bluuebunny/crossref_metadata_2025_split huggingface dataset:
CHANGES IN THE CONTENT OF DOPAMINE AND ITS METABOLITES IN THE BASAL GANGLIA FOLLOWING RIGHT MIDDLE CEREBRAL ARTERY OCCLUSION AND REFLOW IN MONKEYS
Authors: Kuruvilla Alice , Cherian Rebecca , Theodore Deepa , Abraham Jacob 
Published: June 2007

SUMMARY1. Focal ischaemia was produced experimentally in Macaca radiata monkeys by occlusion of middle cerebral artery (MCA). There was a lowering of the dopamine (DA) content of basal ganglia after 4 and 12 h of occlusion.2. DA content was restored to normal in basal ganglia after restoration of blood flow. With the progress of time the DA content was increased above that of sham controls. Changes were also observed in the non‐occluded left basal ganglia.3. The homovanillic acid (HVA) content was decreased significantly at 12 h after occlusion. After the onset of reflow, the HVA content of the right basal ganglia was higher than that of sham controls.4. The 3, 4 dihydroxyphenylacetic acid (DOPAC) content of right basal ganglia was significantly decreased after 12 h occlusion. Reflow restored the level of DOPAC to normal within 1 h after removal of clip.5. Discrete changes were also observed in the left basal ganglia at some of the time intervals.
IN VIVO ESTIMATION OF CHANGES IN DISTAL TUBULE FLOW AND THEIR ROLE IN DEXAMETHASONE‐INDUCED KALIURESIS IN CONTROL AND POTASSIUM‐ADAPTED RATS
Authors: Adam William R. , Adams Beverlie A. , Ellis Andrew G. 
Published: June 2007

SUMMARY1. The aim of this study was to determine whether the kaliuresis associated with glucocorticoids is due to a direct tubular action or is secondary to effects of glucocorticoids on distal tubule flow.2. A whole kidney technique was used to avoid the problem, inherent in microperfusion and micropuncture studies, of deciding whether (all) the appropriate nephron segment(s) are being studied.3. The method used was to determine the best whole kidney measure of distal tubule flow (the independent variable) by correlating this with the dependent variable (potassium excretion, corrected for differences in plasma potassium, UkV/PlK+) in conscious intact and adrenalectomized control and potassium‐adapted rats.4. After an intragastric potassium chloride load, the correlation of UkV/PlK+ with UkV + UNaV was better than with either UNaV or UV, as measures of distal tubule flow. From the relationship a measure of potassium excretion independent of distal tubule flow can thus be calculated as UkV/PlK+÷ (UkV + UNaV), defined as UK#.5. Measurement of UK# clearly demonstrates decreases in potassium excretion with adrenalectomy and increases in potassium excretion with aldosterone and in the potassium‐adapted rat, consistent with described changes in potassium secretion. In contrast, with dexamethasone treatment, whilst there was an increase in UkV and UkV/PIK+, there was no change in UK# either in the control of potassium‐adapted rats.6. These results suggest that the kaliuretic effect of dexamethasone cannot be attributed to direct tubular effects of glucocorticoids but rather can be explained by its effect on distal tubule flow.
THE EFFECTS OF CALCIUM ANTAGONISTS ON BLOOD PRESSURE AND RESPONSES TO α‐ADRENOCEPTOR AGONISTS IN HYPERTENSIVE RABBITS
Authors: Hamilton C A. , Jardine E. , Sumner D. J. , Reid J. L. 
Published: June 2007

SUMMARY1. The effects of the calcium antagonists verapamil and nifedipine on mean arterial blood pressure, heart rate and pressor responses to a range of α‐adrenoceptor agonists were examined in male normotensive New Zealand white rabbits and in rabbits with perinephritis hypertension.2. Verapamil and nifedipine caused a greater fall in mean arterial pressure in hypertensive compared to normotensive rabbits both when the fall was expressed as an absolute and as a percentage change. Effects on heart rate were similar in normotensive and hypertensive animals.3. Pressor responses to phenylephrine were attenuated by nifedipine and verapamil in normotensive and hypertensive rabbits. Pressor responses to alphamethyl noradrenaline were also attenuated by nifedipine, but pressor responses to BHT 920 were not significantly altered by either calcium antagonist in normotensive or hypertensive rabbits at the dose used. Thus the calcium antagonists had a greater effect on α1‐than α2‐adrenoceptor mediated responses in both normotensive and hypertensive rabbits.4. Hypertensive animals showed an increased responsiveness to phenylephrine and alphamethyl noradrenaline but not BHT 920 compared to normotensives. This difference remained after treatment with both the calcium antagonists.
COMBINED BRONCHODILATOR PROTECTION AGAINST HISTAMINE‐INDUCED BRONCHOCONSTRICTION IN MAN
Authors: Ruffin R. E. , Meki M. , Alpers J. H. 
Published: June 2007

