bluuebunny/crossref_metadata_2025_split huggingface dataset:
ACCELERATED ENDOTHELIAL REGENERATION AND INTIMAL HYPERPLASIA FOLLOWING A REPEATED DENUDATION OF RABBIT CAROTID ARTERIES: MORPHOLOGICAL AND IMMUNOHISTOCHEMICAL STUDIES
Authors: Azuma H. , Niimi Y. , Terada T. , Hamasaki H. 
Published: June 2007

SUMMARY1. We compared endothelial regeneration and intimal thickening after endothelial denudation between normal and sclerotic carotid arteries (CA). Endothelial denudation of the right CA of rabbits formed intimal thickening covered with regenerated endothelial cells (EC) in 6 weeks, which was considered as the sclerosis model. Both CA were then denuded. Morphological and immunohistochemical studies using antibodies for proliferating cell nuclear antigen (PCNA), von Willebrand factor and macrophages were performed.2. Regeneration of EC were observed 24h after denudation on both CA, but completed earlier in the double‐denuded right CA. The density of EC in both CA increased after regeneration and gradually decreased afterwards.3. After a single denudation on the left CA, PCNA‐positive cells clearly appeared in 24h, markedly increased in 72h both in the intima and media, then greatly decreased in 4 and 6 weeks.4. After a double denudation of the right CA, enhancement of the intimal hyperplasia was observed. PCNA‐positive cells markedly increased in 1 week and remained significantly increased in 6 weeks both in the intima and the media.5. We concluded from these results that the repeated endothelial denudation caused more sustained proliferation of smooth muscle cells which led to an enhancement of the intimal hyperplasia.
URAEMIA IS NECESSARY FOR ERYTHROPOIETIN‐INDUCED HYPERTENSION IN RATS
Authors: Poux Jean‐Michel , Lartigue Martine , Chaisemartin Rose‐Anne , Galen Francois Xavier , Leroux‐Robert Claude 
Published: June 2007

SUMMARY1. There is no experimental proof that renal insufficiency is a necessary condition for hypertension during erythropoietin treatment.2. The present study compares the effect of 3 weeks treatment with r‐hu EPO (50i.u./kg) on systolic blood pressure (SBP), haematocrit and plasma cGMP in an animal model of chronic renal failure (remnant kidney model excision) and sham‐operated rats.3. Sub‐total nephrectomy induced a significant fall in haematocrit and a significant increase in plasma creatinine levels. Treatment with r‐hu EPO resulted in a significant haematocrit increase in uraemic as well as in non‐uraemic rats. Despite this effect, r‐hu EPO treatment had no effect on SBP in sham‐operated rats. On the contrary, this treatment caused significant SBP elevation in uraemic ratq in these rats, SBP increase did not correlate with haematocrit increase.4. Plasma cGMP concentrations were significantly higher in uraemic compared to sham‐operated rats and were not modified by r‐hu EPO treatment.5. This study provides evidence that renal insufficiency in rats is a prerequisite for the development of hypertension during erythropoietin treatment.
24 HOUR AMBULATORY BLOOD PRESSURE PROFILES IN THE ACUTE PHASE OF STROKE
Authors: Morfis L. , Schwartz R. , Lykos D. , Zagami A. , Pryor D. , Howes L. G. 
Published: June 2007

SUMMARY1. Twenty‐four hour ambulatory blood pressure monitoring (ABPM) was used to evaluate the blood pressure (BP) changes in acute stroke.2. Stroke was categorized according to the probable underlying vascular mechanism into lacunar infarction (L), thrombotic infarction (T) and intracerebral haemorrhage (ICH). A total of 37 stroke patients were studied (T = 21, L = 9, ICH = 7). Control patients (n= 15) were acute medical admissions not severely ill or in significant pain. ABPM was performed on day 1 and day 7 following admission.3. Day 1 mean ± s.d. 24h systolic BP (SBP) were L (159 ± 15.8), ICH (151 ± 33.4), T (147 ± 15.2) and controls (134 ± 17.8). Day 7 mean 24h SBP were L (138 ± 9.8), ICH (143 ± 26.9), T (138 ± 19) and controls (134 ± 14.8). In each stroke group BP fell to levels similar to control on day 7, while control mean SBP remained unchanged between days 1 and 7. The highest day 1 BP and the greatest subsequent fall on day 7 occurred for lacunar infarction. Diastolic BP showed similar changes to SBP.4. The acute stress of hospitalization does not appear to explain elevated BP in acute stroke. Lacunar infarction appears to be particularly associated with temporary BP elevation.
PROCEEDINGS OF THE HBPRCA EFFECT OF DOSE ON TROUGH PEAK RATIO OF ANTIHYPERTENSIVE DRUGS IN ELDERLY HYPERTENSIVE MALES
Authors: Morgan T. O. , Morgan O. , Anderson A. 
Published: June 2007

