bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of DHA+EPA on oxidative stress and apoptosis induced by ischemia‐reperfusion in rat kidneys
Authors: Ajami Marjan , Davoodi Sayed Hossein , Habibey Rouhollah , Namazi Nasim , Soleimani Mansoureh , Pazoki‐Toroudi Hamidreza 
Published: July 2012

AbstractApoptosis, as well as necrosis, has an important role in post‐ischemic renal pathology. The effect of pretreatment with Docosahexaenoic acid+Eicosapentaenoic acid (DHA+EPA) on renal injury and apoptotic protein expression was evaluated. Right nephrectomy was completed on male Wistar rats (255–300 g). The rats received DHA+EPA (200 mg/kg/day) of distilled water orally for 14 days before ischemia reperfusion (IR) or sham operation. A total of 81 rats were divided into three main groups with 6, 24 and 48 h of post‐operation or reperfusion period. Serum creatinine (SCr), BUN, creatinine clearance (CCr) and fractional excretion of sodium (FENa) were measured. Tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) activities, Bax and Bcl‐2 protein expressions and renal histological injury were determined. SCr, BUN and FENa increased 6–48 h of reperfusion (P < 0.01). Tissue MDA content and Bax expression increased (P < 0.01) and CAT and SOD activities decreased (P < 0.05) in the IR group. DHA+EPA decreased SCr and BUN, FENa, tissue MDA levels (P < 0.05 vs. IR) and increased CAT and SOD activities and Bcl‐2 expression (P < 0.05 vs. IR) for 6–48 h after ischemia. IR induced mild (6 h, P < 0.05) and severe (24–48 h, P < 0.01) tissue damage. Mild‐to‐moderate tissue damage was observed in DHA+EPA groups from 6 to 48 h of reperfusion period (P < 0.05 vs. IR, 24–48 h). In conclusion, the results suggest that pre‐ischemic exposure to DHA+EPA could improve the outcome of early graft function by inhibition of IR‐induced oxidative stress and apoptosis.
Outcomes for Whites and Blacks at Hospitals That Disproportionately Care for Black Medicare Beneficiaries
Authors: López Lenny , Jha Ashish K. 
Published: July 2012

ObjectiveHospital care for blacks is concentrated among a small number of hospitals and whether they have worse outcomes across common medical conditions is unknown.Data SourceWe used the 2007 100% Medicare file to calculate 30‐ and 90‐day mortality rates for white and black patients admitted for acute myocardial infarction (AMI), congestive heart failure (CHF), or pneumonia.Study DesignWe ranked all hospitals in the country by their proportion of discharged black patients and identified the top 10 percent of these hospitals as black serving. We examined race‐specific adjusted mortality rates and adjusted for differences in hospital characteristics.Principal FindingsAt 30 days, black‐serving hospitals had, compared with nonblack‐serving hospitals, similar mortality for AMI, lower mortality for CHF, and higher mortality for pneumonia. At 90 days, mortality was higher at black‐serving hospitals for both AMI and pneumonia and comparable for CHF compared with nonblack‐serving hospitals. White patients had worse outcomes at black‐serving hospitals for two conditions at 30 days and all three conditions at 90 days. Blacks also had worse outcomes at black‐serving hospitals.ConclusionsHospitals with a high proportion of black patients had worse outcomes than other hospitals for both their white and black elderly patients.
Accidental and experimentally induced 5‐fluorouracil toxicity in dogs
Authors: Sayre Rebecca S. , Barr James W. , Bailey E. Murl 
Published: July 2012

AbstractObjectiveTo summarize the literature involving 5‐fluorouracil (5‐FU) toxicosis in dogs.Etiology5‐Fluorouracil's mechanism of action revolves around the metabolism of 5‐FU into fluorouridine triphosphate which then interferes with RNA synthesis and function as well as the inhibition of thymidylate synthase which ultimately impairs DNA stability. Toxicity of 5‐FU is the most pronounced on rapidly dividing cells. Toxicity manifests itself mainly in the neurologic, gastrointestinal, respiratory, or hematopoietic systems.DiagnosisHistory of accidental exposure to 5‐FU‐containing products.TherapyTherapy for 5‐FU toxicosis involves typical decontamination procedures and symptomatic therapy for the subsequent toxicity. Seizure control and treatment of the severe gastrointestinal signs that follow are the primary goals in the acute setting. As the disease progresses, management of the sequelae to bone marrow suppression and pulmonary complications are essential.PrognosisThe prognosis for dogs with ingestion of 5‐FU is dependent on the amount consumed, with severe intoxication carrying a poor prognosis. Toxic doses can be as little as 5 mg/kg, and doses ≥40 mg/kg are reported to be uniformly fatal.
Effects of amiloride on active sodium transport by the isolated frog skin: evidence concerning site of action
Authors: SALAKO L. A. , SMITH A. J. 
Published: July 2012

