bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE MARINE NATURAL PRODUCT 3,5‐DIBROMO‐2‐(2,4‐DIBROMO‐PHENOXY)PHENOL, INHIBITS CONTRACTILE ACTIVITY IN THE GUINEA‐PIG ILEUM
Authors: Bussau Lindsay J. , Beveridge Andrew A. , Nadeson Ray , Anderson Andrew P. 
Published: June 2007

SUMMARY1. The tetrabrominated diphenyl ether 3,5‐dibromo‐2‐(2,4‐dibromophenoxy)phenol (BPE), a natural marine product isolated from a sponge, was tested for pharmacological activity in guinea‐pig ileum.2. BPE (2 μmol/ L) decreased basal force and the frequency of spontaneous contractions of the ileum. It also significantly decreased contractions of the ileum induced by 5 mmol/L barium and to electrical stimulation at parameters which stimulated intrinsic nerves.3. The slopes of concentration‐response curves to acetylcholine (ACh), histamine and 5‐hydroxytryptamine (5‐HT) were significantly reduced by BPE at concentrations of 2 μmol/L or greater.4. BPE (2 μmol/L) did not affect calcium‐induced contractions of longitudinal muscle fibres from guinea‐pig ileum which were stripped of their cellular membrane. It (6 μmol/L) also had no effect on ATP levels in longitudinal muscle fibres.5. BPE (2 μmol/L) reduced both phasic and tonic components of contractions induced by raising the extracellular concentration of K+ to 15, 30, 45 or 60 mmol/ L (in the presence of atropine, propranolol, phentolamine and desensitization to 5‐HT to inhibit the effects of nerve transmitter release).6. BPE (2 μmol/L) reduced carbachol‐induced contractions of ileum pre‐incubated in 1 μmol/L felodipine, a blocker of l‐type voltage‐operated calcium channels (VOCC).7. BPE dose dependently (0.6–6 μmol/L) reduced contractions induced by Ca2+ in both K+ depolarized ileum and in tissue exposed to carbachol (10 μmol/L) in the presence of felodipine (0.1 μmol/L).8. These results suggest that BPE affects intracellular messenger systems controlling cytosolic calcium and/or blocks entry of calcium into the cell through both VOCC and receptor‐operated channels (ROC).
INHIBITORY EFFECT OF OCTOPAMINE ON THE RELEASE OF ENDOGENOUS ACETYLCHOLINE FROM ISOLATED MYENTERIC SYNAPTOSOMES OF GUINEA‐PIG
Authors: Chang Shu‐Shi , Cheng Juei‐Tang 
Published: June 2007

SUMMARY1. The effect of octopamine on the release of endogenous acetylcholine (ACh) from isolated ileal synaptosomal preparations of guinea‐pigs was examined using high pressure liquid chromatography with electrochemical detection. Release of ACh was induced by substance P or by depolarization with high potassium (50 mmol/ L) in medium containing atropine, propranolol and naloxone.2. Octopamine produced a dose‐dependent inhibition of substance P‐induced ACh release. A simiiar inhibitory action of octopamine was found in the samples depolarized by high potassium as a reference.3. The action of octopamine was not reversed by the dopamine receptor antagonists either for the DA‐2 subtype, domperidone, or for the DA‐1 subtype, SCH23390, or by haloperidol. However, idazoxan and yohimbine antagonized this octopamine‐induced inhibition at concentrations sufficient to abolish the action of clonidine.4. Failure of guanethidine or nomifensine to inhibit octopamine ruled out mediation by noradrenergic neurotransmitters.5. Octopamine decreased the influx of [45Ca] stimulated by substance P into synaptosomal preparations and this was reversed by idazoxan or yohimbine at concentrations sufficient to block the action of clonidine.6. Pertussis toxin abolished the inhibitory action of octopamine at a dose high enough to block the action of clonidine.7. These results indicate that octopamine suppresses the influx of calcium ions into cholinergic nerve terminals of ileal synaptosomes of guinea‐pigs via an activation of α2‐adrenoceptors coupled with a pertussis toxin‐sensitive GTP‐binding protein which results in a decrease of ACh release.
PERFUSION PRESSURE AND TRANSMURAL FLOW DISTRIBUTION IN THE LEFT VENTRICLES OF ISOLATED RAT HEARTS
Authors: Walland A. , Weihs H. , Mutschler E. 
Published: June 2007

