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Introduction: Quality improvement systems (QIS) that are based on empirical performance assessment have increasingly been implemented as a mandatory part of health systems across countries. This study aims to describe national mandatory QIS in Europe in 2014., Materials and Methods: Relevant national agencies for national mandatory QIS in Europe were identified through online searches and key informants. A questionnaire was compiled during a workshop with these agencies and filled out by representatives from these particular agencies., Results: Agencies in charge of national mandatory QIS in seven countries (Denmark, France, Germany, Israel, Scotland, Sweden and Switzerland) were included in the study. An analysis of QIS revealed similarities, such as the use of routine data for performance assessment and the aim to hold healthcare providers accountable. Differences relate to the different forms of feedback systems and improvement mechanisms used. Trends include the development towards greater implementation of QIS within health systems, the inclusion of the patient's perspective in performance assessment, and experiments with pay for performance-related measures., Conclusion: On a country level, for health systems striving for newly implementing QIS it is recommended to start where routine data is available, add qualitative methodologies once the QIS is getting more complex, report performance data back to service providers and be patient centred. On the inter-country level exchange of information between agencies commissioned with implementing national QIS is very much needed for., (Crown Copyright © 2016. Published by Elsevier Ireland Ltd. All rights reserved.)

Objectives: Accreditation in France relies on a mandatory 4-year cycle of self-assessment and a peer review of 82 standards, among which 14 focus priority standards (FPS). Hospitals are also required to measure yearly quality indicators (QIs-5 in 2010). On advice given by the accreditation committee of HAS (Haute Autorité en Santé), based on surveyors proposals and relying mostly on compliance to standards, accreditation decisions are taken by the board of HAS. Accreditation is still perceived by hospitals as a burdensome process and a simplification would be welcomed. The hypothesis was that a more limited number of criteria might give sufficient amount of information on hospitals overall quality level, appraised today by accreditation decisions., Design: The accuracy of predictions of accreditation decisions given by a model, Partial Least Square-2 Discriminant Analysis (PLS2-DA), using only the results of FPS and QIs was measured. Accreditation decisions (full accreditation (A), recommendations or reservation (B), remit decision or non-accreditation (C)), results of FPS and QIs were considered qualitative variables. Stability was assessed by leave one out cross validation (LOOCV)., Setting and Participants: All French 489 acute care organisations (ACO) accredited between June 2010 and January 2012 were considered, 304 of them having a rehabilitation care sector (RCS)., Results: Accuracy of prediction of accreditation decisions was good (89% of ACOs and 91% of ACO-RCS well classified). Stability of results appeared satisfactory when using LOOCV (87% of ACOs and 89% of ACO-RCS well classified). Identification of worse hospitals was correct (90% of ACOs and 97% of ACO-RCS predicted C were actually C)., Conclusions: Using PLS2-DA with a limited number of criteria (QIs and FPS) provides an accurate prediction of accreditation decisions, especially for underperforming hospitals. This could support accreditation committees which give advices on accreditation decisions, and allow fast-track handling of 'safe' reports.

Objectives: Because the synthesis of aldosterone is mainly modulated by angiotensin II through type I receptor stimulation and because converting enzyme inhibition (CEI) does not modify aortic extracellular matrix in old normotensive rats, the aim of the present study was to determine whether inhibition of aldosterone formation was able to prevent aortic fibrosis in old Sprague-Dawley normotensive rats., Background: We have previously shown that long-term aldosterone antagonism prevents the age-related increase in aortic collagen accumulation in young spontaneously hypertensive rats, independent of blood pressure changes. In contrast, we reported that the positive effects of CEI in the prevention of aortic collagen accumulation were related to the inhibition of angiotensin II actions on angiotensin II type I receptors., Methods: For this purpose, we studied the histomorphometric and stiffness (echo-tracking technique) changes of an eight-week treatment with the aldosterone antagonist spironolactone by comparison with placebo., Results: At the end of treatment, spironolactone in conscious animals did not change intra-arterial blood pressure, aortic and carotid wall thickness, and cardiac weight. Cardiac collagen density and, to a lesser extent, carotid collagen and elastin densities and contents were significantly decreased in association with an increase of carotid distensibility., Conclusions: These results show that in old normotensive rats, spironolactone can markedly prevent cardiac and, to a lesser extent, arterial fibrosis and improve arterial stiffness, despite a lack of hypotensive effect.

