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PubMed2005

[Pathophysiology of radicular pain].

Pathophysiological mechanisms of low back pain and radicular pain produced by lumbar disorders are still controversial. We have made experimental animal models and have elucidated the mechanisms of hyperalgesia, which is a pain related behavior, in these animals. We have not demonstrated that only mechanical compression of the nerve roots in the lumbar spine results in hyperalgesia in rat. We found that application of the nucleus pulposus to the nerve roots produces time-dependent reversible hyperalgesia in the affected hindpaw of the rat, and that the hyperalgesia is related to bioactive substances in the arachidonic acid cascade. We have also reported that inflammatory granulation tissue around the nerve root is related to hyperalgesia rather than the nucleus pulposus itself, and that mechanical compression to the nerve root after application of the nucleus pulposus produces different type of hyperalgesia. Collectively, not only mechanical compression of the cauda equina and nerve root but also various inflammatory substances are related to pathophysiological mechanisms of radicular pain in patients with lumbar disorders such as disc herniation. Elucidating pathophysiological mechanisms of pain-related behaviors such as hyperalgesia is important to establish a new strategy for the treatment of lumbar painful radiculopathy.

Animals↗
PubMed2005

[The role of metalloproteinases in kidney pathophysiology].

Disturbances in extracellular matrix changes underlie many diseases. Metalloproteinases (MMP) are thought to play a very important role in the maintenance of proper balance between degradation and regeneration of tissue basic substance. MMP is a group of enzymes capable of digesting almost all extracellular matrix (ECM) components. Extracellular matrix of the tissues not only constitutes the support for its cells but also participates in cell metabolism regulation. Any disturbance in the balance between matrix degradation and regeneration is the clue to pathophysiology of many diseases. Metalloproteinases of ECM are a big family of zinc-dependent enzymes that include, among others, interstitial collagenases, matrix lysines, gelatinases, elastases and membrane-type matrix metalloproteinases (MT-MMP). Studies performed in animal models with MMP deficiency that have been carried out in the last few years have supplied a unique tool for the analysis of the role of gelatinase in physiological and pathophysiological development processes. However, the studies have proved complexity of the problem revealing not only protective but also destructive role of MMP depending on the experimental animal model which leaves a wide area for further investigations not only in animals but also patients with chronic kidney diseases. In the later part of our study we would like to focus on previous results of studies and views on the influence of MMP on kidney pathophysiology on the basis of available literature.

Extracellular Matrix↗
PubMed2000

Shock: a review of pathophysiology and management. Part II.

OBJECTIVE: To review pathophysiology and management of hypovolaemic, cardiogenic and septic shock in a two part presentation. DATA SOURCES: Articles and published peer-review abstracts and a review of studies reported from 1994 to 1998 and identified through a MEDLINE search of the English language literature on septic shock, cardiogenic shock and hypovolaemic shock. SUMMARY OF REVIEW: The pathophysiological effects of cardiogenic and hypovolaemic shock are related predominantly to a reduction in preload and myocardial contractility, respectively, whereas the pathophysiological effects of septic shock result largely from the overwhelming production of inflammatory mediators. The excessive inflammatory response results in haemodynamic compromise and widespread tissue injury. While the understanding of the acute inflammatory reaction has improved, therapies to modulate the chemical mediators responsible for the organ dysfunction associated with this reaction have not altered mortality, and in some instances may have increased it. Treatment of septic shock is still largely supportive, using intravenous fluids and inotropic agents to provide adequate tissue perfusion while the infective lesion is managed with antibiotic therapy and surgical drainage of septic focus. CONCLUSIONS: Septic shock is provoked by an excessive acute inflammatory response to an infection. Management of the shock is supportive using fluids and inotropic agents, while antibiotic therapy and surgical drainage of the septic focus take effect. Immunomodulation of the acute inflammatory response causing septic shock has not improved mortality.

Journal Article↗
PubMedDate not supplied

Signals through CD40 play a critical role in the pathophysiology of Schistosoma mansoni egg antigen--induced allergic rhinitis in mice.