SUMMARY1. The influence of perfusion pressure on flow distribution in the left ventricular wall was investigated with a newly developed microsphere method in Langendorff preparations of the rat heart.2. Microspheres with a diameter of 10 μm stained with the fluorescent dye yellow‐green were infused into the perfusion medium. The hearts were then relaxed with a calcium‐chelator, fixed with formaldehyde and cut transversally with a freezing microtome. Photographs were taken of the 52 μm slices with a fluorescence photomacroscope. The ventricular wall was subdivided into four zones, evaluated planimetrically and the beads were counted for calculation of microsphere density.3. Perfusion of groups of hearts, paced at 5 Hz, with Tyrode's solution at pressures of 30, 50, 80 or 120 cmH2O for 30 min revealed an increase of left ventricular pressure amplitude, coronary flow, myocardial oxygen consumption and flow redistribution towards the endocardium of the left ventricular wall with increasing perfusion pressure.4. The quotient of the sphere densities in the inner endocardium over that in the outer epicardium, however, was already maximal at a pressure of 80 cmH2O and amounted to 1.59 ± 0.15. This quotient was only 0.52 ± 0.11 at a perfusion pressure of 30 cmH2O, thus indicating massive change in flow distribution upon hypoperfusion.5. These results indicate that transmural left ventricular flow redistribution in response to hypoperfusion in the isolated rat heart is similar to that in hearts of much larger species.
METHODOLOGICAL EVALUATION OF INDIRECT CALORIMETRY DATA IN LEAN AND OBESE RATS
Authors: Rafecas Immaculada , Esteve Montserrat , Fernández‐López José‐Antonio , Remesar Xavier , Alemany Marià 
Published: June 2007

SUMMARY1. The applicability of current indirect calorimetry formulae to the study of energy and substrate balances on obese rats has been evaluated. The energy consumption of series of 60‐day rats of Wistar, lean and obese Zucker stock were studied by means of direct and indirect calorimetry, and by establishing their energy balance through measurement of food intake and retention. Calorimetric studies encompassed a 24 h period, with gas and heat output measurements every 2 or 5 min, respectively, for direct and indirect calorimetry.2. The analysis of fat composition (diet, whole rat, and synthesized and oxidized fat) showed only small variations that had only a limited effect on the overall energy equation parameters.3. A gap in the nitrogen balance, which represents a urinary N excretion lower than the actual protein oxidized, resulted in significant deviations in the estimation of carbohydrate and lipid oxidized when using the equations currently available for indirect calorimetry.4. Analysis of the amino acid composition of diet and rat protein as well as of the portion actually oxidized, and correcting for the nitrogen gap allowed the establishment of a set of equations that gave better coincidence of the calculated data with the measured substrate balance.5. The measured heat output of all rats was lower than the estimated values calculated by means of either indirect calorimetry or direct energy balance measurement; the difference corresponded to the energy lost in water evaporation, and was in the range of one‐fifth of total energy produced in the three rat stocks.6. Wistar rats showed a biphasic circadian rhythm of substrate utilization, with alternate lipid synthesis/ degradation that reversed that of carbohydrate, concordant with nocturnal feeding habits. Zucker rats did not show this rhythm; obese rats synthesized large amounts of fat during most of the light period, consuming fat at the end of the dark period, which suggests more diurnal feeding habits. Lean Zucker rats showed a similar, but less marked pattern.7. The results obtained indicate that lean and obese rats can be studied using the same indirect calorimetry formulae provided that there is an adequate measure of protein oxidation and the composition of diet does not differ.
THE ANGIOTENSIN‐CONVERTING ENZYME INHIBITOR, PERINDOPRIL, PREVENTS CARDIAC HYPERTROPHY IN LOW‐RENIN HYPERTENSIVE RATS
Authors: Nakamura Fumiaki , Nagano Masahiro , Higaki Jitsuo , Higashimori Koichi , Morishita Ryuichi , Mikami Hiroshi , Ogihara Toshio 
Published: June 2007