SUMMARY1. The study was undertaken in male patients aged 61–73 years with essential hypertension.2. The patients had previously had their blood pressure controlled with the drug studied.3. A randomized crossover study compared the effect of different drug doses on peak (3h) and trough (24h) blood pressure compared to placebo.4. All drug doses used lowered blood pressure at peak response and the responses with different doses of angiotensin converting enzyme inhibitors were similar. The peak response to felodipine had some dose dependency.5. Trough blood pressure was not different from placebo with enalapril, 5 and 10 mg, perindopril, 2mg, felodipine, 2.5 mg but was different with enalapril, 20 and 40 mg, perindopril, 4 and 8 mg and felodipine, 5 and 10 mg.6. Trough peak ratio was dose dependent, with the greatest dependency seen with enalapril which has the shortest half‐life.7. When low doses of enalapril (5 or 10 mg), perindopril (2 mg) or felodipine ER (2.5 mg) are used it is important to check blood pressure prior to the next dose to ensure that control is achieved and maintained.
Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists, 1994: PHARMACODYNAMICS OF LEVODOPA IN PARKINSON'S DISEASE
Authors: Nutt J. G. 
Published: June 2007

SUMMARY1. Levodopa markedly reduces parkinsonism during the first years of treatment. However, with continued therapy the response to levodopa becomes erratic and is complicated by involuntary movements. To improve the therapy of parkinsonism, the challenge is to understand why fluctuations in response develop and, once developed, what controls the moment to moment motor status.2. In patients with a fluctuating response to levodopa, three distinct responses can be recognized: a short‐duration response, a long‐duration response and a negative response.3. The short‐duration response, measured in minutes to hours, has a steep concentration‐response relationship such that the response appears ‘all or nothing.’ The duration of effect is dose‐responsive. The short‐duration response becomes shorter during chronic therapy, possibly because of tolerance. The onset to effect becomes briefer and the magnitude of the response becomes larger during chronic therapy, possibly because of sensitization.4. The long‐duration response, measured in days to weeks, develops and decays slowly. The rate of decay is proportional to the severity of the parkinsonism and therefore this response may relate to dopamine storage capacity of remaining nerve terminals.5. The negative response, measured in minutes, is a worsening of motor function as the short‐duration improvement wears off. It may reflect a biphasic concentration‐response relationship.6. The response to levodopa in parkinsonian patients is a complex interplay between responses with different time courses and variably affected by sensitization, tolerance and disease progression.
Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists, 1994: HYPOTHESIS: APOPTOSIS CAUSED BY CYTOTOXINS REPRESENTS A DEFENSIVE RESPONSE THAT EVOLVED TO COMBAT INTRACELLULAR PATHOGENS
Authors: Vaux David L. , Häcker Georg 
Published: June 2007

SUMMARY1. Over 100 different agents have been shown, under certain circumstances, to cause apoptosis, a form of cell death with characteristic morphology. In most cases, the mechanism of cell death is likely to be the same, as expression of the cell death inhibitory gene bcl‐2 can frequently prevent apoptotic changes and/or delay cell death.2. These observations raise the question of how and why cells detect these agents and why they respond by implementing the suicide mechanism that bcl‐2 can control. Our hypothesis is that apoptosis is used as an anti‐viral strategy, and that cells interpret any metabolic disturbance as evidence of infection by a virus and thereby kill themselves in response to these toxins before they are killed by the action of the toxin itself.3. Experiments on the effect of sodium azide upon growth factor‐dependent cells support this idea. Bcl‐2 can delay cell death caused by azide, and inhibit apoptotic changes seen by electron microscopy, but cannot prevent the eventual death of the cells.4. These ideas suggest that drugs designed to regulate cell death may be useful for the treatment of ischaemic or neoplastic diseases. For example, human cells may activate a suicide pathway in response to sub‐lethal amounts of anoxia following a stroke or heart attack and so blocking apoptosis may be a useful therapy to limit tissue damage. On the other hand, increasing the propensity of cells to activate their physiological cell death mechanisms may enhance the effectiveness of toxins designed to kill tumour cells.
Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists, 1994: ANIMAL MODELS OF HEART FAILURE FOR PHARMACOLOGICAL STUDIES
Authors: Einstein R. , Abdul‐Hussein N. 
Published: June 2007

