bluuebunny/crossref_metadata_2025_split huggingface dataset:
PLASMA VASOPRESSIN AND ATRIAL NATRIURETIC FACTOR DURING HAEMORRHAGE: INFLUENCE OF CARDIAC AND AORTIC RECEPTORS
Authors: Courneya C. A. , Wilson N. , Ledsome J. R. 
Published: June 2007

SUMMARY1. The changes in plasma concentrations of immunoreactive vasopressin (iVP) and atrial natriuretic factor (iANF) in response to haemorrhage (10–30% blood volume) were measured in 10 anaesthetized rabbits before and after cardiac receptor denervation (vagal nerve section). Carotid sinus pressure was maintained constant (60 mmHg) to eliminate any changing input from carotid baroreceptors.2. Haemorrhage increased iVP before and after vagal nerve section indicating that withdrawal of input from aortic baroreceptors may have contributed to the increase in iVP.3. Section of the vagus nerves attenuated the iVP response to haemorrhage.4. There was no correlation between release of iVP and iANF.5. Haemorrhage decreased iAF before and after vagal nerve section. Section of the vagus nerves increased iANF. Plasma iANF was highly correlated with atrial pressure and mean arterial pressure suggesting iANF release was secondary to changes in cardiac haemodynamics.
RAMIPRIL REDUCES ALBUMINURIA IN DIABETIC RATS FED A HIGH PROTEIN DIET
Authors: O'Brien R. C. , Cooper M. E. , Allen T. J. , Jerums G. 
Published: June 2007

SUMMARY1. Streptozotocin diabetes was induced in Wistar‐Kyoto rats fed a 50% protein diet. Animals were randomized to receive either the ACE inhibitor ramipril, 1 mg/L in drinking water (n= 7), or no treatment (n= 7), and were studied for 6 months. Blood glucose, body weight and glomerular filtration rate (GFR) were measured at 0, 1, 4, 8 and 16 weeks of diabetes and urinary albumin excretion was measured every 8 weeks.2. In both groups, GFR increased significantly within 1 week of induction of diabetes (P < 0.001) and thereafter remained stable. There was no difference in GFR between the treated and untreated groups.3. Urinary albumin excretion increased progressively in both groups throughout the study. Ramipril treatment reduced albuminuria by approximately 50% at weeks 16 and 24 (P < 0.01).4. The amelioration of diabetic albuminuria by ACE inhibition, in the setting of high dietary protein intake, may have important implications for the treatment of human diabetic nephropathy.
RENAL VENOUS WEDGE PRESSURE IN RENAL WRAP HYPERTENSION IN RABBITS
Authors: Denton Kate M. , Anderson Warwick P. 
Published: June 2007

SUMMARY1. Renal cellophane wrapping to produce hypertension causes thickening of the capsule of the kidney. To determine whether this compresses the kidney, deep renal vein wedge pressure was measured as an estimate of tissue pressure in anaesthetized rabbits 1 month after cellophane wrapping (n= 5) or a sham operation (n= 3).2. Renal vein wedge pressure was 18.3 ± 2.0 mmHg in hypertensive rabbits and 8.4 ± 1.1 mmHg in the sham‐operated rabbits.3. Arterial pressure was raised or lowered with angiotensin II or glyceryl trinitrate, respectively. Arterial and wedge pressures were approximately linearly related and, at any given arterial pressure, wedge pressure was approximately 8 mmHg higher in the cellophane‐wrapped kidney than in the kidney of the sham‐operated group.4. These results, showing that renal wedge pressure is elevated in renal wrap rabbits, indicate that the kidneys are compressed, probably by the thickened renal capsule. This may explain the increased renal vascular resistance seen in this form of hypertension.
DIURETIC EFFECT INDUCED BY INTRARENAL INFUSION OF NISOLDIPINE IN ANAESTHETIZED DOGS
Authors: Kageyama M. , Matsumura Y. , Hayashi K. , Hosokawa T. , Morimoto S. 
Published: June 2007