SUMMARY1. Sixteen stable asthmatics had the protective effects of inhaled fenoterol (200 μg) and inhaled ipratropium bromide (60 μg) against standardized histamine inhalation tests at 1 h examined in a randomized double blind fashion.2. There was no significant difference in the baseline forced expired volume in 1 s (FEV1) for the two study days (P >0.05).3. There was an increase in FEV, at 1 h on the fenoterol and ipratropium day compared with the fenoterol day (0.26 versus 0.17 1; P < 0.05).4. The geometric mean provocative concentration of histamine to cause a 20% fall in FEV, (PC20) was 6.31 mg/ml after fenoterol and 8.51 mg/ml after fenoterol and ipratropium (P= 0.038).5. There was no significant relationship between bronchodilator effect of the bronchodilators and the increase in PC20 from pre‐study values, r= 0.307 (P=0.25) for fenoterol alone and r=0.195 (P=0.47) for fenoterol and ipratropium.6. The relationship between pre‐study histamine responsiveness and the increase in PC20 caused by the bronchodilators just failed to reach statistical significance, r= ‐0.441 (P= 0.09) for fenoterol alone and r= ‐0.47 (P=0.06) for fenoterol and ipratropium.7. The study has shown a greater right shift of histamine responsiveness for combined inhaled fenoterol and ipratropium compared with inhaled fenoterol alone in this group of asthmatics.
THE EFFECT OF β‐ADRENOCEPTOR BLOCKERS ON THE ABSORPTION AND EXCRETION OF CHLOROTHIAZIDE IN MAN
Authors: Adebayo G. I. , Oyenuga A. B. , Mabadeje A. F. B. 
Published: June 2007

SUMMARY1. The effect of β‐adrenoceptor blockers on the absorption and elimination of the diuretic chlorothiazide was studied in healthy subjects.2. A week of pretreatment with either pindolol (10 mg twice daily) or propranolol (80 mg twice daily) resulted in significant reduction in 36 h mean cumulative urinary recovery of chlorothiazide in two groups of six subjects compared with a control (untreated) group.3. A week of pretreatment with atenolol (100 mg daily) did not significantly alter 36 h cumulative urinary excretion in another group of six subjects.4. None of the β‐blockers significantly changed chlorothiazide half‐life.5. It is suggested that the non‐selective (as opposed to the cardioselective) β‐blockers reduce chlorothiazide absorption by the mechanism(s) discussed.
THE EFFECTS OF NALOXONE, DEXAMETHASONE, DEOXYCORTICOSTERONE AND 17‐HYDROXYPROGESTERONE ON BLOOD PRESSURE RESPONSES OF NORMAL AND ADRENALECTOMIZED RATS DURING HYPOVOLAEMIC SHOCK
Authors: Khalid B. A. K. , Moral Paden , Merican Zainuddin 
Published: June 2007

SUMMARY1. The roles of, and interactions between, steroids and naloxone, an opioid antagonist, in the reversal of experimental hypotensive shock were studied in normal and adrenalectomized rats.2. In normal rats treated with dexamethasone or deoxycorticosterone or 17‐hydroxyprogesterone the hypotension and shock caused by 1% bodyweight and 2% bodyweight haemorrhage could be substantially reversed by naloxone in a dose‐related manner. In contrast, the reversal of hypotension by naloxone was markedly less in adrenalectomized rats.3. It is concluded that there is a co‐ordinate release of pressor catecholamines and depressor enkephalins from adrenal glands in hypovolaemic shock. Eventually, the use of naloxone would be of much less value in the treatment of hypotension or shock in patients with Addison's disease.
MICROINJECTION OF KAINIC ACID INTO THE ROSTRAL VENTROLATERAL MEDULLA CAUSES HYPERTENSION AND RELEASE OF NEUROPEPTIDE Y‐LIKE IMMUNOREACTIVITY FROM RABBIT SPINAL CORD
Authors: Morris M. J. , Pilowsky P. M. , Minson J. B. , West M. J. , Chalmers J. P. 
Published: June 2007