SUMMARY1. Animals for the study of congestive heart failure (HF) should have chronic, stable disease produced by methods which allow controllable damage and hence predictable disease severity.2. Pressure and volume loading have commonly been used in the past but these methods are limited by the difficulty of controlling the disease severity.3. HF induced by cardiotoxic agents, particularly doxorubicin, has been widely used for experimental purposes, but again, control of the degree of damage may be difficult.4. Coronary artery ligation or occlusion produces heart failure in experimental animals, with clear clinical relevance. Disadvantages of such techniques include fatal arrhythmias and collateral vessel growth that prevents or slows the onset of HF.5. A minimally invasive model of HF which is relatively controllable can be produced by repeated or single DC shocks across the left ventricle.6. Chronic rapid ventricular pacing produces a technically simple, predictable, stable and controllable preparation of HF with neurohumoral and haemodynamic changes which mimic the clinical pattern. These changes are reversible in the short term but after pacing for 1 year or longer complete recovery does not occur after cessation of pacing.7. It has recently been suggested that a single DC shock, three to seven times the threshold defibrillating current, administered to the left ventricle, might provide the basis for the development of a model of heart failure which is technically simple and controllable (Ceddeset al. 1994).
HOW DO FISH OILS AFFECT VASCULAR FUNCTION?
Authors: Chin Jaye P. F. , Dart Anthony M. 
Published: June 2007

SUMMARY1. This is a review on the mechanisms by which fish oils affect vascular function and how such changes contribute to their documented cardioprotective effects.2. Evidence that fish oils depress vascular responses to contractile agents will be examined. It is concluded that this effect of fish oils is mediated predominantly by alterations in prostanoid profile.3. Effects of fish oils on arterial relaxation are discussed with particular emphasis on endothelium dependent relaxation. It is suggested that the functional impairment of endothelium dependent relaxation documented in a number of cardiovascular disease states can be reversed by dietary fish oils.4. In addition, possible effects of fish oils on growth factors, inositol trisphosphate and lipid metabolism, the sympathetic nervous system, rheological and membrane properties and inducible nitric oxide are reviewed.
EFFECTS OF NG‐NITRO‐l‐ARGININE ON PRESSURE NATRIURESIS IN ANAESTHETIZED RABBITS
Authors: Evans Roger G. , Szenasi Gabor , Anderson Warwick P. 
Published: June 2007

SUMMARY1. We tested the effects of blockade of nitric oxide synthesis on renal function under conditions of controlled renal artery pressure. Our hypothesis was that endogenous nitric oxide plays a role in the natriuresis that accompanies increased renal perfusion pressure. We used a novel technique which employed an extracorporeal circuit to produce step changes over a wide range of renal artery pressures in pentobarbitone‐anaesthetized rabbits.2. Rabbits were treated with either NG‐itro‐l‐arginine (NOLA, 20 mg/kg, i.v.; n = 8) or its vehicle (n= 8). Renal artery pressure was set (by adjusting the extracorporeal circuit) at 65, 80, 95, 110 and then 130mmHg respectively, at the beginning of each of five 30 min experimental periods.3. NOLA treatment caused profound renal vasoconstriction that was largely independent of the level of renal artery pressure, renal blood flow being 35–43% lower in NOLA‐treated than in vehicle‐treated rabbits across the range of renal artery pressures tested (P= 0.002). NOLA treatment increased filtration fraction (P = 0.02), and tended to reduce glomerular filtration rate (P= 0.09).4. NOLA‐treatment affected sodium excretion in a manner dependent on the level of renal artery pressure, with the slope of the relationship between sodium excretion and renal artery pressure being lower in NOLA‐treated than in vehicle‐treated rabbits (P= 0.006).5. These data provide direct evidence that in anaesthetized rabbits endogenous nitric oxide (i) tonically dilates the renal vasculature across a wide range of renal perfusion pressures, and (ii) enhances sodium excretion to a progressively greater degree as renal artery pressure is increased. It may therefore play a role in pressure‐induced natriuresis.
REGULATION OF COLLECTING DUCT Na+ REABSORPTION BY ANP 31–67
Authors: Zeidel Mark L. 
Published: June 2007