BACKGROUND: Interaction between CD40 and CD40L is thought to regulate immune responses in several allergic diseases. However, little is known about its in vivo role in the pathophysiology of allergic rhinitis. We sought to determine whether the lack of signals through CD40 affects the pathophysiology of allergic rhinitis using a murine model. METHODS: Wild type (WT) and CD40-deficient BALB/c (CD40-/-) mice were sensitized intranasally to Schistosoma mansoni egg antigen (SEA). After repeated sensitization, histamine responsiveness, serum antibody titer including immunoglobulin E (IgE), nasal eosinophilia, and cytokine production by nasal mononuclear cells were determined in each group. RESULTS: Intranasal sensitization with SEA in WT mice elicited a strong Th2 response including SEA-specific IgE production, nasal eosinophilia, and interleukin (IL)-4, and IL-5 production by nasal mononuclear cells after antigen challenge. Production of SEA-specific IgE and IgG1 was abolished in SEA-sensitized CD40-/- mice. These mice showed impaired nasal eosinophilia and displayed markedly reduced histamine-induced nasal hyperresponsiveness as compared with WT mice. Furthermore, reduced production of IL-4 and IL-5 by nasal mononuclear cells was seen in CD40-/- mice. CONCLUSION: These results show that signals through CD40 play a critical role in not only IgE production but also pathophysiology of allergic rhinitis such as nasal hyperresponsiveness and nasal eosinophilia.

Animals↗
PubMed1991

[The importance of sports for the prevention of coronary heart disease--physiological and pathophysiological aspects].

For the application of physical conditioning in the prevention of coronary heart disease to be meaningful, account must be taken of physiological and pathophysiological baselines. Physical activity is associated with an increase in metabolic rate, and the prophylactic effect of exercise is due mainly to metabolic effects and not, as commonly thought, to hemodynamic factors. Raising the metabolic rate has a positive effect on risk factors which--with the exception of smoking--are largely metabolic. For this reason, the physiological aspects of the release of energy and its increase under physical exercise are described. Of decisive importance for prophylaxis is not so much the nature of the exercise--for example endurance training in particular--as the overall extent of physical exercise, and the resulting energy consumption. The hemodynamic effect of physical activity, in particular the optimization of cardiovascular function, is of importance not so much for primary preventive reasons as for reducing the oxygen requirement of the myocardium--a secondary preventive measure. For producing a cardiovascular training effect, forms of exercise performed close to the aerobic-anaerobic threshold (AAT) are optimal. A common mistake is to assume that the training effect achieved under physiological conditions can simply be extrapolated to the pathophysiological situation. Exercise workloads that are below the aerobic-anaerobic threshold fail to produce a training effect. Here, the major aim must be to achieve metabolic, coordinative and motivational effects. If the physiological responses to exercise, in particular heart rate, are modified by pathophysiological or pharmacological mechanisms, other, in particular respiratory and metabolic parameters should be used as regulators of training. Such parameters are considered in detail.

Adrenergic beta-Antagonists↗
PubMed1991

The pathophysiological basis of arrhythmogenesis in myocardial ischemia and reperfusion: possible target for intervention.

Regional ischemia and reperfusion alter the homeostasis of many substances in the myocardium. Which, if any play a role as pathophysiological progenitors of the associated arrhythmias? The key questions which must be answered in relation to each are: (i) is the presence of the substance sufficient to account for arrhythmogenesis and (ii) is the presence of the substance necessary for arrhythmogenesis to occur? Although there are many candidates for the role of pathophysiological progenitor, and although there is much evidence in support of a role for various of these, the evidence is largely circumstantial. Some of this evidence is reviewed here. I am of the view that new models must be developed if unequivocal data are to be derived. An example which may be of value in this regard is the newly developed rabbit dual perfusion model. The technical aspects of this model are described herein. Using this model I have examined the role of one prospective pathophysiological progenitor of arrhythmogenesis, K+, the intra-extracellular homeostasis of which is disturbed by ischemia and reperfusion in a manner related on a temporal basis with development of susceptibility to arrhythmogenesis. The article concludes with some speculation on possible future research directions.

Angiotensin II↗
PubMed1990

Pathogenesis and pathophysiology of meningitis.

Advances in the understanding of the pathogenesis and pathophysiology of meningitis have occurred primarily through the use of experimental animal models. These models have proven to be particularly valuable in experimental bacterial meningitis, focusing on the bacterial virulence factors responsible for the initiation of infections, CNS invasion, and induction of SAS inflammation. Recent studies have examined the formation of host inflammatory cytokines in response to these virulence factors. These cytokines may be responsible for many of the pathophysiologic consequences of bacterial meningitis (eg. increased BBB permeability, cerebral edema, and increased intracranial pressure). Meningitis due to C. neoformans occurs most commonly in patients with defects in cell-mediated immunity (eg, AIDS), and the depletion of T helper cells in AIDS patients may allow unrestricted cryptococcal growth. Viral meningitis is an illness of low prevalence when compared with the overall occurrence of viral infections at other sites. CNS infection usually occurs by means of traversal across barriers that normally exclude viral invasion of the CNS, primarily through hematogenous dissemination from initial sites of infection. These advances in the pathogenesis and pathophysiology of bacterial, fungal, and viral meningitis may lead to the development of innovative treatment strategies for these disorders.