SUMMARY1. To examine whether an angiotensin‐converting enzyme (ACE) inhibitor prevents left ventricular (LV) hypertrophy even in low‐renin hypertension, we studied the effect of the administration of perindopril on cardiac hypertrophy induced by partial renal ablation in hypertensive rats.2. Rats that had undergone partial nephrectomy were randomly divided into four groups that received the following as drinking water: Group A, tap water; Group B, 1% sodium chloride (NaCl); Group C, NaCl + perindopril 3 mg/ kg per day; and Group D, NaCl + perindopril 1 mg/ kg per day. Plasma renin activity (PRA), angiotensin‐II (AII) concentration and cardiac tissue AII were measured.3. Supplementation of NaCl following nephrectomy increased the blood pressure and cardiac weight compared with rats that had undergone nephrectomy alone (P<0.05). Treatment with perindopril (3 mg/kg per day) did not affect the blood pressure and plasma AII but inhibited the increase of cardiac weight (P<0.05). Left ventricular AII was decreased in cases of reduced renal mass hypertension, but was not changed by treatment with perindopril.4. These results demonstrate that perindopril may be able to prevent LV hypertrophy even in low‐renin hypertension, which was not mediated by a reduction of blood pressure or suppression of the circulating and cardiac renin‐angiotensin systems. Other mechanisms of ACE inhibitors may contribute to the cardioprotective effects.
THE INHIBITION OF NITRIC OXIDE‐MEDIATED RELAXATIONS IN RAT AORTA AND ANOCOCCYGEUS MUSCLE BY DIPHENYLENE IODONIUM
Authors: Rand M. J. , Li C. G. 
Published: June 2007

SUMMARY1. The effects of diphenylene iodonium (DPI), an inhibitor of reduced nicotinamide adenine dinucleotide phosphate‐dependent oxidases (which generate superoxide anions), were studied on nitric oxide (NO)‐mediated responses in isolated preparations of the rat aorta and anococcygeus muscle.2. In aortic rings, the endothelium‐dependent relaxant action of acetylcholine was reduced by DPI (0.3–10 μmol/L) in a concentration‐dependent manner and abolished by the NO synthase (NOS) inhibitor L‐nitro‐NG‐arginine methylester (l‐NAME; 100 μmol/L). Relaxations induced by sodium nitroprusside (SNP) or NO were not affected by DPI or l‐NAME.3. In anococcygeus muscles, DPI (0.3–10 μmol/ L) as well as l‐NAME (5–100 μmol/L) produced concentration‐dependent reductions of relaxations produced by nitrergic nerve stimulation. Relaxations induced by NO and SNP were not affected by either DPI or l‐NAME. l‐Arginine (1 mmol/L) prevented the reduction of nitrergic relaxations by l‐NAME but not by DPI.4. Contractions of anococcygeus muscles elicited by exogenous noradrenaline (1 μmol/ L) were not affected or were inhibited by DPI (0.3–10 μmol/L), but the contractions elicited by noradrenergic nerve stimulation were significantly enhanced by DPI and l‐NAME. When noradrenergic contractions had already been maximally enhanced by l‐NAME (100 μmol/L), DPI produced no further enhancement. l‐Arginine (1 mmol/L) prevented the enhancement of noradrenergic contractions by l‐NAME but not by DPI.5. The efflux of radioactivity induced by field stimulation from anococcygeus muscles previously incubated with [3H]‐noradrenaline was not affected by either DPI or l‐NAME.6. Superoxide dismutase (SOD, 100 U/mL) had no significant effects on noradrenergic contractions, nitrergic relaxations, relaxations induced by NO or the actions of DPI in the rat anococcygeus muscle.7. The results suggest that the effects of DPI in reducing the NO‐mediated relaxations produced by acetylcholine in rat aortic rings and stimulation of nitrergic nerves in the rat anococcygeus muscle are due to the inhibition of NOS in these tissues. The effects of DPI were not sensitive to l‐arginine, and thus the mechanism of inhibition of NOS differs from that of l‐NAME.
CIRCADIAN VARIATIONS OF BLOOD PRESSURE AND PULSE RATE IN ESSENTIAL HYPERTENSIVES WITH DIABETES MELLITUS
Authors: Matsumura Kiyoshi , Abe Isao , Tsuchihashi Takuya , Kobayashi Kazuo , Fujishima Masatoshi 
Published: June 2007