SUMMARY1. Microinjections of kainic acid were made into the pressor area of the rostral ventrolateral medulla oblongata of anaesthetized rabbits, in the region of the C1 adrenaline‐containing neurons.2. Over the 65 min following the microinjection, there was a significant increase in blood pressure, as well as an increase in the release of neuropeptide Y‐like immunoreactivity into the spinal subarachnoid space.3. These data provide evidence for a functional bulbospinal neuropeptide Y‐containing projection which may be responsible for mediating the pressor effects of stimulation of the rostral ventrolateral medulla.
MODULATION OF RENAL NORADRENALINE RELEASE BY PREJUNCTIONAL RECEPTOR SYSTEMS IN VITRO
Authors: Rump L. C. 
Published: June 2007

SUMMARY1. The amount of noradrenaline released per nerve impulse from renal sympathetic nerves can be modulated through specific prejunctional receptors.2. Under in vitro conditions activation of α1, α2‐, prostaglandin, adenosine, dopamine and serotonin receptors inhibits noradrenaline release from the kidney.3. Stimulation of prejunctional β‐adrenoceptors, probably of the β2‐subtype, as well as stimulation of prejunctional angiotensin II receptors facilitates noradrenaline release. Moreover, neuronally released noradrenaline inhibits its own release through activation of both prejunctional α1‐and α2‐adrenoceptors.4. Locally produced PGE2, which is formed and released via stimulation of postjunctional α1‐adrenoceptors, as well as adenosine, released from postjunctional sites by renal nerve stimulation (RNS), seems to inhibit noradrenaline release through their specific prejunctional receptor systems.
AUTORADIOGRAPHIC LOCALIZATION OF RECEPTORS IN THE MAMMALIAN CARDIOVASCULAR SYSTEM
Authors: Summers R. J. , Molenaar P. , Stephenson J. A. , Jones C. R. 
Published: June 2007

SUMMARY1. Autoradiographic techniques have been used to examine the location of β‐adrenoceptors in the heart and β‐adrenoceptors, substance P receptors and muscarinic cholinoceptors in blood vessels.2. Both β1‐adrenoceptors and β2‐adrenoceptors were present in guinea‐pig and human heart, on the myocardium and associated with the cardiac nerves and blood vessels.3. Nerves on the vasculature and vascular smooth muscle contained β‐adrenoceptors and muscarinic cholinoceptors.4. Receptors for substance P and β‐adrenoceptors, but not muscarinic cholinoceptors were present on endothelial cells.
SENSITIVITY CHANGES OF THE PERFUSED HINDQUARTERS’ VASCULATURE IN RATS WITH ALLOXAN‐INDUCED DIABETES MELLITUS
Authors: Boura A. L. A. , Hodgson W. C. , King R. G. 
Published: June 2007

SUMMARY1. Arachidonic acid (AA, 0.125–1.0 mg/kg) injected via the aorta into the autoperfused hindquarters caused dose‐dependent increases in perfusion pressure. This effect was reduced after intravenous administration of the thromboxane receptor antagonist AH23848 (5 mg/kg) or indomethacin (5 mg/kg).2. Responses to AA (0.125–1.0 mg/kg) were reduced markedly in the Krebs‐perfused hindquarters when compared with those occurring in the blood‐perfused preparation.3. Doses of guanethidine (1 mg/kg) and pentacynium (1 mg/kg) blocking pressor responses to intravenous administration of the ganglion stimulants McN‐A‐343 and DMPP, respectively, did not affect responses to AA.4. Constrictor responses to AA (0.5–1.0 mg/kg) in blood‐perfused hindquarters were increased in 14 day alloxan‐diabetic rats but those to the thromboxane A2‐mimetic U46619 (0.5–8.0 μg/kg, i.a.) were reduced when compared with non‐diabetic controls.5. In 14 day alloxan‐diabetic rats vasoconstrictor responses to noradrenaline and methoxamine were potentiated but those to 5‐hydroxytryptamine were reduced compared with non‐diabetic animals.6. It is concluded that AA causes constriction in the blood‐perfused hindquarters by release of a product of cyclo‐oxygenase acting on thromboxane A2‐receptors. A constituent of blood, perhaps the platelet, appears necessary for this effect. Conversion of AA to the constrictor metabolite is augmented during experimentally induced diabetes.
EFFECTS OF ANGIOTENSINS II AND III ON GLOMERULOTUBULAR BALANCE IN RATS
Authors: Harris Peter J. , Zhuo Jialong , Skinner Sandford L. 
Published: June 2007