SUMMARY1. Renal effects of nisoldipine, a potent calcium channel blocker, were examined in anaesthetized dogs.2. Intrarenal arterial infusion of nisoldipine (10, 50 ng/kg per min) did not influence mean systemic blood pressure and renal haemodynamics, but did cause dose‐related increases in urine flow and urinary excretion of electrolytes. During nisoldipine infusion at the higher dose, the levels of fractional excretion of sodium, potassium and chloride were significantly elevated.3. In the lithium clearance study, fractional lithium excretion, an index of fractional sodium excretion in the proximal tubules, was unchanged even with the higher dose of nisoldipine, whereas fractional sodium excretion in the distal tubules markedly increased.4. Nisoldipine elicited a significant increment in osmolar clearance without altering the reabsorption of free water.5. Thus, intrarenal administration of nisoldipine at a non‐hypotensive dose to anaesthetized dogs produced a significant diuretic effect without alteration in renal haemodynamics. Results in lithium clearance and free water clearance studies suggest that nisoldipine exerts a diuretic action by inhibiting sodium transport at the distal nephron segments beyond the proximal tubules.
BLOOD PRESSURE, PLASMA AND PITUITARY PROLACTIN RESPONSES TO BROMOCRIPTINE IN NEW ZEALAND GENETICALLY HYPERTENSIVE AND NORMOTENSIVE RATS
Authors: Tan B. K. H. , Hutchinson J. S. 
Published: June 2007

SUMMARY1. The effects on blood pressure (BP), plasma and pituitary prolactin (PRL) of a 13 day intraperitoneal infusion of bromocriptine (BRC) delivered by osmotic minipump were investigated in genetically hypertensive rats (GHR) and their normotensive (NT) controls.2. In the GHR, the mean BP in the BRC‐treated group over the 13 day period of study was significantly lower than in the vehicle‐treated group. In the NT rats, the mean BP in the BRC‐treated group over the 13 day period was also significantly lower than in the vehicle‐treated group.3. Mean plasma PRL concentration in the GHR and NT rats were comparable. In the GHR, the mean plasma PRL concentration taken on day 13 was significantly lower in the BRC‐treated group than in the vehicle‐treated group. In the NT rats, the mean plasma PRL concentration taken on day 13 in the BRC‐treated group was, however, not significantly different from that in the vehicle‐treated group.4. The mean pituitary PRL content was not significantly different in the GH and NT rats. There was a greater suppression of pituitary PRL content in the BRC‐treated GHR than in the BRC‐treated NT rats compared with their respective vehicle‐treated groups.5. The results raise the possibility that PRL may have an indirect role in the pathogenesis of the hypertension of the GHR.
CARDIOVASCULAR EFFECTS OF CENTRAL ADMINISTRATION OF β‐ENDORPHIN IN RATS RECEIVING NEONATAL INJECTION OF MONOSODIUM GLUTAMATE
Authors: Wong T. M. , Lee A. Y. S. , Chan R. K. W. 
Published: June 2007

SUMMARY1. The effects of intracerebroventricular (i.c.v.) and intracisternal (i.e.) injection of β‐endorphin on arterial blood pressure (BP) in rats that received five intraperitoneal injections of monosodium glutamate (MSG) on alternate days in the first 10 days of life were studied.2. β‐endorphin administered into the lateral ventricles caused a prolonged elevation in BP, whereas i.c. injection of the peptide resulted in an even longer lasting reduction in BP. In the MSG‐treated rat, the prolonged hypertensive effect of i.c.v. injection of β‐endorphin was completely abolished, but the effect of i.c. injection of the peptide was the same as that in the control. Since MSG treatment destroyed selectively the structures around the third ventricle, it is suggested that these structures, including the arcuate nucleus, may be responsible for mediating the cardiovascular effects of β‐endorphin.3. The effects of central administration of β‐endorphin were completely blocked by naloxone, which mainly antagonizes the actions of μ‐receptor agonists and has no cardiovascular effects itself. The results suggest that μ‐receptors may be involved in mediation of the effects of β‐endorphin on the cardiovascular system and that β‐endorphin in the brain may not exert a tonic influence on the cardiovascular functions.
PERHEXILENE: EFFECTS ON HEPATIC LYSOSOMAL FUNCTION IN RATS
Authors: Sewell Richard B. , Horowitz John D. , Grinpukel Susan A. , Martin Glenn 
Published: June 2007