Animals↗
PubMedDate not supplied

Pathophysiology and pathogenesis of generalized peritonitis.

Peritonitis is a complex disease state that results in many pathophysiologic alterations that affect multiple organs. The clinician must possess a thorough understanding of the pathophysiology and pathogenesis of the disease so that effective treatment can be instituted. Treatment should be directed at eliminating the cause of peritonitis and preventing or reversing the resulting pathophysiologic alterations.

Animals↗
PubMedDate not supplied

Neuroanatomic and pathophysiologic aspects of intervertebral disc disease in the dog.

A sound understanding of anatomy and the pathophysiology of disease is important in all branches of medicine, but nowhere is it more critical to success than in the medical and surgical management of intervertebral disc disease. Due to the remote location and unforgiving nature of the spinal cord, the veterinary surgeon must possess an intimate working knowledge of the surgical anatomy of the vertebrae, ligaments and joints of the spine, intervertebral discs, spinal cord, and spinal nerves. In addition, proper localization of spinal cord lesions during the neurological evaluation requires awareness of the functional neuroanatomy of the upper and lower motor motor neurons, the sensory systems and tracts, and the reflex arcs. Knowledge of the pathophysiology the intervertebral disc degeneration and the response of the spinal cord to disc extrusions are also important in the overall understanding of the disease and enhances proper decision making for its management. This chapter reviews the portions of the gross and functional neuroanatomy and the pathophysiology of the intervertebral disc and the spinal cord that are pertinent to the dog with intervertebral disc disease. Emphasis is placed on concepts that are critical for the veterinary surgeon who is involved in the surgical management of the disc patient.

Animals↗
PubMed1989

Interpretation of pathophysiology by laboratory data (2). Graphic display of data, dynamic pattern.

In order to display the pathophysiology of a patient more efficiently and adequately than in the static radar chart presented in the first report, a dynamic radar chart and serial line graphs using colored lines were presented. A dynamic radar chart prepared as described particularly in this report, shows the whole data of a patient along with the time course of illness by the space-saving "overlapped-drawing". Moreover serial line graphs are employed for items important for the understanding of a patient's pathophysiology or for items which show obscure change due to overlapping in the dynamic radar chart. Although this line graph is space-occupying it reveals more clearly the changes of data throughout the entire course of a patient's disease. In this second report the dynamic presentation of data and its interpretation, were presented for nine cases. This was done more efficiently and adequately than in the cases described in the first report where the display and interpretation of pathophysiology of a patient was made using merely the data of a single point.

Biometry↗
PubMed1989

Proposed role for leukotrienes in the pathophysiology of multiple systems organ failure.

The leukotrienes are a group of biologically active products of arachidonic acid metabolism that have been demonstrated to possess the capability to alter vascular reactivity as well as vascular permeability when applied topically to tissues or infused into the vascular bed of various organs. These biologic effects of the exogenous leukotrienes have led to the speculation that these arachidonic acid metabolites could be important mediators in the pathophysiologic events that culminate in the development of acute lung injury and MSOF. Increased production of inflammatory mediators is undoubtedly a contributing factor to the pathophysiologic events that culminate in MSOF. LTB4 has been shown to be a potent stimulator of neutrophil chemotaxis and adhesion. It is possible that LTB4 may be responsible for initiation or amplification of the inflammatory response in this syndrome. The sulfidopeptide leukotrienes have profound effects on cardiac function, which may be mediated through effects on both coronary blood flow and cardiac contractility. These arachidonic acid metabolites are also capable of altering blood flow to several vascular beds and, when synthesized endogenously and released, may be important in the regulation of the peripheral circulation. Endogenous leukotrienes may have physiologic or pathophysiologic effects on cardiac output and its distribution to peripheral vascular beds or on systemic blood pressure. In view of the observations that alterations in cardiac output, blood pressure, and individual organ blood flow have been demonstrated in the clinical setting of ARDs and MSOF, it is attractive to suggest that the leukotrienes may contribute to the hemodynamic alterations observed in these clinical conditions. In addition to their effects on vascular smooth muscle and the myocardium, the leukotrienes have been shown to increase the permeability of blood vessels. In the case of the sulfidopeptide leukotrienes, the enhanced vascular permeability appears to be a direct effect of these lipoxygenase metabolites. Although LTB4 may directly increase vascular permeability, several lines of evidence suggest that the recruitment and activity of neutrophils is required for edema formation to develop following application of this leukotriene. Enhanced capillary permeability, at least in the pulmonary circulation, is a hallmark of ARDS and is also frequently present in MSOF. The leukotrienes, either through direct effects on vessels or through recruitment of inflammatory cells, are likely contributors to the nonhydrostatic edema associated with these syndromes.