SUMMARY1. The role of angiotensin as a modulator of proximal glomerulotubular (GT) balance was investigated in anaesthetized rats by examining the relationship between glomerular filtration rate (GFR) and absolute proximal reabsorption (APR) during removal of endogenous angiotensin II (AII) and III (AIII) with enalaprilat (CEI) and then during their subsequent replacement by intravenous infusions.2. Enalaprilat lowered mean arterial blood pressure (MABP) and increased renal blood flow (RBF), GFR, urine flow rate and sodium excretion. Filtration fraction (FF) was not altered. Absolute proximal reabsorption, derived from fractional lithium clearance, increased by only 48% of the change expected for ‘perfect’ GT balance.3. Angiotensin II replacement corrected MABP, GFR and plasma renin level, but reduced RBF and increased FF; APR was decreased and GT balance was restored. Urine flow and sodium excretion remained above control values with AII.4. Replacement with AIII did not correct the hypotension but completely reversed the renal and renin responses to enalaprilat and restored GT balance without affecting FF.5. It was concluded that the relation between proximal reabsorption and GFR is considerably modified by the intrarenal angiotensin concentration. The findings are best explained by a direct stimulation of proximal tubular sodium transport by angiotensin at the concentrations existing in anaesthetized rats.
β‐ADRENOCEPTORS ON ENDOTHELIAL CELLS DO NOT INFLUENCE RELEASE OF RELAXING FACTOR IN DOG CORONARY ARTERIES
Authors: Macdonald Peter S. , Dubbin Philip N. , Dusting Gregory J. 
Published: June 2007

SUMMARY1. The aim of this study was to determine if stimulation of a β‐adrenoceptor on endothelial cells could release an endothelium‐derived relaxing factor (EDRF) similar to that released by acetylcholine.2. In dog coronary rings preconstricted with PGF2α or serotonin, removal of the endothelium did not alter the relaxant responses to isoprenaline. However, in rings preconstricted with the thromboxane‐mimetic U46619, removal of the endothelium enhanced the response to isoprenaline.3. The vasorelaxant responses to isoprenaline in endothelium‐denuded rings were inhibited in a concentration‐dependent manner by the specific β1‐adrenoceptor antagonist CGP‐20712A (3–100 nmol/l), but were not altered by the β2‐adrenoceptor antagonist ICI‐118551 (30 nmol/l).4. The vasorelaxant responses to isoprenaline in the presence of CGP‐20712A (30 nmol/l) or ICI‐118551 (30 nmol/l) were not impaired by removal of the endothelium.5. Endothelium‐dependent vasorelaxant responses to acetylcholine and bradykinin were not altered by isoprenaline (0.1 μmol/l) in the presence of CGP‐20712A (30 nmol/l).6. Therefore, the β‐adrenoceptors on dog coronary artery smooth muscle which produce relaxation are predominantly of the β1‐subtype. Stimulation of any β2‐adrenoceptors on the endothelium in dog coronary artery does not release EDRF, and does not modulate endothelium‐dependent vasodilatation induced by other agents.
EFFECTS OF PANAX GINSENG ON BLOOD ALCOHOL CLEARANCE IN MAN
Authors: Lee F. C. , Ko J. H. , Park J. K. , Lee J. S. 
Published: June 2007

SUMMARY1. Fourteen healthy male volunteers were studied to assess the effects of Panax ginseng on blood alcohol clearance, utilizing each subject as his own control.2. At 40 min after the last drink, the blood alcohol level in the test group receiving ginseng extract (3 g/65 kg body weight) along with alcohol (72 g/65 kg body weight) was about 35% lower than their control values.3. When the blood alcohol level was compared on individual bases, alcohol concentrations in 10 out of 14 test subjects ranged from 32 to 51% lower than their control values.4. These results demonstrate that P. ginseng extract enhances blood alcohol clearance in man.
CHRONOTOXICITY OF β‐ADRENOCEPTOR BLOCKING AGENT IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Fujimura Akio , Ebihara Akio 
Published: June 2007