SUMMARY1. The circadian variations of blood pressure and pulse rate in essential hypertensives either with or without diabetes mellitus were studied.2. Diabetic patients with orthostatic hypotension showed an increase in variability of blood pressure and a decrease in that of pulse rate when assessed by coefficient of variation. Cosinor analysis showed no significant circadian rhythm in both blood pressure and pulse rate in these patients.3. There were no differences in the circadian variations of blood pressure and pulse rate between essential hypertensives with and without diabetes mellitus unless orthostatic hypotension was present.4. These results suggest that diabetes mellitus per se does not have any effects on the circadian variations of blood pressure and pulse rate in essential hypertensives unless autonomic neuropathy is present.
NEUROLEPTICS INDUCE PENILE ERECTION IN THE RABBIT
Authors: Naganuma H. , Egashira T. , Fujii I. 
Published: June 2007

SUMMARY1. Intramuscular (i.m.) administration of the neuroleptics chlorpromazine, haloperidol and spiperone at doses ranging from 0.1 to 0.4 mg/kg in male rabbits induced a dose‐dependent penile erection.2. The i.m. administration of the α1‐adrenoceptor antagonists prazosin and bunazosin (0.1–0.4 mg/kg), induced a dose‐dependent penile erection. However, that of the peripheral dopamine receptor antagonist domperidone (0.4–4.0 mg/kg) and the dopamine receptor agonist apomorphine (0.1–1.0 mg/kg) did not. Penile erection was not induced by i.m. injection of chlorpromazine in combination with intrapenile administration of the α1‐adrenoceptor agonist methoxamine.3. Penile erection was induced by the administration of chlorpromazine (0.25–1.00 mg/body) into the lateral cerebral ventricle. At a low dose, however, the administration of chlorpromazine into the lateral ventricle induced a less notable penile erection than that induced intramuscularly.4. Penile erection was induced by i.m. injection of the ganglionic blocker hexamethonium (5–20 mg/ kg). When chlorpromazine was given after pretreatment with hexamethonium, penile erection was more notable than that induced by either drug given alone.5. These results suggest that neuroleptics could act locally in the penile structure to cause penile erection by α1‐adrenoceptor‐blocking actions.
BILIARY HYPERPRESSURE IN RAT EXTRAHEPATIC CHOLESTASIS ALTERS HORSERADISH PEROXIDASE BILIARY EXCRETION
Authors: Panozzo Maria P. , Fabris Carlo , Basso Daniela , Favero Giuseppe Del , Infantino Aldo , Cecchetto Attilio , Plebani Mario , Naccarato Remo 
Published: June 2007

SUMMARY1. The authors investigated the effect of two extrahepatic cholestasis models (one by bile duct ligation and the other by choledocho‐jugular fistula) on the hepatic clearance of horseradish peroxidase in male Sprague‐Dawley rats divided into four groups.2. In groups A (n = 5 rats) and B (n = 5), bile duct ligation was performed, while a choledocho‐jugular fistula was created in groups C (n = 5) and D (n= 7). A 10 mg intravenous bolus of horseradish peroxidase was injected after 24 h (groups A and C), 48 h (groups B and D) or 1 h (Group E; five sham‐operated rats). Serum and bile samples were then serially collected for 2 h.3. In all groups, serum horseradish peroxidase levels increased soon after injection and then rapidly decreased, the curves being similar. Biliary excretion increased for 30 min and then slowly decreased. The highest horseradish peroxidase biliary concentrations and outputs were found in Group B followed by Group A; both groups had significantly higher levels than Group E. No difference was found between horseradish peroxidase biliary excretion of groups C and D and that of sham‐operated rats.4. When each group was considered separately, sampling times correlated with the corresponding ratios of bile/ plasma HRP. Significant differences were found between the relative slopes of groups A, B and E, but not between those of groups C, D and E.5. In conclusion, bile duct obstruction greatly affects the plasma‐bile transfer of fluid phase markers, such as horseradish peroxidase, while single retention, caused by choledocho‐jugular fistula, has no influence. The increased biliary hyperpressure related to the duration of cholestasis may account for the degree of horseradish peroxidase transfer which, in turn, probably depends on an enhanced paracellular passage.
A STUDY ON THE ROLE OF CHOLINERGIC AND GAMMA AMINO BUTYRIC ACID SYSTEMS IN THE ANTI‐NOCICEPTIVE EFFECT OF GOSSYPIN
Authors: Viswanathan S. , Thirugnanasambantham P. , Ramaswamy S. , Bapna J. S. 
Published: June 2007