SUMMARY1. The bulk of studies of the actions of atrial natriuretic peptides (ANP) have focussed on the carboxyterminal derivative (ANP 99–126) of the prohormone (ANP 1–126), but recent evidence indicates that an additional peptide derived from ANP 1–126, namely, ANP 31–67 also circulates, and has natriuretic actions.2. The effects of ANP 31–67 on inner medullary collecting duct (IMCD) Na+ transport have been examined in freshly prepared suspensions of rabbit IMCD cells. Like ANP 99–126, ANP 31–67 reduces Na+ transport in these cells.3. However, unlike ANP 99–126, this effect is not mediated by cGMP, and does not result from inhibition of apical Na+ channels. Rather, ANP 31–67 inhibits basolateral Na/K‐ATPase, probably via the stimulation of PGE2 synthesis.4. These results are discussed in the context of other natriuretic substances (interleukin 1 and endothelin), which also inhibit Na+ reabsorption by PGE2 ‐mediated inhibition of Na/K‐ATPase.
PREGNANCY ATTENUATES ACTIVITY OF THE BARORECEPTOR REFLEX
Authors: Brooks Virginia L. , Quesnell Rebecca R. , Cumbee Sharon R. , Bishop Vernon S. 
Published: June 2007

SUMMARY1. Pregnancy‐induced changes in acute blood pressure regulation are reviewed.2. Pregnant animals are less able to maintain arterial pressure during haemorrhage than non‐pregnant animals.3. Baroreceptor reflex‐mediated increases in heart rate, renal sympathetic activity, vasopressin, ACTH and cortisol are reduced during pregnancy. Therefore, one explanation for the subnormal ability of pregnant animals to regulate arterial pressure during haemorrhage is that the baroreceptor reflex is not as effective.4. Chronic increases in oestrogen levels in non‐pregnant rabbits do not reduce the gain of baroreflex control of renal sympathetic activity. This and other findings suggest that oestrogen alone does not mediate the blunted baroreflex activity observed during pregnancy.
NITRIC OXIDE BIOSYNTHESIS DURING PREGNANCY: IMPLICATIONS FOR CIRCULATORY CHANGES
Authors: McLaughlin Margaret K. , Conrad Kirk P. 
Published: June 2007

SUMMARY1. The biosynthesis of NO and its second messenger, cGMP, increases from pre‐pregnant levels during rat gestation. An increase in plasma level and urinary excretion of cGMP is also evident during human pregnancy. However, the relative contribution of the maternal vasculature and other tissues to increased NO and cGMP biosynthesis during gestation is uncertain. Consensus is lacking about the contribution of NO to reduced maternal vascular tone and reactivity during gestation in various organ beds; clearly, further investigation is still needed. That NO may also regulate vascular smooth muscle behaviour during pregnancy by altering membrane potential is another intriguing possibility.2. The syncytiotrophoblast of the human placenta expresses significant NO synthase activity, and along with the fetoplacental endothelium undoubtedly contributes to NO production during pregnancy.3. Finally, it should be emphasized that vascular studies in gravid animal models need to be extended to pregnant women.
VEGETARIAN DIET COMPONENTS, PROTEIN AND BLOOD PRESSURE: WHICH NUTRIENTS ARE IMPORTANT?
Authors: Beilin L. J. , Burke V. 
Published: June 2007

SUMMARY1. Evidence that vegetarian dietary patterns lower blood pressure (BP) comes from both population studies and randomized controlled trials in normotensive and hypertensive subjects.2. The effect has been shown most clearly in those who keep to a strict lacto‐ovo vegetarian diet characterized by a relatively low intake of saturated fat, a high polyunsaturated/saturated fat ratio, and a high intake of fruit, vegetables and other fibre containing products. Randomized controlled dietary trials suggest the effects are independent of dietary sodium, additive to that of calorie restriction, and not due to the absence of meat protein per se. Indeed, recent population studies suggest an inverse relationship between dietary protein and BP.4. Dietary fats, fibre, potassium, magnesium and calcium do not independently seem to account for the effects. A possible role for complex carbohydrate in conjunction with the other dietary factors has yet to be fully explored.
AMBULATORY BLOOD PRESSURE MONITORING FOR EVALUATING THE RELATIONSHIPS BETWEEN LIFESTYLE, HYPERTENSION AND CARDIOVASCULAR RISK
Authors: Pickering Thomas G. , Schwartz Joseph E. , James Gary D. 
Published: June 2007