Summary
Amiloride reduces short‐circuit current and potential difference across the isolated frog skin.
Isotopically measured sodium influx and efflux are diminished.
Total electrical conductance and partial sodium conductance are diminished, the reduction in total conductance being entirely accounted for by the reduction in partial sodium conductance.
The effect of antidiuretic hormone (ADH), cyclic 3′5′‐adenosine monophosphate (cyclic AMP) and theophylline can be antagonized by pretreatment with amiloride but the antagonism can be abolished by increasing the concentration of these compounds.
Amiloride has no effect on oxygen consumption in concentrations which inhibit sodium transport. However, it prevents the stimulatory effect of ADH on oxygen consumption.
The results are consistent with an action of amiloride at the passive outside membrane of the transporting cells of isolated frog skin.
Changes in the molecular composition of circulating hydroxyethyl starch
Authors: FARROW S. P. , HALL M. , RICKETTS C. R. 
Published: July 2012

Summary
Hydroxyethyl starch (HES) of molecular weight 450,000 has been extensively investigated as a plasma volume expander and HES of molecular weight 60,000 has been proposed for use as a cryoprotective agent in the freezing for preservation of red blood cells. In these applications considerable amounts of HES may be injected intravenously and it is therefore desirable to understand its behaviour in vivo.
After intravenous injection into rabbits, plasma levels of HES and clinical dextrans were determined using anthrone. HES persisted longer in the circulation than did the dextrans.
HES was recovered from the bloodstream of rabbits and shown by gel filtration to be of a narrower molecular size distribution than the injected material. Smaller molecules were removed, presumably by filtration at the glomerulus. Larger molecules may have been removed by cells of the reticuloendothelial system or possibly through the action of amylase.
The amylase in saliva was shown to break down HES into molecules of intermediate size with very little production of maltose units.
Regional circulatory effects of pancreatic glucagon
Authors: ROSS G. 
Published: July 2012

Summary
The effects of close intra‐arterial injections and infusions of glucagon on blood flow in the femoral, hepatic and superior mesenteric arteries of anaesthetized cats were studied using non‐cannulating electromagnetic flow probes.
Glucagon dilated the mesenteric vasculature. The threshold dose for rapid injections was less than 1 μg and maximal changes were produced by 10–20 μg. The dilatation began within a few seconds of injection and was unaffected by prior denervation or by pre‐treatment with propranolol or atropine.
Close intra‐arterial glucagon increased the resistance of the hepatic arterial bed but had no effect on femoral vascular resistance. Intravenous glucagon failed to alter renal blood flow.
Glucagon is therefore a potent vasoactive substance with its effect wholly or predominantly confined to the splanchnic area.
It has been suggested that the cardiac effects of glucagon and isoprenaline resemble each other because both compounds act on the β‐adrenoceptor mechanism. The different regional vascular effects of glucagon and isoprenaline suggest that glucagon vasodilatation may not be mediated via β‐adrenoceptors.
The effects of cholinomimetic drugs on responses to sympathetic nerve stimulation and noradrenaline in the rabbit ear artery
Authors: RAND M. J. , VARMA B. 
Published: July 2012

Summary
The effects of infusions of the cholinomimetic drugs acetylcholine, methacholine, muscarine, carbachol, arecoline and pilocarpine were examined on vasoconstrictor responses of the perfused rabbit ear artery to sympathetic nerve stimulation and to injections of noradrenaline.
The first effect of very low concentrations of acetylcholine or muscarine was a slight enhancement of responses to sympathetic nerve stimulation, but when higher concentrations of acetylcholine, methacholine, muscarine, carbachol and arecoline were infused, these vasoconstrictor responses were decreased. With still higher concentrations the responses tended to increase in size during the infusion. After stopping an infusion, the depressed vasoconstrictor responses rapidly recovered and became enhanced.
Infusions of pilocarpine in a wide range of concentrations generally caused enhancement of responses.
The depressant effects of cholinomimetic drugs on the responses to sympathetic nerve stimulation were antagonized by atropine. Larger concentrations of the drugs overcame the blockade by atropine.
The effects of acetylcholine, methacholine and muscarine on the responses to sympathetic nerve stimulation were more pronounced at low than at high frequencies of stimulation.
Vasoconstrictor responses to injected noradrenaline were enhanced by acetylcholine or methacholine, whereas responses to sympathetic nerve stimulation were decreased by the same concentrations of these choline esters.
It is suggested that cholinomimetic drugs may act on receptor sites associated with the adrenergic terminal axon and that they may facilitate or impair the release of noradrenaline and impair noradrenaline uptake.
Mechanism of the antagonism of the hypotensive action of guanethidine by propranolol
Authors: GREWAL R. S. , KAUL C. L. 
Published: July 2012