SUMMARY1. Chronotoxicity of a single LD50 dosage of β‐adrenoceptor blocking agent, pindolol, was determined in spontaneously hypertensive rats (SHR) and Wistar‐Kyoto control rats (WKY).2. The 24 h mortality was greater when pindolol was administered at 00.00 h than when it was administered at 12.00 h in both SHR and WKY.3. The chronogram of the mortality in SHR was similar to that in WKY.4. These results indicate that the mode of circadian variation in the acute toxicity of pindolol in SHR is not different from that in WKY.
THE HAEMODYNAMIC EFFECTS OF CYCLOSPORIN A IN SHEEP
Authors: Whitworth Judith A. , Mills Eric H. , Coghlan John P. , McDougall John G. , Nelson Mark A. , Spence Campbell D. , Tresham Janette J. , Scoggins Bruce A. 
Published: June 2007

SUMMARY1. Cyclosporin A (CyA; 12 mg/kg/day) was infused into six conscious sheep over 5 days to examine the haemodynamic effects of the drug in normal animals.2. Mean arterial pressure was increased from 73(1) mmHg to 90(4) mmHg (P < 0.001). There was no change in cardiac output but calculated total peripheral resistance was elevated from 16(1) to 21(2) mmHg min/1 (P < 0.001) on day 4.3. There was no change in plasma [Na], but a fall in plasma [K]. Urinary Na excretion decreased. Glomerular filtration rate, filtration fraction, renal blood flow, renal vascular resistance, body weight, plasma renin and blood aldosterone concentration were unchanged.4. CyA produces an increase in blood pressure in sheep associated with an increase in total peripheral resistance on days 1, 3, and 4, in the absence of changes in renal function. This suggests that CyA hypertension is not simply a consequence of nephrotoxicity.
RENAL RESPONSES TO ANGIOTENSIN II IN CONSCIOUS DOGS: EFFECTS OF ASPIRIN AND INDOMETHACIN
Authors: Anderson W. P. , Selig S. E. , Woods R. L. , Gilchrist A. I. 
Published: June 2007

SUMMARY1. Angiotensin II was infused into the renal artery of unanaesthetized dogs at 0.4 and 2.0 ng/kg per min for 40 min each.2. Indomethacin (3 mg/kg, and 1 mg/kg per h infusion i.v.) accentuated the angiotensin II‐induced falls in glomerular filtration rate, renal blood flow and urine flow rate. Indomethacin did not alter the effects of angiotensin II on Na+ or K+ excretions.3. Aspirin (35 mg/kg p.o. 2.5 h and 0.5 h prior to experiment) did not significantly change the renal effects of angiotensin II.4. Both aspirin and indomethacin accentuated renal vasoconstriction during briefer (5 min) angiotensin II infusion.5. Thus indomethacin and aspirin had markedly different effects on the actions of angiotensin II in the kidney. This suggests that at least one of these drugs has actions which affect angiotensin II‐mediated vasoconstriction other than via cyclooxygenase inhibition.
CHARACTERIZATION AND LOCALIZATION OF (—‐)[125I]‐CYANOPINDOLOL BINDING TO NON‐β‐ADRENOCEPTOR SITES IN DOG KIDNEY
Authors: Lew R. , Summers R. J. 
Published: June 2007