SUMMARY1. The participation of cholinergic and gamma amino butyric acid (GABA) neurotransmitter systems in the anti‐nociceptive effect of gossypin was investigated using pharmacological tools.2. Physostigmine potentiated its anti‐nociceptive response while atropine failed to modify it significantly.3. THIP (4,5,6,7‐tetra hydroisoxazolo (5,4‐C) pyridin‐3‐ol) and gossypin treatment produced an additive response while bicuculline attenuated the anti‐nociceptive response of gossypin. Similar observations were recorded for morphine.4. It is suggested that cholinergic and GABAergic systems play a role in gossypin‐induced anti‐nociception.
INVESTIGATION OF CLASS I ANTI‐ARRHYTHMIC DRUG ACTIONS ON GUINEA‐PIG CARDIAC MITOCHONDRIAL LACTATE DEHYDROGENASE ACTIVITY
Authors: Dzimiri Nduna , Almotrefi Abdulrahman A. 
Published: June 2007

SUMMARY1. The effects of the Class I anti‐arrhythmic drugs quinidine, procainamide, lidocaine, phenytoin and tocainide on mitochondrial lactate dehydrogenase activity were compared in guinea‐pig heart preparations.2. All the tested drugs inhibited the enzyme activity in a concentration‐dependent fashion, exhibiting varying profiles in their actions. Lidocaine exhibited inhibitory concentration 20% (IC20) and IC50 values of 0.52 ± 0.02 mmol/L and 25.6 ± 0.5 mmol/ L, procainamide 6.0 ± 0.2 mmol/ L and 108 ± 7.2 mmol/L, phenytoin 3.4 ± 0.06 μmol/L and 0.34 ± 0.02 mmol/L, quinidine 39.2 ± 1.2 μmol/L and 9.8 ± 0.8 mmol/L and tocainide 2.7 ± 0.3 mmol/L and 44.6 ± 2.5 mmol/L.3. According to the IC50 values, this is the order of their inhibitory potencies: phenytoin > quinidine > lidocaine > tocainide > procainamide. This trend is in general agreement with the lipophilicity rank of the drugs.4. It is concluded, therefore, that inhibition of mitochondrial lactate dehydrogenase is a property shared by most Class I anti‐arrhythmic drugs which may depend on their lipophilicity and possibly their membrane stabilizing effects.
EFFECTS OF ALDOSE REDUCTASE INHIBITION WITH EPALRESTAT ON DIABETES‐INDUCED CHANGES IN RAT ISOLATED ATRIA
Authors: Booth Richard J. , Hodgson Wayne C. 
Published: June 2007