Animals↗
PubMed1984

The pathophysiology of movement disorders.

This review concentrated on the more recent findings of investigations into the functional anatomy and pathophysiology of movement disorders. Attempts were made to provide explanations for rigidity, bradykinesia, and tremor. What little is known of the pathophysiology of chorea, tics, and dystonia is discussed. Greater information is available to allow pathophysiologic classification of different types of myoclonus.

Chorea↗
PubMed1983

Variation in the pathophysiology of involutional entropion and its treatment.

It is essential to understand the anatomy in detail, the normal physiology and pathophysiology of the lower eyelid to properly correct an involution entropion surgically. The fact that 50% of involutional entropion causes show an actual defect (dehiscence or complete detachment) of the retractor aponeurosis of the lower eyelid is important. The surgeon must be cognizant of the high rate of occurrence of these defects and look for them during the surgical repair. The direct external approach of the imbrication procedure makes it easy to identify these aponeurotic retractor defects. The pathophysiologic changes can vary with each case and are as follows involutional changes (attenuation, dehiscence, detachment) taking place in the lower lid retractors; atony of the lateral and medial canthal tendons may be present and must be recognized; enophthalmus of the aging is present; the septal oribicularis loses it firm attachment to the orbital septum. It is paramount that the pathophysiologic changes present in each case be recognized and surgically corrected to prevent recurrences.

Entropion↗
PubMed1995

Pathophysiology of status epilepticus.

The cellular and molecular pathophysiology of status epilepticus (SE) provides a conceptual framework for understanding clinical scenarios and prospectively designing logical therapies. SE is a dynamic process that evolves over time in a predictable manner with an established sequence of EEG, motor, physiologic, and cellular changes. Neuronal injury and death are the result of processes intrinsic to the brain, mediated by a complex neurotoxic cascade consisting of multiple serial and parallel processes. The risk of cell injury depends also on the overall pathophysiologic profile, including the presence of alterations resulting from SE and occurring independent of SE. On neurophysiologic grounds, we divide SE into "spike-wave" and "nonspike-wave" forms. Spike-wave "absence" status epilepticus carries a low risk of epileptic brain damage, and therapy should be adjusted accordingly. All nonspike-wave SE has a theoretical basis for epileptic brain damage, but the actual risk is variable. There is a significant known risk of cell injury during generalized convulsive SE, a variety of nonspike-wave SE, so aggressive treatment is warranted to prevent sequelae. There is also a theoretical basis for epileptic brain damage in nonspike-wave nonconvulsive SE, but prospective studies are needed to determine which of these patients warrant aggressive therapy. Based on pathophysiologic principles, future treatment of nonspike-wave SE may use a combination of anti-ictal agents, including gamma-aminobutyric acid agonists and N-methyl-D-aspartate antagonists, as well as various neuroprotectants.

Animals↗
PubMed1995

Muscle atonia is triggered by cholinergic stimulation of the basal forebrain: implication for the pathophysiology of canine narcolepsy.

Narcolepsy is a sleep disorder characterized by excessive daytime sleepiness and rapid eye movement (REM) sleep-related symptoms, such as cataplexy. The exact pathophysiology underlying the disease is unknown but may involve central cholinergic systems. It is known that the brainstem cholinergic system is activated during REM sleep. Furthermore, REM sleep and REM sleep atonia similar to cataplexy can be triggered in normal and narcoleptic dogs by stimulating cholinergic receptors within the pontine brainstem. The pontine cholinergic system is, therefore, likely to play a role in triggering cataplexy and other REM-related abnormalities seen in narcolepsy. The other cholinergic system that could be involved in the pathophysiology of narcolepsy is located in the basal forebrain (BF). This system sends projections to the entire cerebral cortex. Since acetylcholine release in the cortex is increased both during REM and wake, the basocortical cholinergic system is believed to be involved in cortical desynchrony. In the current study, we analyzed the effect of cholinergic compounds injected into the forebrain structures of narcoleptic and control dogs. We found that carbachol (a cholinergic agonist) injected into the BF triggers cataplexy in narcoleptic dogs while it increases wakefulness in control dogs. Much higher doses of carbachol bilaterally injected in the BF were, however, shown to trigger muscle atonia even in control dogs. These results suggest that a cholinoceptive site in the BF is critically implicated in triggering muscle atonia and cataplexy. Together with similar results previously obtained in the pontine brainstem, it appears that a widespread hypersensitivity to cholinergic stimulation may be central to the pathophysiology of canine narcolepsy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Pathophysiologic sequelae of intracranial disease.