SUMMARY1. Perhexilene, a long‐acting anti‐anginal drug, can induce adverse effects on the liver which may be dose‐dependent. At high concentrations, perhexilene causes marked morphological change in hepatocyte lysosomes. The current study examined the effect of ‘therapeutic’ doses of perhexilene on hepatic lysosomal function, particularly the biliary release of lysosomal enzymes, using an isolated perfused rat liver (IPRL) model.2. Pharmacokinetic studies demonstrated that clearance of single doses of perhexilene by the perfused rat liver was dose‐dependent and established a ‘therapeutic’ dose of 0.6 mg using the IPRL. A 5 day pretreatment regimen of 20 mg/kg per day was shown to produce ‘therapeutic’ perhexilene concentrations of 150–210 ng/ml.3. At perhexilene concentrations equating the ‘therapeutic’ range in man, the major effect of perhexilene was at the biliary pole of the hepatocyte. In 5 day pretreatment dose studies, lysosomal enzyme excretion into bile was markedly increased. In single dose studies, the increase in biliary lysosomal enzyme output partially reflected an increase in bile water production which was not seen with the 5 day pretreatment regimen. Hepatic and perfusate lysosomal enzyme activities were not affected.4. This selective effect of perhexilene on hepatocyte‐to‐bile lysosomal excretion may reflect intracellular lysosomal drug localization.
COMPARISON OF THE PROPERTIES OF [3H]‐d‐2‐AMINO‐5‐PHOSPHONOPENTANOIC ACID AND [3H]‐dl‐2‐AMINO‐7‐PHOSPHONOHEPTANOIC ACID BINDING TO HOMOGENATES OF RAT CEREBRAL CORTEX
Authors: Manallack David T. , Sheehan Kerrie‐Anne M. , Beart Philip M. 
Published: June 2007

SUMMARY1. The pharmacology and ionic regulation of [3H]‐2‐d‐2‐amino‐5‐phosphonopentanoic acid ([3H]‐d‐AP5) and [3H]‐dl‐2‐amino‐7‐phosphonoheptanoic acid ([3H]‐dl‐AP7) binding to homogenates of rat cerebral cortex were examined using radioligand binding methodology.2. Both [3H]‐d‐AP5 and [3H]‐dl‐AP7 labelled a single population of binding sites with dissociation constants of 0.39 and 1.8 μmol/l, respectively. The density of binding sites found with [3H]‐dl‐AP7 was 13 times greater than that found with [3H]‐d‐AP5.3. The ionic requirements of the [3H]‐d‐AP5 binding site in the presence of chloride were such that calcium acetate enhanced binding, while magnesium and sodium acetate both decreased binding. In the absence of chloride both calcium and chloride ions stimulated binding.4. In a chloride‐free buffer calcium acetate stimulated binding of [3H]‐dl‐AP7 in a biphasic manner. Chloride ions (ammonium salt) enhanced binding slightly at low concentrations (0.1–1.0 mmol/l) above which binding was reduced to non‐specific levels. The ionic dependence of [3H]‐dl‐AP7 binding had some similarities to the previously defined GLU‐C site.5. The pharmacological profile of the site labelled by [3H]‐d‐AP5 was consistent with that of a recognition site for N‐methyl‐d‐aspartate (NMDA) as defined in electrophysiological experiments. [3H]‐dl‐AP7 did not label an NMDA site as several non‐NMDA ligands displaced binding with high affinity and the binding was not stereospecific as found for [3H]‐d‐AP5. Moreover, the pharmacological profile of the [3H]‐dl‐AP7 site did not correspond to any excitatory amino acid receptor as presently defined.
EVIDENCE FOR A ROLE OF NITRIC OXIDE IN THE NEUROTRANSMITTER SYSTEM MEDIATING RELAXATION OF THE RAT ANOCOCCYGEUS MUSCLEC
Authors: Li C. G. , Rand M. J. 
Published: June 2007