The purpose of the present study was to determine the effects of chronic sinoaortic denervation on the mechanical properties and composition of the abdominal aorta in Wistar rats. We used a high-resolution echotracking system to determine in situ under physiological conditions of blood flow and arterial wall innervation the aortic diameter-, compliance-, and distensibility-pressure curves in 16-week-old anesthetized rats that had been denervated at 10 weeks of age for 6 weeks (n = 8). Compared with sham-operated rats (n = 8) we observed a marked reduction of baroreflex response and increase in overall mean blood pressure variability as measured by standard deviation and spectral analysis in sinoaortic-denervated rats. Mean blood pressure was not affected by sinoaortic denervation in both conscious and anesthetized rats. Sinoaortic denervation significantly shifted the distensibility-pressure curve toward lower levels of distensibility, indicating a decreased aortic distensibility for a given level of arterial pressure. Sinoaortic denervation produced a significant increase of aortic wall cross-sectional area and collagen content, one of the less-distensible components of the arterial wall. These results suggest that intact arterial baroreceptors are necessary for maintaining normal functional and structural properties of large arteries in rats. The reduction in arterial distensibility in chronic sinoaortic-denervated rats may have resulted from different factors, including the initial hypertensive phase, aortic wall hypertrophy, and increase in collagen content. The changes in aortic wall structure and related reduction in aortic distensibility, in addition to other mechanisms, might have been direct consequences of an increased blood pressure variability.

Arteries, when they are subjected in vitro to cyclic loading and unloading, are reported to be stiffer than in static conditions and to be poorly influenced by changes in vasomotor tone. However, such parameters have never been studied in living animals. This study used very high resolution echotracking technics to evaluate pulsatile changes of carotid blood pressure and diameter and the resulting dynamic pressure-cross-sectional (CSA) curve in anesthetized Wistar-Kyoto rats before and following changes of arteriolar vasomotor tone produced by vasoconstrictive [phenylephrine, L-NG nitro-arginine (LNA)] or vasodilating (hydralazine, nitroprusside) agents. Phenylephrine and LNA caused a progressive upward shift of the pressure-CSA curve toward significantly higher values of mean blood pressure and diameter. Since the two vasoconstrictive agents produced exactly the same arterial hemodynamic pattern, their effects may be considered as 'passive', i.e. predominantly due to the mechanical effect of pressure distension. From this observation, a simple model was validated, permitting evaluation in vivo of the passive static properties of the pressure-CSA curve from the relationship between mean arterial diameter and mean arterial pressure at the various steady states produced by the two vasoconstrictive agents. This static relationship had a significantly steeper slope than the corresponding dynamic relationships determined for the same steady-state mean arterial pressures. With hydralazine, a downward shift of the pulsatile pressure-CSA curve was obtained, with exactly the same characteristics as for phenylephrine and LNA, but within lower ranges of blood pressure and with a corresponding decrease in arterial diameter. In contrast, nitroprusside shifted the pulsatile pressure diameter curve toward both lower values of blood pressure and higher values of arterial diameter, thus indicating an active change in arterial tone. At any given value of mean blood pressure and arterial diameter, operational pulsatile compliance was significantly higher with sodium nitroprusside than with hydralazine. This study provides evidence that in living rats (1) the described static carotid pressure-diameter curve has a significantly steeper slope than the corresponding dynamic curve for the same mean arterial pressure, (2) for the same mean arterial pressure and diameter, sodium nitroprusside has a significantly higher dynamic compliance than hydralazine, implicating the role of nonhemodynamic factors in the stiffness of changes, and (3) vasomotor tone influences markedly the dynamic pressure-diameter (or CSA) curve within intermediate and lower blood pressure ranges through active mechanisms involving the GMP cyclic pathway.

