the other hand, protected the animals against morphine‐induced convulsions and toxicity. Similarly, clonidine pretreatment also had a protective action against morphine‐induced convulsions.
THE MECHANISM OF POLYURIA IN RATS PRETREATED WITH LITHIUM STUDIES BY IN VITRO MICROPERFUSION
Authors: Ray C. , Morgan T. , Carney S. 
Published: June 2007

SUMMARYThe collecting ducts in papillae taken from normal rats have a measurable increase in diffusional tritiated water (THO) permeability with ADH 5 μunit/ml and this increase is maximal with antidiuretic hormone (ADH) 100 μunit/ml added to the media.2 The presence of plasma from rats pretreated with lithium to make them polyuric inhibited the response to ADH. The lowest concentration of ADH that caused a measurable increase in diffusional water permeability was 50 μunit/ml and the increase was maximal with ADH 2000 μunit/ml.3 The maximum response to ADH did not differ whether plasma from control or lithium pretreated rats was used. However, the dose‐response curve to ADH was shifted to the right by the plasma from lithium‐pretreated rats.4 Lithium added to the plasma from control rats did not alter the response to ADH.5 It is proposed that lithium given to rats causes a circulatory factor to be produced that inhibits in a competitive fashion the response of the collecting duct to ADH. Such an effect would explain many features of the impairment of water excretion associated with lithium use.
GRADED EFFECTS OF SARALASIN ON PROSTAGLANDIN E, PLASMA RENIN ACTIVITY AND RENAL BLOOD FLOW IN ANAESTHETIZED DOGS
Authors: Wong Pancras C. , Zimmerman Ben G. 
Published: June 2007

SUMMARY1. The objective of this study was to examine in anaesthetized dogs the graded effect of saralasin on renal prostaglandin E (PGE) release and to attempt to associate this change with its effects on plasma renin activity and renal blood flow.2. Blood pressure and renal blood flow were monitored. Renal PGE concentration and plasma renin activity were measured by radioimmunoassay. Saralasin or saline vehicle was infused into the renal artery for 20 min.3. Infusion of saralasin at the lowest dose of 0.25 &#x006d;̈g/kg per min or saline vehicle did not alter either renal blood flow or plasma renin activity. Saralasin increased renal blood flow and caused a complete blockade of the renal vasoconstrictor response to exogenous angiotensin II at the two higher doses used (0.5 and 1 &#x006d;̈g/kg per, min). Only the highest dose of saralasin increased plasma renin activity significantly.4. Renal venous PGE concentration at the 5, 10 and 20 min periods of infusion was not changed significantly by any of these three doses of saralasin. We conclude therefore that the increases in renal blood flow and plasma renin activity caused by saralasin in the anaesthetized dog occur by mechanisms independent of changes in renal PGE.
ATTENUATION OF THE ANTIHYPERTENSIVE EFFECT OF CAPTOPRIL BY THE OPIOID RECEPTOR ANTAGONIST NALOXONE
Authors: Millar J. A. , Sturani A. , Rubin P. C. , Lawrie C. , Reid J. L. 
Published: June 2007