SUMMARY1. Ambulatory monitoring provides a unique opportunity for studying the temporal relationships between lifestyle factors and blood pressure (BP). These include physical activity, mental activity, environmental stressors, substances ingested for pleasure such as smoking, alcohol and caffeine, and nutrition.2. Changes in physical activity play a major role in determining the diurnal profile of BP, whereas the influence of mood is small.3. Environmental stress, in the form of job strain, has been shown to be associated with a sustained increase of BP throughout the day and night in men, and also with an increased left ventricular mass. The effects are most marked in men who drink alcohol regularly. Job strain does not appear to influence BP in women.4. Although it is recognized that smoking raises BP acutely, its long‐term effects have been unclear. Ambulatory monitoring shows that smokers have a larger diurnal swing of BP than non‐smokers, because of a higher daytime pressure. Alcohol also increases the diurnal swing of BP.5. Ambulatory monitoring has been used relatively little for evaluating nutritional factors, but has the possibility of quantifying their effects on BP more reliably than traditional methods, and also elucidating the underlying mechanisms.
ALTERED LIPID PEROXIDATION/GLUTATHIONE RATIO IN EXPERIMENTAL EXTRAHEPATIC CHOLESTASIS
Authors: Panozzo M. P. , Basso D. , Balint L. , Biasin M. R. , Bonvicini P. , Metus P. , Infantoho D. , Plebani M. 
Published: June 2007

SUMMARY1. Lipid peroxidation can occur in the presence of a cellular antioxidant‐oxidant imbalance, but the role of lipid peroxides in cholestasis is not well understood.2. This study was undertaken in order to: (i) evaluate the behaviour of a product of lipid peroxidation (thiobarbituric acid‐reactive species), and of an important antioxidant tripeptide, reduced glutathione, in the course of experimental extrahepatic cholestasis; and (ii) ascertain whether there was a link between this aspect and the alterations in liver morphology.3. Forty‐five male Sprague‐Dawley rats (250–300 g) were double bile duct ligated and followed from 1 to 28 days. At the end of each experimental period, blood and liver samples were collected for thiobarbituric acid‐reactive species and glutathione determinations.4. Bile duct ligated rats showed a marked increase in liver weight which was related to cholestasis duration and to some anatomical alterations such as bile duct proliferation and dilation and liver fibrosis (periportal, perivenular, perineoductular and parenchymal).5. An increase in serum lipid peroxidation was also observed but this was not linked to hepatic thiobarbiturie acid‐reactive species. Erythrocyte and hepatic glutathione decreased in relation to cholestasis duration. Serum lipid peroxides and erythrocyte glutathione were correlated with liver cell necrosis.6. In conclusion, experimental extrahepatic cholestasis determines bile duct proliferation and fibrosis, the degree of which is directly related to the duration of cholestasis itself and to liver cell necrotic phenomena. Furthermore, extrahepatic cholestasis is associated with increased lipid peroxide formation and with a depletion of reduced glutathione both in the liver and in the erythrocytes. The alteration in the oxidative balance may be a contributory factor in necrotic liver cell phenomena.
USING NEUROBLASTOMA CELL LINES TO ADDRESS DIFFERENTIAL SPECIFICITY TO ORGANOPHOSPHATES
Authors: Ehrich Marion 
Published: June 2007

SUMMARY1. Organophosphates can cause acute toxicity, which follows inhibition of ncetylcholinesterase (AChE), or delayed neuropathy, which follows inhibition of neuropathy target esterase (NTE).2. Human neuroblastoma SH‐SY5Y cells contain AChE and NTE.3. Organophosphates actively able to inhibit AChE in animal models inhibited AChE in neuroblastoma cells.4. Inhibition of NTE in neuroblastoma cells could identify active organophosphates capable of causing delayed neuropathy in animal models and distinguish these organophosphates from those that do not cause delayed neuropathg in animal models.
EFFECTS OF SELECTED ORGANIC SOLVENTS ON THE ASTROCYTE MEMBRANE ATPase IN VITRO
Authors: Vaalavirta Leila , Tähti Hanna 
Published: June 2007

SUMMARY1. The present study deals with astrocyte cultures as a model for studying the membrane‐mediated central nervous system‐depressing effect of organic solvents.2. The primary astrocyte cultures were prepared from neonatal rat cerebella. The cells were cultured in modified essential medium. The astrocyte membranes isolated from the cultures were exposed to solvents in incubation mixture at different dose levels (3, 6 and 9 mmol/L) for 1h. The physiologically important integral proteins Na+, K+‐ATPase and Mg2+‐ATPase were studied.3. The aromatic hydrocarbons (benzene, toluene, styrene, xylene and ethylbenzene) inhibited the ATPase activities according to their lipid solubilities. n‐Hexane and cyclohexane clearly had less effect than aromatic hydrocarbons, despite their greater lipid solubilities.4. Astrocytes were shown to be sensitive targets to the effects of organic solvents, measured as the inhibition of the integral enzymes Na+, K+‐ATPase and Mg2+‐ATPase.