Study of factors which modify the development of norepinephrine-induced acute renal failure in the dog

Study of factors which modify the development of norepinephrine-induced acute renal failure in the dog. Previous studies have demonstrated that the fall in inulin clearance which occurs 3 hours after the intrarenal administration of norepinephrine can be markedly attenuated by the prior administration of intrarenal prostaglandin E2 (PGE). Since in the previous studies PGE led to a marked increase in both renal blood flow and solute excretion, we designed the present series of experiments to investigate whether an increase in renal blood flow, solute excretion, or other factors were responsible for the protective effect in the norepinephrine model. Two renal vasodilators, bradykinin and secretin, were evaluated initially. Bradykinin administration prior to norepinephrine administration had a protective effect similar to that previously found with PGE, whereas secretin did not. Both of these vasodilators increased renal blood flow to the same degree, but only bradykinin increased urine flow and solute excretion. The fall in inulin clearance 3 hours after the administration of norepinephrine was also attenuated by two diuretics (mannitol and furosemide) which tended to increase renal blood flow. In contrast, two natriuretic agents, which are also renal vasoconstrictors (chlorothiazide and benzolamide), had no protective effect. Further, chlorothiazide and benzolamide obvicited the protective effect of bradykinin. These studies demonstrate that there are several types of pharmacologic agents which can modify the magnitude of renal functional impairment resulting from extreme renal ischemia. Although the mechanism of the protective effects remain unclear, the findings are compatible with the view that the protective effect noted with PGE, bradykinin, mannitol, and furosemide may be related to an increase in osmolar excretion which occurred with administration of each of these agents. This potentially salutory effect (increased osmolar excretion), however, could be overcome by an agent (e.g., chlorothictzide or benzolamide) which also increased renal resistance prior to the administration of norepinephrine.Etude des facteurs qui modifient l'évolution de l'insuffisance rénale aiguë par la norépinéphrine chez le chien. Des travaux antérieurs ont démontré que la chute de la clearance de l'inuline qui survient 3 heures après l'administration intra-rénale de norépinéphrine peut être atténuée de façon importante par l'injection intrarénale préalable de prostaglandine E2 (PGE). Puisque dans les travaux antérieurs, la PGE a déterminé une augmentation importante à la fois du débit sanguin rénal et de l'excrétion de substances dissoutes, cette série d'expériences a pour but de savoir si une augmentation du débit sanguin rénal ou de l'excrétion de substances dissoutes ou bien d'autres facteurs sont responsables de l'effet protecteur dans le modèle de la norépinéphrine. Deux vasodilatateurs rénaux, la bradykinine et la secrétine ont été initialement étudiés. L'administration de bradykinine préalable à celle de norépinéphrine a un effet protecteur semblable à celui antérieurement observé avec la PGE alors que la secrétine n'a pas cet effet. Ces deux vasodilatateurs augmentent le débit sanguin rénal de la même façon, mais seule la bradykinine augmente le débit urinaire et l'excrétion de substances dissoutes. La chute de la clearance de l'inuline 3 heures après la norépinéphrine est aussi atténuée par deux diurétiques qui tendent à augmenter le débit sanguin rénal (mannitol et furosémide). Au contraire, deux agents natriurétiques qui sont aussi des vasoconstricteurs rénaux (chlorothiazide et benzolamide) n'ont pas d'effet protecteur. De plus, ces deux corps empêchent l'effet protecteur de la bradykinine. Ces études démontrent qu'il y a plusieurs catégories d'agents pharmacologiques qui peuvent modifier l'importance de l'altération fonctionnelle qui résulte d'une ischémie rénale extrême. Quoique le mécanisme de l'effet protecteur reste obscur, ces constatations sont compatibles avec l'idée que l'effet observé avec la PGE, la bradykinine, le mannitol et le furosémide puisse être lié à une augmentation de l'excrétion osmolaire qui est observée au cours de l'administration de chacun de ces corps. Cet effet bénéfique potentiel (l'augmentation de l'excrétion osmolaire) peut, cependant, être annulé par un agent (comme le chlorothiazide ou la benzolamide) qui augmente aussi la résistance rénale préalablement à l'administration de norépinéphrine