Summary
Propranolol antagonizes the hypotensive effect of guanethidine in renal hypertensive but not in adrenal demedullated renal hypertensive rats.
Guanethidine does not interfere with the release of catecholamines from the adrenal gland which follows splanchnic nerve stimulation in cats anaesthetized with pentobarbitone.
Guanethidine does not release or interfere with the release of catecholamines after the intravenous injection of physostigmine in the rat.
Propranolol antagonizes the antihypertensive effect of guanethidine by potentiating the vasopressor effects of catecholamines released from the adrenal glands during the induction stage of ether anaesthesia.
Uptake and metabolism of catecholamines in the perfused hearts of different species
Authors: JARROTT B. 
Published: July 2012

Summary
The uptake of (±)‐3H‐noradrenaline was studied in isolated perfused hearts of rat, mouse, guinea‐pig, pigeon and toad (Bufo marinus), and the IC50 (concentration causing 50% inhibition) values for inhibition of uptake of (±)‐3H‐noradrenaline by (–)‐noradrenaline were calculated. IC50 values ranging from 0·28 μm (rat heart) to 2·34 μm (toad heart) were found.
In all species except the toad, (–)‐noradrenaline showed a higher affinity than (–)‐adrenaline for the uptake process, but the reverse was found for the toad heart.
Mouse and pigeon hearts contained increasing amounts of metabolites of noradrenaline with increasing perfusion concentrations of noradrenaline, but the guinea‐pig and toad hearts did not. The in vitro activities of noradrenaline catabolizing enzymes in heart homogenates were measured but did not explain the differences in the pattern of catabolism of noradrenaline found in the intact hearts of the different species.
In all hearts except the toad, cocaine was an effective blocking agent for the uptake of (±)‐3H‐noradrenaline and led to an increase in 3H‐normetanephrine in these hearts. In the pigeon heart, cocaine plus phenoxybenzamine in the perfusate resulted in an inhibition of both 3H‐noradrenaline uptake and 3H‐normetanephrine formation.
In guinea‐pig and pigeon perfused hearts, the uptake of 3H‐noradrenaline into atria and ventricles reflected the relative concentrations of endogenous catecholamines in these regions, but this was not found for rat, mouse and toad hearts.
It was concluded that species differences exist for both the accumulation and metabolism of catecholamines in isolated perfused hearts.
Cardiac actions in the dog of a new antagonist of adrenergic excitation which does not produce competitive blockade of adrenoceptors
Authors: CHARLIER R. 
Published: July 2012

Summary
The cardiac actions of amiodarone, a benzofuran derivative used in the treatment of angina pectoris, have been compared with those of (±)‐propranolol in anaesthetized dogs.
After three successive intravenous injections of propranolol, 0·5 mg/kg, had reduced the heart rate by 25%, a fourth dose had no further negative chronotropic action, but amiodarone, 10 mg/kg intravenously, at this point reduced the heart rate by 23%.
Amiodarone, 10 mg/kg intravenously, reduced, but did not abolish, cardiac responses to isoprenaline, 2 μg/kg intravenously. Subsequent successive injections of 10 mg/kg of amiodarone did not further block the responses to isoprenaline, but propranolol, 1 mg/kg intravenously, abolished them.
Amiodarone reduced cardiac chronotropic and inotropic responses to glucagon, which were not affected by propranolol.
Cardiac output was increased 5 min after amiodarone, 10 mg/kg intravenously, but at 10 min and thereafter it did not differ from control values. Propranolol, 1 mg/kg intravenously, reduced cardiac output by 17% at 5 min, and by 30% after 30 min.
From this and other evidence which is discussed, it is concluded that the cardiac actions of amiodarone are not produced by competitive blockade of β‐adrenoceptors.
Role of the vagus nerves in anaphylaxis and histamine‐induced bronchoconstrictions in guinea‐pigs
Authors: MILLS JANET E. , WIDDICOMBE J. G. 
Published: July 2012