SUMMARY1. Isoprenaline and cardiac responsiveness of isolated atria from 2 and 6 week streptozotocindiabetic rats, and their age‐matched controls, was examined. The effects of chronic administration of epalrestat (40 mg/kg orally, by gavage) on diabetes‐induced changes were also investigated.2. Spontaneously beating atria, bathed in either normal or high glucose (30 mmol/ L) Krebs’ solution, from both 2 and 6 week diabetic rats beat more slowly and with greater force than atria from control rats. These changes in basal parameters were normalized by 2 weeks of insulin (5 U/day s.c.) treatment but not by 2 or 6 weeks of chronic treatment with epalrestat.3. Isoprenaline (0.1 nmol‐0.1 μmol/L) produced concentration‐dependent increases in inotropy and chronotropy in atria from both control and diabetic rats.4. Atria from 2 week diabetic rats displayed decreased sensitivity to the positive inotropic effects of isoprenaline. This change was normalized by chronic insulin treatment but not by chronic epalrestat treatment.5. Atria from 6 week diabetic rats displayed increased sensitivity to the positive chronotropic effects of isoprenaline which was normalized by epalrestat.6. These results suggest that changes observed in atria from 2 week diabetic rats may be due to hyperglycaemia per se whereas in atria from 6 week diabetic rats abnormal activity of the polyol pathway may be a contributing factor.
THE EFFECT OF CROMAKALIM ON THE ELECTRICAL PROPERTIES OF AND [86Rb+] EFFLUX FROM NORMAL AND HYPERTROPHIED RAT BLADDER
Authors: Creed K. E. , Malmgren A. 
Published: June 2007

SUMMARY1. The activity of smooth muscle strips from normal and hypertrophied rat bladders was compared. The hypertrophied bladders were produced by partially obstructing the urethra 8–13 weeks previously.2. Spontaneous mechanical activity was more frequent and smaller in amplitude in strips from normal than hypertrophied bladders and was less sensitive to cromakalim, being reversibly abolished by cromakalim at 10−6 mol/L compared with 10−7 mol/L for hypertrophied bladder.3. The mean resting membrane potentials of smooth muscle cells from normal and hypertrophied rat bladders were ‐47.2 and ‐47.6 mV, respectively. Bursts of spontaneous action potentials, corresponding to the mechanical activity, were seen in some cells.4. Nifedipine at 10−6 mol/L had no significant effect on the resting membrane potential. Occasional single spikes occurred with increased duration and the afterhyperpolarization was abolished. Cromakalim at 10−5 mol/L produced hyperpolarization of 3–9 mV and, in the continued presence of the drug, occasional singe spikes could be recorded from both normal and hypertrophied bladders.5. Nifedipine at 10−6 mol/L abolished movement but did not significantly alter [86Rb+] efflux from strips from either normal or hypertrophied bladders. Addition of cromakalim at 5± 10−6 or 5 ± 10−5 mol/L in the presence or absence of nifedipine increased efflux from the normal bladder by 30–40%. In the hypertrophied bladder the efflux increased by about 14% and 28% in the presence of 5 ± 10−6 and 5 ± 10−5 mol/L cromakalim, respectively.6. No significant differences between electrical properties of normal and hypertrophied bladders were therefore found and we are unable to explain why the mechanical activity of hypertrophied rat bladders was more sensitive to cromakalim than normal bladders.
THE EFFECT OF ATRIAL NATRIURETIC PEPTIDE INFUSION ON RENAL HAEMODYNAMICS AND PLASMA LIPOPROTEINS IN PUROMYCIN AMINONUCLEOSIDE NEPHROSIS IN RATS
Authors: Radin M. Judith , McCune Sylvia A. 
Published: June 2007

SUMMARY1. The effect of continuous intravenous administration of 1 UmUg/h atrial natriuretic peptide (ANP) for 4 days was studied in normal male Sprague‐Dawley rats and rats made nephrotic with puromycin aminonucleoside (PA).2. ANP infusion significantly increased urinary sodium and potassium excretion by 3 days of infusion in control rats but not in PA‐treated rats. ANP infusion significantly increased glomerular filtration rate in PA‐treated rats, while effective renal plasma flow was similarly decreased compared with non‐infused nephrotic rats.3. Plasma high density lipoproteins (HDL) were significantly decreased and low density lipoproteins (LDL) were increased in PA‐treated rats that received ANP; HDL were increased in normal rats infused with ANP.4. Competitive binding studies demonstrated a lower density of specific ANP receptors in glomerular membranes from rats injected with PA, while binding affinity was unchanged.5. Infusion with exogenous ANP did not promote natriuresis in PA nephrosis despite an enhancement of glomerular filtration rate (GFR), thus suggesting that sodium retention in this model is due to a post‐glomerular defect. Plasma lipoprotein composition in both normal and nephrotic rats may be affected by ANP.