Redundancy in Logic I: CNF Propositional Formulae

A knowledge base is redundant if it contains parts that can be inferred from the rest of it. We study the problem of checking whether a CNF formula (a set of clauses) is redundant, that is, it contains clauses that can be derived from the other ones. Any CNF formula can be made irredundant by deleting some of its clauses: what results is an irredundant equivalent subset (I.E.S.) We study the complexity of some related problems: verification, checking existence of a I.E.S. with a given size, checking necessary and possible presence of clauses in I.E.S.'s, and uniqueness. We also consider the problem of redundancy with different definitions of equivalence.Comment: Extended and revised version of a paper that has been presented at ECAI 200

Organic conductors in high magnetic fields: model systems for quantum oscillations physics

Even though organic conductors have complicated crystalline structure with low symmetry and large unit cell, band structure calculations predict multiband quasi-two dimensional electronic structure yielding very simple Fermi surface in most cases. Although few puzzling experimental results are observed, data of numerous compounds are in agreement with calculations which make them suitable systems for studying magnetic quantum oscillations in networks of orbits connected by magnetic breakdown. The state of the art of this problematics is reviewed.Comment: Comptes-Rendus Physique, in pres

Real-time Relaxation and Kinetics in Hot Scalar QED: Landau Damping

The real time evolution of field condensates with soft length scales k^{-1}>(eT)^{-1} is solved in hot scalar electrodynamics, with a view towards understanding relaxational phenomena in the QGP and the electroweak plasma. We find that transverse gauge invariant non-equilibrium expectation values of fields relax via {\em power laws} to asymptotic amplitudes that are determined by the quasiparticle poles. The long time relaxational dynamics and relevant time scales are determined by the behaviour of the retarded self-energy not at the small frequencies, but at the Landau damping thresholds. This explains the presence of power laws and not of exponential decay. Furthermore, we derive the influence functional, the Langevin equation and the fluctuation-dissipation theorem for the soft modes, identifying the correlation functions that emerge in the classical limit. We show that a Markovian approximation fails to describe the dynamics {\em both} at short and long times. We also introduce a novel kinetic approach that goes beyond the standard Boltzmann equation and incorporates off-shell processes and find that the distribution function for soft quasiparticles relaxes with a power law through Landau damping. We also find an unusual dressing dynamics of bare particles and anomalous (logarithmic) relaxation of hard quasiparticles.Comment: 41 pages, 5 figures, uses revtex, replaced with version to appear in Phys. Rev.

The Unappreciated Role of Extrarenal and Gut Sensors in Modulating Renal Potassium Handling: Implications for Diagnosis of Dyskalemias and Interpreting Clinical Trials

In addition to the classic and well-established “feedback control” of potassium balance, increasing investigative attention has focused on a novel and not widely recognized complementary regulatory paradigm for maintaining potassium homeostasis—the “feed-forward control” of potassium balance. This regulatory mechanism, initially defined in rumen, has recently been validated in normal human subjects. Studies are being conducted to determine the location for this putative potassium sensor and to evaluate potential signals, which might increase renal potassium excretion. Awareness of this more updated integrative control mechanism for potassium homeostasis is ever more relevant today, when the medical community is increasingly focused on the challenges of managing the hyperkalemia provoked by renin–angiotensin–aldosterone system inhibitors (RAASis). Recent studies have demonstrated a wide gap between RAASi prescribing guidelines and real-world experience and have highlighted that this gap is thought to be attributable in great part to hyperkalemia. Consequently we require a greater knowledge of the complexities of the regulatory mechanisms subserving potassium homeostasis. Sodium polystyrene sulfonate has long been the mainstay for treating hyperkalemia, but its administration is fraught with challenges related to patient discomfort and colonic necrosis. The current and imminent availability of newer potassium binders with better tolerability and more predictive dose–response potassium removal should enhance the management of hyperkalemia. Consequently it is essential to better understand the intricacies of mammalian colonic K+ handling. We discuss colonic transport of K+ and review evidence for potassium (BK) channels being responsible for increased stool K+ in patients with diseases such as ulcerative colitis