Summary
The effects of vagotomy on the respiratory responses of guinea‐pigs to anaphylactic reactions and to intravenous injections of histamine acid phosphate are described.
In spontaneously breathing guinea‐pigs, vagotomy reduced by 50% or more the decreases in total lung conductance (bronchoconstriction) and the decreases in lung compliance, and almost abolished the rapid shallow breathing due to histamine.
In paralysed, artificially ventilated guinea‐pigs, vagotomy reduced by more than 33% the decreases in total lung conductance, but had little effect on the changes in lung compliance due to histamine.
In paralysed, artificially ventilated guinea‐pigs, vagotomy reduced by 75% the decrease in total lung conductance and halved the decrease in lung compliance due to anaphylaxis.
We conclude that a vagal reflex is mainly responsible for the rapid shallow breathing due to histamine, and partly responsible for the bronchoconstrictions due to histamine and to anaphylaxis in guinea‐pigs. We suggest that “lung irritant receptors” in the bronchial epithelium are the afferent end‐organs involved.
Acetylcholine content in the brain of rats treated with paraoxon and obidoxime
Authors: MILOŠEVIĆ M. P. 
Published: July 2012

Summary
The effect of obidoxime on the rise in brain acetylcholine caused by the anticholinesterase paraoxon was studied in the rat.
In animals poisoned with a sublethal dose of paraoxon and thereafter treated with obidoxime the levels of both “free” and total brain acetylcholine were practically the same as those in rats injected with paraoxon only.
After poisoning with doses of paraoxon which are lethal unless an oxime is also given, the total acetylcholine in the brain of obidoxime‐protected rats continued to accumulate, reaching a peak 2 h after injection of paraoxon. At this time no signs of central effects such as convulsions or tremor were seen.
Atropine, given 30 min before paraoxon, markedly reduced the rise in total brain acetylcholine seen when the anticholinesterase is given alone.
In rats pretreated with atropine and obidoxime excessive doses of paraoxon which are lethal in the absence of the antidotes produced a rise in total brain acetylcholine which was directly proportional to the dose of paraoxon administered.
Effects of some drugs on the responses of the rat isolated, innervated urinary bladder to indirect electrical stimulation
Authors: DHATTIWALA A. S. , JINDAL M. N. , KELKAR V. V. 
Published: July 2012

Summary
The effects of some drugs known to inhibit transmission in the superior cervical ganglion and at the neuromuscular junction were investigated on the cholinergic nerve‐smooth muscle junction, using the rat isolated innervated urinary bladder preparation.
HC‐3 and Win 4981 inhibited the indirectly evoked contractions; the block was typically slow in onset, depended on the rate of stimulation and was partially reversed by choline. The moderate coincident inhibition of acetylcholine‐responses disappeared after washing the tissue, while the block of the neuronally evoked contractions persisted.
Morphine, methylpentynol carbamate, chloral hydrate and strychnine inhibited indirectly evoked contractions without inhibiting the responses to acetylcholine. Paraldehyde inhibited both types of response.
Hexamethonium, mecamylamine and tubocurarine had no effect on either type of response. Tetraethylammonium augmented both types of response; the augmentation due to lower concentration was followed by a moderate block of the neuronally evoked contractions.
Small concentrations of procaine markedly inhibited responses to acetylcholine and produced a partial block of the neuronally evoked contractions.
None of the drugs affected conduction in the isolated phrenic nerve.
All the drugs other than paraldehyde and procaine appeared to act at the nerve terminals. The results are generally consistent with the view that HC‐3 and Win 4981 act by limiting transport of choline across nerve membrane and that the other drugs act by inhibiting the release of acetylcholine. A reduction in sensitivity of the effector cell membrane may account, wholly or in part, for the action of paraldehyde and procaine.
A comparison of the sensitivities of innervated and denervated rat vasa deferentia to agonist drugs
Authors: BIRMINGHAM A. T. , PATERSON G. , WÓJCICKI J. 
Published: July 2012

Summary
One vas deferens of a rat was denervated by stripping away the serous coat; the other vas was left intact as a control. One week later the sensitivity in vitro of both vasa deferentia to noradrenaline, adrenaline, dopamine, oxymetazoline or acetylcholine was measured.
Log concentration response curves for the mean responses of both vasa from a group of four rats for each drug were plotted. Denervated vasa were more sensitive than control vasa to noradrenaline (16‐fold), to adrenaline (8‐fold), to dopamine (2‐fold) and to oxymetazoline (2‐fold). Denervated vasa were more sensitive to acetylcholine over the lower half of the concentration range only.
It is concluded that these results support the theory that at least part of the increased sensitivity of denervated smooth muscle to catecholamines is due to an abolition or reduction of the neuronal uptake process. There is also a small non‐specific increase in sensitivity.
Accumulation of dopamine by blood platelets from normal subjects and parkinsonian patients under treatment with l‐DOPA
Authors: BOULLIN D. J. , O'BRIEN R. A. 
Published: July 2012