A variety of intracranial diseases affect dogs and cats. Clinical signs often result not only from mechanical destruction of normal brain but also from associated pathophysiologic alterations induced secondary to the primary disease process. Effective management of intracranial disease requires recognition and treatment of the primary as well as of many of these secondary pathophysiologic sequelae. This article discusses the evolution, ramifications, diagnosis, and treatment of these pathophysiologic sequelae.

Animals↗
PubMed1997

Distribution and pathophysiologic role of molybdenum-containing enzymes.

The importance of molybdenum-containing enzymes in the pathophysiology of a number of clinical disorders necessitates a comprehensive understanding of their histological localization and expression. The objectives of this review are to cover such enzymes so far reported and their enzyme- and immunohistochemical localization in various tissues and species, and to discuss their possible pathophysiological effects. The molybdenum cofactor is essential for the activity of the three molybdenum-containing enzymes, sulfite oxidase, xanthine oxidase and aldehyde oxidase. Sulfite oxidase serves as the terminal enzyme in the pathway of the oxidative degradation of sulfur amino acids, and is also involved in preventing the toxic effects of sulfur dioxide. Biochemical study has revealed a high activity of sulfite oxidase mainly in the liver, heart and kidney with lesser activity observed in other tissues. Subcellular observations have shown that this enzyme is present in the mitochondrial intermembraneous spaces. Xanthine oxidase is the final enzyme in the conversion of hypoxanthine to xanthine, and subsequently, to uric acid. Unlike sulfite and aldehyde oxidases, xanthine oxidase can be converted to xanthine dehydrogenase, and vice versa. Xanthine oxidase has been widely investigated for its role in post-ischemic reperfusion tissue injury. Enzyme- and immunohistochemical studies of its localization in various animal species and tissues have shown its ubiquitous distribution in the liver, small and large intestine, lung and kidney, and other tissues. Aldehyde oxidase shares a similar substrate specificity with xanthine oxidase. Although the tissue localization of this enzyme has not been studied as thoroughly as that of xanthine oxidase, aldehyde oxidase is reportedly found in the digestive gland of terrestrial gastropods, the antennae of certain moths as well as the mammalian liver. Recently, the ubiquitous distribution of aldehyde oxidase has been demonstrated in rat tissues. The aldehyde oxidase activity of herbivores exceeds that of carnivores, suggesting a possible role of this enzyme as a protection against the effects of toxic plants. The relationship between the tissue localization of these enzymes and their pathophysiological roles is reviewed.

Animals↗
PubMed1997

Pathophysiology of the thalassemias. The Albion Walter Hewlett Award presentation.

The Albion Walter Hewlett Award (named for Professor of Medicine and Chair of the Stanford Department of Medicine 1916-1925) recognizes a role model, accomplished in discovery of the biological sciences and at the same time a consummate and compassionate physician. In introductory remarks, Dr. Stanley L. Schrier, Professor of Medicine (Hematology), the tenth recipient of the Award, indicated that the person so identified is no longer a viable model in academic medicine. The loss of this sort of person is serious because this appropriately trained physician-investigator was uniquely positioned to study pathophysiology, defined as the processes by which disordered biology produces disease. He used his own studies on the clinical manifestations of the thalassemias to clarify what he meant by pathophysiology. Thus he and his colleagues first defined membrane material properties of alpha and beta thalassemic RBC membranes and the states of hydration of alpha and beta thalassemic RBC and found them to be strikingly divergent. The biochemical counterparts of these alterations proved to be the accumulation of the excess unmatched partially oxidized globin chains on the membrane skeleton. In vitro studies with chemical oxidants selectively oxidized alpha and beta globin chains which then attached to the RBC membrane skeleton and reproduced the membrane material properties characteristic of beta and alpha thalassemia respectively. Many of these alterations had occurred prior to the reticulocyte stage so that pursuit of pathophysiology shifted to studies of marrow erythroid precursors, and it was shown that in beta thalassemia major there was accelerated programmed cell death as well as defective assembly of the membrane skeleton.

Awards and Prizes↗