Intracerebroventricular (i.c.v.) injection of the 1,4-dihydropyridine (DHP) calcium channel agonist, Bay K8644 (30 micrograms/kg) increased mean blood pressure and the K+-evoked release of [3H]acetylcholine ([3H]ACh) from hippocampal slices in spontaneously hypertensive rats (SHR). The Bay K8644-induced hypertension was inhibited by a pretreatment with methylatropine (80 micrograms/kg i.c.v.). In SHR, nicardipine, a DHP calcium channel antagonist, reduced mean blood pressure when i.c.v. injected (10 micrograms/kg). The nicardipine-induced hypotension was reduced by a pretreatment with hemicholinium-3 (20 micrograms, i.c.v.). Nicardipine (1 microM) did not modify, in SHR, the K+-evoked release of [3H]ACh, but inhibited the Bay K8644-induced increase in the ACh release. In normotensive rats, neither Bay K8644 nor nicardipine modify blood pressure, when centrally injected, or the stimulated release of [3H]ACh from hippocampal slices. The participation of central DHP sites in the cholinergic transmission in genetic hypertension is discussed.

Central and peripheral hypotensive effects of (+)- and (-)-nicardipine (1-10 micrograms/kg i.v. or i.c.v.) were investigated in normotensive and SH rats. The results suggest that a stereoselectivity exists for the peripheral and central hypotensive effects of the nicardipine isomers. (+)-Nicardipine was shown to be 3-8 times as potent as the (-) isomer in reducing blood pressure in all the experiments.

In dogs anaesthetized with pentobarbital (30 mg. kg -1 i.v.), clonidine (0,01 mg.kg-1 i.v.) reduced the tachycardia induced at low frequencies by stimulation of the cardiac nerve. The effects of some alpha-adrenoceptor blocking agents on this effect have been studied. Small doses of yohimbine (0.3 mg. kg-1 i.v.) or piperoxan (0.3 mg. kg-1 i.v.) increased the effects of the stimulation and in addition antagonized the inhibitory effects of clonidine and reversed the pressor response to adrenaline. Thymoxamine (1 mg.kg-1 i.v.) and prazosin (1 mg.kg-1 i.v.) did not increase the effect of the stimulation of the cardiac nerve, but reduced the effect of clonidine. ARC239 (0.05 mg.kg-1) reversed the pressor response to adrenaline but even at high doses did not increase the effects of the stimulation of the cardiac nerve or the effects of clonidine. These observations afford further evidence for a dissimilarity between pre and post-synaptic alpha-adrenoceptors.

In pentobarbitalized closed-chest dogs, nicergoline (10--100 microgram/kg, i.v.) reduced blood pressure, heart rate, and splanchnic nerve activity. Intracisternal administration of nicergoline (3 microgram/kg) only reduced splanchnic nerve activity. In open-chest dogs, nicergoline reduced blood pressure, cardiac output, and total peripheral resistance but did not change heart rate. In pithed rats treated with a beta-adrenoceptor-blocking agent, nicergoline reduced the pressor responses to noradrenaline and adrenaline. Nicergoline slightly attenuated the pressor responses of dogs to noradrenaline and tyramine and, in addition, reversed the hypertension induced by adrenaline and dimethylphenylpiperazinium. Nicergoline (100 microgram/kg) increased the tachycardia induced in dogs by stimulation of the right cardiovascular nerve and prevented the inhibitory effect of clonidine on this response. However, nicergoline only partially antagonized the effect of clonidine once it was fully established. Nicergoline did not antagonize the hypotensive and bradycardic effects of clonidine when they were established. Nicergoline did not affect the vagally mediated bradycardia evoked by carotid nerve stimulation in beta-adrenoceptor-blocked dogs. The compound did not change blood pressure in Cl spinal cord transected dogs. In conclusion, nicergoline appears to decrease blood pressure by blocking alpha-adrenoceptors and, at least at some doses, by a central inhibition of the sympathetic tone. Nicergoline appears to be a preferential alpha 1-adrenoceptor-blocking agent.