Summary
Human blood platelets have been shown to take up dopamine by an energy‐dependent, saturable process that is inhibited by 5‐hydroxytryptamine (5‐HT), desipramine and other drugs.
Platelets from parkinsonian subjects receiving oral l‐DOPA also took up dopamine.
When the responses of normal and parkinsonian platelets were compared, the parkinsonian cells showed the following differences: increased affinity for the dopamine transport process; decreased equilibrium concentrations of dopamine after incubation for 90 min, and greater efflux of dopamine from loaded platelets during a 10 min incubation.
There were no differences in the uptake of 5‐HT by parkinsonian platelets, but endogenous 5‐HT was significantly reduced; ATP was normal.
In two out of three samples of platelets from parkinsonian subjects, traces of a dopamine‐like substance were detected, but this finding requires confirmation.
If the platelet is a valid model for dopaminergic brain neurones, then the results described would suggest that dopamine uptake and storage may be abnormal in brain neurones in Parkinson's disease.
Hyposensitivity to drugs induced by morphine and some related substances in the cat
Authors: CONTRERAS E. , HUIDOBRO F. 
Published: July 2012

Summary
Hyposensitivity to noradrenaline occurred concomitantly with morphine tachyphylaxis in the absence of any obvious depressant effect on the heart or peripheral circulation.
The actions of adrenaline, noradrenaline and angiotensin and, occasionally, other drugs were tested before and after repeated injections of morphine or one of ten related substances in various preparations of the spinal cat.
Tachyphylaxis in response to morphine could be related to a simultaneous decrease in the tissue responses to adrenaline, noradrenaline and angiotensin but such a parallelism has not been shown for the substances related to morphine.The authors wish to express their gratitude to Professor C. Eyzaguirre for his invaluable suggestions and criticism and to Dr. N. F. Grundy for his assistance in the preparation of the paper for publication. This work was partially aided by a grant from the Gildmeister Foundation, Santiago, Chile.
Changes in the composition of hind limb lymph after chemical injury
Authors: BOYLES SUSAN , LEWIS G. P. , WESTCOTT BARBARA 
Published: July 2012

Summary
Lymph was collected directly from the hind limbs of rabbits and cats anaesthetized with pentobarbitone.
Injury to the hind limb was caused by injection of one of two chemicals; either dimethylsulphoxide (DMSO) which produced a mild injury, or croton oil which produced severe injury.
After subcutaneous injection (6 × 0·2 ml) into the right hind limb there was a good correlation between the changes in concentration of intracellular enzyme systems in the lymph draining the limb and the histological appearance of the injured tissue. DMSO caused an increase in cytoplasmic enzymes only, while after croton oil, which caused cell necrosis, there was an increase in the concentration of all intracellular enzymes examined.
There was an increased lymph flow accompanied by a fall in protein concentration after DMSO, while croton oil caused an increase in protein concentration and a variable effect on lymph flow.
Effects of (±)‐propranolol, (±)‐, (+)‐, and (–)‐alprenolol on unanaesthetized dogs with ventricular arrhythmias resulting from coronary artery ligation
Authors: DUCE B. R. , GARBERG L. , SMITH E. R. 
Published: July 2012

SummaryThe effects of (±)‐propranolol, (±)‐, (+)‐ and (–)‐alprenolol were studied in unanaesthetized dogs with ventricular arrhythmias produced by ligation of the left coronary artery. The responses were compared with those of similar control dogs which were given only isotonic saline.The ventricular arrhythmias were abolished by cumulative doses of 3·5 mg/kg of (±)‐alprenolol, 7·5 mg/kg of (–)‐alprenolol and (±)‐propranolol and by 15·5 mg/kg of (+)‐alprenolol.At the time of maximum antiarrhythmic activity none of the drugs produced significant alterations in mean arterial pressure or atrial rate.Cumulative doses of 7·5 mg/kg and 15·5 mg/kg of the four drugs resulted in some instances of lip licking, emesis and/or head tremors while 31·5 mg/kg was invariably lethal.Since the β‐adrenoceptor blocking activity of (–)‐alprenolol is 100 times greater than that of (+)‐alprenolol, suppression of these ventricular arrhythmias was apparently unrelated to antagonism of sympathetic influences.Alprenolol and propranolol have myocardial depressant properties apart from their effects on β‐adrenoceptors which could account for the antiarrhythmic activity observed.