SUMMARY1. The nitric oxide (NO) synthesis inhibitor NG‐monomethyl‐l‐arginine (l‐NMMA), but not d‐NMMA, inhibited the NANC‐mediated relaxations of the rat anococcygeus muscle, but did not affect the relaxation produced by sodium nitroprusside.2. The inhibitory effect of l‐NMMA was reversed by l‐arginine but not by d‐arginine, and prior exposure to l‐arginine blocked the effect of l‐NMMA.3. The noradrenergically mediated contractions of the anococcygeus elicited by field stimulation were slightly enhanced by l‐NMMA, but the response to noradrenaline was not affected.4. The results suggest that NANC transmission in the rat anococcygeus muscle involves the generation of NO from arginine.
ANTICONVULSANT ACTIVITY OF DI‐N‐PROPYLACETATE AND BRAIN MONOAMINE METABOLISM IN THE RAT
Authors: Abed Wadie T. 
Published: June 2007

SUMMARY1. Sodium di‐n‐propylacetate (DPA) treatment induced significant increases in brain contents of gamma‐aminobutyric acid (GABA), 5‐hydroxyindoleacetic acid (5‐HIAA) and homovanillic acid (HVA). Furthermore, the threshold for pentylenetetrazol (PTZ) clonic convulsions was also increased in response to DPA administration.2. Pretreatment with inhibitors of monoamine synthesis α‐methyl‐p‐tyrosine (AMPT) and p‐chlorophenylalanine (PCPA) did not alter the anticonvulsant activity of DPA, but when given alone, both AMPT and PCPA caused significant decreases in brain monoamine contents and PTZ threshold seizures.3. Experiments using probenecid suggest that the increases in 5‐HIAA and HVA seen after DPA treatment could have resulted from inhibition of their active transport out of the brain. These data indicate that the anticonvulsant action of DPA is not dependent on changes in monoamine metabolism in the brain.
PRELIMINARY STUDY ON THE ANTINOCICEPTIVE EFFECT OF ELEPHANT β‐ENDORPHIN
Authors: Wong Chak‐Lam , Wai Man‐Keung , Cheng Heung‐Chin , Chung David , Yamashiro Donald 
Published: June 2007

SUMMARY1. Intraventricular administration of human β‐endorphin and elephant β‐endorphin significantly prolonged the tail flick response tested 30 min later. However, elephant β‐endorphin was about 7–8 times more potent than human β‐endorphin in the tail flick test.2. β‐Endorphin1‐27 antagonized the antinociceptive effect of both human β‐endorphin and elephant β‐endorphin by the same extent. Naloxone also antagonized the antinociceptive effects of the β‐endorphins but it was less effective than β‐endorphin1‐27.3. Human β‐endorphin and elephant β‐endorphin were of equal potency in inhibiting the abdominal constriction response induced by intraperitoneal (i.p.) acetic acid. Both β‐endorphin1‐27 and naloxone antagonized these effects of the β‐endorphins with naloxone being more effective.4. The present study showed that different opioid receptor subtypes may be involved in the tail flick test and the abdominal constriction test. Furthermore, elephant β‐endorphin was a better antinociceptive agent than human β‐endorphin in the tail flick test.
VASODILATORY EFFECTS OF MILRINONE ON PULMONARY VASCULATURE IN DOGS WITH PULMONARY HYPERTENSION DUE TO PULMONARY EMBOLISM: A COMPARISON WITH THOSE OF DOPAMINE AND DOBUTAMINE
Authors: Tanaka Hiroyuki , Tajimi Kimitaka , Matsumoto Akinori , Kobayashi Kunio 
Published: June 2007

SUMMARY1. The limited therapeutic role of pulmonary vasodilation reflects lack of their selectivity for the pulmonary vasculature, and many drugs have been evaluated for effectiveness; however, none has gained widespread clinical use.2. Milrinone (MIL) is a newly synthetized phosphodiesterase inhibitor, which has potent positive inotropic and vasodilatory effects.3. The present study shows the effects of MIL on the pulmonary circulation in dogs with pulmonary hypertension due to autologous muscle‐induced pulmonary embolism, and also demonstrates a comparison with those of dopamine and dobutamine.4. As MIL showed potent vasodilatory effects on the pulmonary vasculature, it had a potential clinical role in the treatment of pulmonary hypertension.
EFFECT OF LIGNOCAINE ON CORONARY BLOOD FLOW, SYSTOLIC MYOCARDIAL FUNCTION AND MYOCARDIAL HIGH ENERGY PHOSPHATE STORES IN SWINE
Authors: Perlmutter Neal , Wilson Richard , Joyce Mary , Angello Debra , Gee David 
Published: June 2007