SUMMARY1. (—)[125I]‐Cyanopindolol (CYP) binding to non‐β‐adrenoceptor sites in dog kidney was characterized in homogenate preparations and their distribution in sections determined using autoradiography.2. In homogenate studies, (—)[125I]‐CYP bound to a single population of non‐interacting sites (Bmax= 5.45, s.e.m. = 1.00 fmol/mg wet weight; nH = 0.99, s.e.m. = 0.01) with high affinity (KD= 3.84, s.e.m. = 0.76 nmol/l, n= 4).3. In competition studies, compounds selective for α‐ and β‐adrenoceptors, muscarinic cholinoceptors and receptors for 5‐HT, histamine and benzodiazepines, calcium channel antagonists, catecholamine uptake inhibitors, MAO inhibitors and adrenergic neurone blockers were ineffective at concentrations of 10 μmol/l.4. Compounds selective for dopamine D1‐receptors (fluphenazine, SCH 23390 and SK & F 82526) and D2‐receptors (pimozide, domperidone, spiperone, haloperidol, sulpiride, cis‐ and trans‐flupenthixol) competed with similar affinities (5–25 μmol/l) for (—)[125I]‐CYP binding.5. In autoradiographic studies, (—) [125I]‐CYP binding to non‐β‐adrenoceptor sites was localized over glomeruli, juxtaglomerular apparatus, distal tubules, blood vessels and medullary rays and tubules.6. It is concluded that in dog kidney, (—)[125I]‐CYP binds to a site closely associated with dopamine receptors.
THE EFFECT OF SUBDIAPHRAGMATIC VAGOTOMY ON THE GASTRIC MUCUS BARRIER IN RATS
Authors: Somasundaram K. , Ganguly A. K. 
Published: June 2007

SUMMARY1. Little information exists on the quantitation of mucus barrier and its vagal control; hence, the effect of vagotomy on the two components of the mucus barrier was studied in the glandular regions of rat stomach.2. Bilateral subdiaphragmatic vagotomy was carried out by cutting both vagus nerves at the level of the lower end of the oesophagus. After 14 days, the glycoproteins in mucosal epithelial cells were identified by periodic acid Schiff's (PAS) staining technique and were assessed by calculating the ratio of the mucosal height to that of the thickness of PAS‐positive materials in it. The adherent mucus was estimated by the Alcian blue binding technique and the results were compared with control animals subjected to mock vagotomy.3. The bilateral subdiaphragmatic vagotomy caused a significant reduction in mucosal epithelial PAS‐stainable materials content in oxyntic and pyloric gland areas.4. The operation also caused a decrease in Alcian blue binding capacity of both the glandular regions.5. The data suggest that the absence of vagal influence causes weakening of both the lines of mucus barrier. The findings support the hypothesis that the vagal system must be intact in the rat in order to maintain gastric mucus glycoproteins and thereby mucosal integrity.
EFFECTS OF CYCLOSPORIN A, GENTAMICIN AND FUROSEMIDE ON RAT RENAL FUNCTION: A LITHIUM CLEARANCE STUDY
Authors: Dieperink Hans , Leyssac Paul P. , Starklint Henrik , Kemp Ejvind 
Published: June 2007

SUMMARY1. This study applied clearance methods of inulin, lithium, potassium, sodium and para‐aminohippuric acid (PAH) for investigation of the effects of cyclosporin A (CyA), furosemide and gentamicin on rat (n= 92) renal function. The drugs were dosed for 2 weeks; CyA 12.5 mg/kg per day, gentamicin 32 mg/kg per day and furosemide 5 mg/kg per day.2. The questions asked were: could these methods differentiate the effects of drugs with different sites of action, and would gentamicin or furosemide exaggerate the nephrotoxicity of CyA?3. Furosemide increased sodium clearance (CNa) 74% and fractional sodium clearance (FENa) 105%, while fractional sodium reabsorption in the distal nephron (FDNR) was reduced, compared with placebo‐treated controls.4. Gentamicin reduced CPAH29% and Cin37%, while FENaincreased 335%. Proximal fractional reabsorption (PFR) and absolute proximal reabsorption (APR) decreased.5. CyA depressed CPAH32% and lithium clearance (CLi) 56%, and increased PFR.6. The effects of CyA and furosemide in reducing renal function were not additive.7. CyA plus gentamicin reduced CPAHto 35% of the value in untreated controls, equal to 52% of the CPAHof CyA‐treated rats; Cinwas reduced to 46% of the Cinof CyA‐treated rats.8. Rats given CyA, furosemide and gentamicin had decreased Cin, CPAH and CLicompared with rats given either CyA plus furosemide or gentamicin plus furosemide.9. Thus, in this investigation of drugs known to have different sites of actions, the differences in renal and tubular function were discernible with the lithium clearance method.10. The nephrotoxicities of CyA and of gentamicin were additive, while furosemide did not aggravate CyA nephrotoxicity.