SUMMARY1 To test a possible role of endogenous opioids in the blood pressure (BP) and heart rate (HR) responses to the converting enzyme inhibitor captopril in man, nine normal subjects were given captopril (50 mg) or placebo with and without the opioid antagonist naloxone (0.2 mg/kg i.v.).2 Treatments were given in random order and under double‐blind conditions. BP and HR were measured supine and after a 5 min head‐up tilt to 60Â˚ before, 90, and 360 min after captopril. BP and HR responses to Valsalva's manoeuvre and isometric exercise (sustained hand grip) were also measured, as indirect tests of baroreceptor reflex function.3 After captopril alone, there was a significant decrease in supine diastolic and tilt systolic and diastolic BP at 90 min (7.8, s.d. = 6; 15.4, s.d. = 13; and 7.0, s.d. = 12 mmHg, respectively). When naloxone was also given, corresponding changes were 0 (s.d. =9), 0 (s.d. = 15) and 3 (s.d. =7) mmHg.4 The effect of naloxone on the changes in supine diastolic and tilt systolic BP were significant (P=0.017, P= 0.030 respectively; analysis of variance). No significant effects of treatment on supine or tilt HR were seen. BP and HR changes during Valsalva's manoeuvre and isometric exercise were not altered by active treatment.5 These results suggest that the BP but not the HR responses to converting enzyme blockade are mediated by endogenous opioids.
ATTENUATION BY CAPTOPRIL OF PRESSOR RESPONSES TO PERIPHERAL SYMPATHETIC NERVE STIMULATION IN RATS IS ABOLISHED AFTER BILATERAL NEPHRECTOMY AND DURING MINERALOCORTICOID HYPERTENSION
Authors: Boura A. L. A. , Hui S‐C. G. , Ishac E. J. N. , Rechtman M. P. , Walters W. A. W. 
Published: June 2007

SUMMARY1. Intravenous administration of captopril (0.1‐0.3 mg/kg) to normotensive pithed rats, with or without unilateral nephrectomy, was followed by a sustained fall in arterial blood pressure. Concomitantly pressor responses to electrical stimulation of the spinal sympathetic outflow (T11‐L3), ganglion stimulation with McNeil‐A‐343 (4‐(m‐chlorophenylcarbamoyloxy)‐2‐butynyl‐trimethylammonium chloride) or intravenous injection of noradrenaline were reduced. Attenuation by captopril (1 mg/kg) of pressor responses to McNeil‐A‐343 persisted after intravenous propranolol (1 mg/kg). Tachycardia caused by electrical stimulation of the spinal sympathetic nerves (C7‐T2) was unchanged after 3.0 mg/kg captopril.2. After procedures reducing the activity of the renin angiotensin system, bilateral nephrectomy or induction of mineralocorticoid hypertension by unilateral nephrectomy and administration of desoxycorticosterone acetate, pressor responses to McNeil‐A‐343 or noradrenaline were unchanged after 1 mg/kg captopril.3. It is concluded that in the pithed rat, basal arterial blood pressure and the height of pressor responses to either postganglionic sympathetic nerve activation or intravenous noradrenaline depend on converting enzyme activity maintaining circulating angiotensin II levels.
CARDIOVASCULAR EFFECTS OF STIMULATION OF NEURONES WITHIN THE ‘DEFENCE AREA’ OF THE HYPOTHALAMUS AND MIDBRAIN OF THE RABBIT
Authors: Tan Esther , Dampney R. A. L. 
Published: June 2007

SUMMARY1. In anaesthetized rabbits, electrical stimulation applied at many sites within the medial hypothalamus and dorsal midbrain elicited a skeletal muscle vasodilatation.2. Vasodilator responses were only elicited by microinjections of glutamate ions (which excite only cell bodies) into a much more restricted region: the periaqueductal grey (PAG) in the midbrain, and the ventromedial nucleus in the hypothalamus.3. The results suggest that cell groups within the PAG and ventromedial nucleus are capable of generating skeletal muscle vasodilatation, which is characteristic of the ‘defence reaction’. At other sites within the ‘defence area’, the cardiovascular response to electrical stimulation arises from axons of passage.
EVIDENCE FOR A FUNCTIONAL CENTRAL DOPAMINERGIC INSUFFICIENCY IN THE SPONTANEOUSLY HYPERTENSIVE RAT
Authors: Hutchinson J. S. , DiNicolantonio R. , Veroni M. , Cleverdon M. 
Published: June 2007