SUMMARY1. To investigate the effect of lignocaine upon coronary blood flow, myocardial systolic wall function and high energy phosphate stores, lignocaine was administered as a rapid intravenous injection to 14 open chest anaesthetized swine.2. Before and after injection, measurements were made of coronary blood flow by electromagnetic flow probe, per cent wall thickening by ultrasonic crystals, adenosine triphosphate (ATP) and creatine phosphate (CP) content by myocardial biopsy, and arterial pressure by central aortic catheter. The animals were divided into two groups based on whether or not they received a continuous low‐dose infusion of lignocaine prior to the study. Group I received the continuous low‐dose infusion of lignocaine and group II did not.3. With a 2 mg/kg lignocaine injection, peak diastolic coronary flow rose significantly in groups I and II by 27±7 and 29±7% respectively. This was followed by a significant decline in per cent wall thickening in groups I and II of ‐11±2 and ‐19±6% respectively. In group I myocardial CP content decreased after lignocaine injection by 58±6% and ATP tended to rise even though systolic and diastolic pressure did not change significantly. In group II neither CP nor ATP changed significantly, but systolic and diastolic blood pressure decreased significantly.4. Repeat lignocaine injections were given over a wider dosage range (0.5–4.0 mg/kg) to determine dose–response for lignocaine versus coronary blood flow. Coronary blood flow increased and per cent wall thickening decreased as doses of lignocaine were increased.5. It was concluded that rapid intravenous lignocaine injection appeared to cause a dose‐dependent coronary dilatation and systolic dysfunction. Pre‐treatment with low‐dose continuous infusion of lignocaine appeared to result in a decrease in CP and a rise in ATP when compared with no pre‐treatment—despite a similar effect on myocardial function and coronary blood flow.
EFFECT OF LONG‐TERM ADMINISTRATION OF TESTOSTERONE OENANTHATE ON SYMPATHETIC NEUROTRANSMISSION TO RAT ISOLATED SEMINAL VESICLES
Authors: Chin Jaye P. F. , Pennefather Jocelyn N. 
Published: June 2007

SUMMARY1. The effects of prolonged administration of testosterone oenanthate (TE) on sympathetic neurotransmission to the rat isolated seminal vesicle were examined.2. TE was administered at either 1.2 or 2.4 mg/kg subcutaneously (s.c.) thrice weekly for 8 weeks. A separate group of rats was administered the vehicle, sesame oil, 0.5 mL/kg, s.c. at the same regime and used as controls. TE administration increased plasma testosterone and dihydrotestosterone levels and seminal vesicle weights. TE 2.4 mg/kg suppressed fertility in male rats.3. The mean ‐log EC50 values of adrenalin and noradrenaline in seminal vesicles from the control group were 5.30 (95% confidence limits: 5.14, 5.58; d.f. = 14) and 4.92 (95% confidence limits: 4.56, 5.49; d.f. = 14) respectively. Neither of these estimates were modified by TE administration.4. The mean noradrenaline content (μg/tissue) in seminal vesicles from control rats was 0.88±0.09 μg/tissue. This did not change with TE treatment. Tissue noradrenaline concentration (μg/g tissue), on the other hand, decreased by more than 50% in preparations from rats treated with TE. This was paralleled by a decrease in the density of catecholamine fluorescence.5. Mean responses to field stimulation (20 pulses, 60 V dial setting, 2 ms, 1–70 Hz) appeared to decrease in preparations from TE treated groups; this decrease was, however, not statistically significant (P>0.05; d.f. = 15).6. It is concluded that prolonged administration of testosterone oenanthate to rats, at doses sufficient to suppress fertility, decreases the density of sympathetic innervation to the seminal vesicle by increasing smooth muscle mass. Treatment does not, however, modify the responses of this preparation to exogenously added catecholamines.
RELATIONSHIP BETWEEN GASTRIC MUCOSAL PROSTAGLANDIN LEVELS AND HEALING OF GASTRIC LESIONS IN RATS
Authors: Kuroiwa Masaki , Sugiyama Satoru , Ohara Atsushi , Goto Hidemi , Tsukamoto Yoshihisa , Nakazawa Saburo , Ozawa Takayuki 
Published: June 2007