In pentobarbital-treated dogs clonidine (10 micrograms/kg) reduced the increase in heart rate caused by electrical stimulation of the cardiac nerve (1-10 Hz). We studied the actions of six alpha-adrenoceptor blocking drugs. Yohimbine (0.3 mg/kg) and phentolamine (1 mg/kg) potentiated the effects of nerve stimulation and antagonized the inhibitory effects of clonidine. Piperoxan (1 mg/kg) increased the response to nerve stimulation but antagonized the effects of clonidine only at the lowest frequency of stimulation. Thymoxamine (1 mg/kg) and prazosin at high doses (1 mg/kg) also antagonized the effects of clonidine but failed to increase the positive chronotropic response to stimulation of the cardiac nerve. AR-C239, a new and potent alpha-adrenoceptor blocking agent, changed neither the response to nerve stimulation nor the inhibitory effect of clonidine. The effects of all these drugs were observed at doses which reduced or reversed the pressor response to adrenaline. Therefore, our results afford further evidence for a dissimilarity between postsynaptic and presynaptic alpha-adrenoceptors in the dog. In addition, they show that the failure of an alpha-adrenoceptor blocking compound to increase the response to nerve stimulation does not necessarily indicate a lack of presynaptic alpha-adrenoceptor blockade.

In the present investigation, the alpha-adrenoceptor blocking effect of (imidazolinyl-2)-2-dihydro 2,3 benzofurane or S 9871 and its stereoisomers was studied. In the pithed rat (+/-) and (+) S 9871 competitively antagonized the pressor effects of azepexole and clonidine more effectively than those of cirazoline and phenylephrine. (-) S 9871 only blocked the pressor response of the alpha 1-agonists used: phenylephrine and cirazoline. (+/-) and (+) S 9871 antagonized the inhibitory effects of clonidine on the increase in heart rate produced by stimulation of the sympathetic efferent fibres of the thoracic spinal cord. (-) S 9871 was twenty times less potent on the decrease in heart rate induced by clonidine. On the vas deferens of the rat, (+/-) and (+) S 9871 appeared to be more potent than (-) S 9871 in antagonizing the inhibitory effects of clonidine on the twitch response produced by electrical stimulation. Therefore, (+/-) and (+) S 9871 appear to be more preferential for alpha 2-adrenoceptors than for alpha 1-adrenoceptors; in contrast (-) S 9871 appears to be selective for alpha 1-adrenoceptors. (+/-) and (+) S 9871 appears to be one of the most selective agents for blocking alpha 2-adrenoceptors.

An overall study of the in vitro plasma coagulation system in the crab Liocarcinus puber has been carried out using various analytical methods, namely thromboelastography, spectrophotometrical examination, and a new one based on changes of the mechanical impedance of the developing clot. From the results reported here the clotting pattern in this species appears surprisingly complex for an invertebrate and unexpectedly closer to that of the vertebrates. Indirect evidences suggest that the fibrinogen polypeptide chains in this species and very likely in the other crustacean, are very different from those of the vertebrates. This would imply that crustacean and vertebrate fibrinogen would have diverged from one another in a far remote past, far beyond the individualization of the vertebrate alpha chain, that is, over 1.5 million years ago.