SUMMARY1. Several neuroendocrine abnormalities reported in the spontaneously hypertensive rat (SHR) suggest that the function of the dopaminergic tuberoinfundibular tract is impaired in this strain.2. SHR were pretreated with the peripheral acting inhibitor of dopa decarboxylase, carbidopa, or vehicle.3. Intravenous injection of L‐dopa, the precursor of dopamine, lowered blood pressure only in the carbidopa treated SHR suggesting a central dopamine action.4. Intracerebroventricular injection of dopamine in SHR lowered blood pressure towards normal.5. The data are in agreement with the hypothesis that SHR have a functional central dopaminergic insufficiency.
THE QUANTITATION OF ARTERIAL ELASTICITY FROM DOPPLER FLOW MEASUREMENTS
Authors: Kenny Peter , Janod Francoise , Bellamy Greg R. , Mann Stewart , Hunyor Stephen N. 
Published: June 2007

SUMMARY1. The pattern of phasic pressure and flow in an artery is related to the components of the impedance of that artery and hence to its compliance.2. Phasic patterns of velocity in peripheral arteries have been recorded by using continuous wave ultrasound Doppler flowmeters coupled to high‐speed spectrum analysers; this has enabled display of the stored spectral ensembles as ‘sonograms’.3. Simultaneous recordings at proximal and distal sites in each limb of a variety of subjects were made under standard resting conditions; characteristic patterns of change in the sonogram are recognized where gross abnormalities of arterial anatomy are present.4. A technique is under development whereby the mean values of velocity for each 7.4 ms time slice are derived, smoothed, and the pulse described by standard Fourier transform analysis. The change of the waveform occurring during passage through the relevant arterial segment is then described by comparing the amplitude/frequency and time‐delay/frequency plots at proximal and distal sites.5. Although results are at present preliminary, changes relating to age and known vascular abnormality are becoming apparent. Further development is in progress to determine the significance of these findings.
PERIPHERAL ADRENOCEPTORS AFTER SINO‐AORTIC DENERVATION
Authors: Morris Margaret J. , Woodcock Elizabeth A. 
Published: June 2007

SUMMARY1. The effect of bilateral sino‐aortic denervation on cardiac and renal cortical α‐and β‐adrenoceptor concentrations was studied in rats by radioligand binding experiments using [3H]‐prazosin (α,), [3H]‐yohimbine (α2) and [125I]‐iodocyanopindolol (β).2. Cardiac α‐ and β‐adrenoceptor concentrations were not altered by sino‐aortic denervation.3. There was a significant increase in β‐adrenoceptor concentration in the renal cortex of sino‐aortic denervated rats compared to sham‐operated controls.
DIFFERENCES IN ARACHIDONIC ACID METABOLISM AND EFFECTS OF ASPIRIN BETWEEN ONE‐ AND TWO‐KIDNEY GOLDBLATT HYPERTENSIVE RATS
Authors: Dusting G. J. , Drysdale T. , Veroni M. , Doyle A. E. 
Published: June 2007

SUMMARY1. Vasodepressor responses to prostacyclin, nitroprusside and arachidonic acid were compared in two groups of anaesthetized, two‐kidney, one‐clip Goldblatt rats. The groups were composed of rats which had high blood pressure (greater than 150 mmHg systolic) or normal blood pressure (less than 140 mmHg systolic).2. The vasodepressor effects of prostacyclin and nitroprusside and arachidonic acid did not differ significantly between hypertensive and normotensive groups when measured as percentages of resting blood pressure.3. Thus, in contrast to one‐kidney Goldblatt hypertensive rats, there is no evidence for increased vascular conversion of arachidonic acid to prostacyclin in the two‐kidney hypertensive model.4. The effect of cyclo‐oxygenase inhibition on development of hypertension in one‐ and two‐kidney Goldblatt rats was also studied by treating them daily with aspirin (200 mg/kg orally) from 3 days before until 3 weeks after clipping the renal artery.5. Aspirin‐treated two‐kidney rats developed significantly higher blood pressures than vehicle‐treated controls, but the blood pressures of aspirin‐treated one‐kidney rats increased less after clipping than those of vehicle‐treated controls.6. It appears paradoxical that transformation of arachidonic acid to prostacyclin is increased, while aspirin has a blood pressure lowering effect in one‐kidney Goldblatt rats. It is suggested that there might be a more fundamental disturbance in arachidonate metabolism in hypertension which might contribute to increased vascular reactivity.