SUMMARY1. This study was designed to determine whether or not endogenous prostaglandins (PG) contribute to the healing of gastric ulcers induced by high concentrations of ethanol or water immersion stress.2. Ethanol‐induced gastric lesions; rats were divided into four groups: (1) the control group: untreated; (2) the indomethacin group: indomethacin (2 mg/kg) was injected intramuscularly (i.m.) once daily until the end of the experiment; (3) the ethanol group: rats were given 1 mL of 50% ethanol intragastrically; (4) the ethanol + indomethacin group: indomethacin (2 mg/kg) was injected (i.m.) once daily from 1 h after administration of 50% ethanol until the end of the experiment.3. Water immersion stress‐induced gastric lesions; rats were divided into three groups: (1) control group: untreated; (2) stress group: rats were placed in a stress cage and immersed into a water bath (23°C) for 6 h; (3) stress + indomethacin group: indomethacin (2 mg/kg) was injected (i.m.) once daily for 3 consecutive days immediately after stress treatment or from 3 days after stress treatment until the end of the experiment.4. Immediately after observation of the lesions, the fundic mucosal layer was separated from the muscle layer and mucosal PG levels were measured by high performance liquid chromatography in each group.5. Indomethacin did not inhibit ulcer healing until 48 h after administration in the ethanol experiment, and until 3 days after administration in the water immersion experiment. In contrast, indomethacin inhibited ulcer healing thereafter in each experiment respectively.6. Four kinds of PG, that is 6‐keto‐PGF1α PGF2α, PGE2 and PGD2 were detected in gastric mucosa. Indomethacin inhibited the recovery of PG levels, and significantly low PG levels were observed after indomethacin treatment.7. It was noted from the effect of indomethacin that there are at least two phases of healing in gastric ulcers (i.e. the early phase and the late phase), and that PG might be linked with the late phase of ulcer healing.
EFFECT OF STRESS ON THE CATECHOLAMINE CONTENT OF THE ADRENAL GLAND OF INTACT AND BURSECTOMIZED CHICKS
Authors: Mahata Sushil K. , De Monisha , Pal Dhananjay , Ghosh Asok 
Published: June 2007

SUMMARY1. Bursa‐intact and bursectomized chicks were exposed to cold–wet immobilization (CWI) stress for 1.5 min. The catecholamines (CA) from the adrenal gland were measured spectrofluorometrically 5, 15, 30 and 60 min after stress.2. In bursa‐intact chicks, the CWI stress caused decrease of both norepinephrine and epinephrine from the adrenal glands 5 min after stress. Resynthesis of epinephrine exceeded the control value 30 and 60 min after stress.3. In bursectomized chicks, the CWI stress brought about a decrease of norepinephrine 15 and 30 min and of epinephrine 30 and 60 min after stress.4. The findings suggest that bursa facilitates early (5 min) release of CA and also helps in quick resynthesis of epinephrine during stress.
MEASUREMENT OF BLOOD‐BRAIN BARRIER PERMEABILITY
Authors: Robinson P. J. 
Published: June 2007

SUMMARY1. Experimental determinations of blood‐brain barrier permeability from measurements of uptake of tracers by brain are limited in two ways. First, there are experimental limitations that are specific to the particular method being used. These limitations include the range of permeability values that a particular method can reliably determine (sensitivity); whether repeated experiments are possible in the same animal; whether regional values can be determined; and to what degree the chemical composition of the perfusate passing through the brain can be controlled.2. A second set of limitations on permeability determinations is of a more general, physiological nature. These constraints apply to a greater or lesser degree to all experimental determinations, and may limit the accuracy and reliability of the permeability values obtained; although certain reliable upper and lower bounds can be determined. These general factors include: capillary heterogeneity (i.e. variations in capillary lengths, surface areas, blood flows, etc.); the possibility of binding to circulating plasma proteins, especially albumin; and the possibility of capillary recruitment and de‐recruitment with changes in cerebral blood flow.