Intracerebroventricular (i.c.v.) injections of dihydropyridine derivatives calcium channel agonist (BAY K8644) and antagonist (nifedipine, nicardipine, PN 200-110) induced opposite long-lasting changes in blood pressure (BP) in pentobarbital anesthetized spontaneously hypertensive rats (SMR). I.c.v. nifedipine (NIF), nicardipine (NIC), and PN 200-110 decreased mean blood pressure dose-dependently and stereoselectively, (+) NIC and (+) PN being 8 and 3 times more potent than their (-) isomers, respectively. The decrease in BP was due to a withdrawal of the sympathetic tone, since NIF- and NIC-induced falls in BP were suppressed after either hexamethonium (HXM), 6 OHDA or bilateral adrenalectomy. I.c.v. BAY K8644 increased BP dose-dependently. The i.c.v. BAY K8644-induced hypertensive effect was inhibited: a), by NIF and (+) PN but not by (-) PN, therefore probably occurring at central DHP sites; b), by HXM and reserpine, thus probably mediated by an increase in sympathetic tone; c) by i.c.v. methylatropine (MA) while i.v. MA and i.c.v. HXM had no inhibitory effect, thus probably involving central muscarinic sites. In SHR, NIC did not after the K(+)-evoked ACh release but suppressed the BAY K8644-induced increase in ACh release. In anesthetized normotensive control rats (WKY), neither i.c.v. NIF, NIC or BAY increased BP and HR while, in conscious SHR it decreased BP without any change in HR. These data increased BP and HR while, in conscious SHR it decreased BP without any change in HR. These data suggest that central DHP sites may be involved in the cholinergic transmission and may participate in genetic hypertension via sympathetic tone.

In pentobarbital-treated dogs and rats, AR-C239, a new and potent alpha-adrenoceptor blocking drug, competitively antagonized pressor responses to adrenaline and inhibited pressor responses to noradrenaline, phenylephrine, tyramine, and dimethylphenylpiperazinium. Injected intravenously into closed-chest dogs, AR-C239 (3-50 micrograms/kg) induced a progressive fall in blood pressure, heart rate, and sympathetic nerve activity. The drug appears to be devoid of direct vasodilator action, and the fall in blood pressure results from the peripheral alpha-blockade. AR-C239 did not change the tachycardia induced by stimulation of the cardiac nerve in dogs and, at least in this preparation, seems to be a specific alpha 1-adrenoceptor blocking drug. When administered into the cisterna magna of dogs, AR-C239 did not have any centrally mediated cardiovascular actions and heart rate. AR-C239 did not modify the functioning of the baroreflex arc. Due to its specificity for alpha 1-Adrenoceptors, AR-C239 may be useful for characterizing alpha-adrenoceptors.

AR-C 239, a new alpha-adrenoceptor blocking drug, appears to act selectively on alpha 1 sites in rats. At peripheral sites, this drug did not change the tachycardia induced by spinal sympathetic outflow stimulation in pithed rats, and did not antagonize the inhibitory effects of clonidine on this preparation. In addition, AR-C 239 showed predominant alpha 1-adrenoceptor blocking properties in the bisected rat vas deferens preparation. AR-C 239 did not prevent or reverse the centrally mediated hypotensive and bradycardic actions induced by clonidine, in intact animals. In conclusion, AR-C 239 seems to be a very useful tool for the characterization of peripheral and central alpha 1-adrenoceptors, in this animal species.

The purpose of the present study was to characterize the effects of mianserin at alpha 2-adrenoceptors. Firstly, the action of mianserin on postganglionic sympathetic fibres has been studied using the tachycardia induced by stimulation of the cardiac nerve in dogs. Mianserin increased this tachycardia, but could not prevent the inhibitory effect of clonidine in this model. However, an antagonistic effect of mianserin against clonidine was observed when animals were pretreated with desipramine. Secondly, mianserin antagonized the inhibitory effect of clonidine on the electrically stimulated guinea-pig ileum. In high concentrations, mianserin reduced both electrically and acetylcholine induced contractions. Thirdly, mianserin antagonised the sleep induced by clonidine in chickens. These results are consistent with alpha 2-adrenoceptor blocking properties of mianserin in peripheral noradrenergic fibres in dogs, in cholinergic fibres in guinea-pig ileum and in the central nervous system in chickens.