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At least 667 records · Page 37Linked to original sources
PubMed2006

Muscarinic stimulation of the rat isolated whole bladder: pathophysiological models of detrusor overactivity.

1 Hypotheses as to the pathophysiological basis of bladder detrusor muscle overactivity (DO) have identified both central nervous and peripheral mechanisms as likely contributory factors. In this paper, we describe peripheral autonomous bladder activity in two animal models of DO and discuss how the differences observed between the two models support the likelihood that clinical DO has a multifactorial basis. 2 A total of 12 adult female Sprague-Dawley rats underwent obstruction or sham operation for 1 or 4 weeks. Six adult female spontaneously hypertensive rats (SHR) were compared with normal Wistar controls. Bladders were microsurgically removed and mounted in whole organ tissue baths. Recordings of intravesical pressure in response to the muscarinic receptor agonist arecaidine were performed under standardized conditions. 3 In the partially obstructed rat bladder, the amplitude of pressure fluctuations elicited by the muscarinic agonist arecaidine was significantly increased compared with sham-operated animals. The tonic component of the response was no different for the two groups. No difference from controls was apparent in the SHR. 4 We conclude that alterations in autonomous bladder activity in the obstructed rat model suggest that peripheral functional changes contribute to the pathophysiological abnormality. In contrast, the fundamental abnormality in the SHR appears to be at a more central level. The observations support the supposition that lesions at widely separate sites can give rise to apparently similar abnormalities of lower urinary tract function.

Animals↗
PubMed2005

Portal hypertension: from pathophysiology to clinical practice.

Portal hypertension (PHT) is responsible for the more severe and often lethal complications of cirrhosis such as bleeding oesophageal varices, ascites, renal dysfunction and hepatic encephalopathy. Because of the combined impact of these complications, PHT remains the most important cause of morbidity and mortality in patients with cirrhosis. Over the years, it has become clear that a decrease in portal pressure is not only protective against the risk of variceal (re)bleeding but is also associated with a lower long-term risk of developing complications and an improved long-term survival. A milestone in therapy was the introduction of non-selective beta-blockers for the prevention of bleeding and rebleeding of gastro-esophageal varices. However, in practice, less than half the patients under beta-blockade are protected from these risks, supporting the overall demand for innovation and expansion of our therapeutic armamentarium. Recent advances in the knowledge of the pathophysiology of cirrhotic PHT have directed future therapy towards the increased intrahepatic vascular resistance, which, in part, is determined by an increased hepatic vascular tone. This increased vasculogenic component provides the rationale for the potential use of therapies aimed at increasing intrahepatic vasorelaxing capacity via gene therapy, liver-selective nitric oxide donors and statines on the one hand, and at antagonizing excessive intrahepatic vasoconstrictor force through the use of endothelin antagonists, angiotensin blockers, alpha(1) adrenergic antagonists or combined alpha(1)- and non-selective beta-blockers or somatostatin analogues on the other. The focus of this review is to give an update on the pathophysiology of PHT in order to elucidate these potential novel strategies subsequently.

Adrenergic beta-Antagonists↗
PubMed2005

Pathophysiology of contrast medium-induced nephropathy.

BACKGROUND: Contrast medium-induced nephropathy (CIN) is a well-known cause of acute renal failure, but the development of CIN remains poorly understood. A number of studies have been performed with the one aim, to shed some light onto the pathophysiology of CIN. These have led to manifold interpretations and sometimes contradicting conclusions. METHODS: This review critically surveys mechanisms believed to mediate CIN by highlighting the complex pathophysiologic entity, including altered rheologic properties, perturbation of renal hemodynamics, regional hypoxia, auto- and paracrine factors [adenosine, endothelin, and reactive oxygen species (ROS)], and direct cytotoxic effects. Moreover, the importance of physicochemical properties of contrast media are made clear. RESULTS: The more recently developed iso-osmolar contrast media are dimers, not monomers as the widely used nonionic low osmolar contrast media. The dimers have physicochemical features different from other contrast media which may be of clinical importance, not only with respect to osmolality. The viscosity of the commercially available dimers is considerably higher than blood. CONCLUSION: Many experimental studies provide evidence for a greater perturbation in renal functions by dimeric contrast media in comparison to nonionic monomeric contrast media. Clinical trials have yielded conflicting results.

Acute Kidney Injury↗
PubMed2002

Bench to bedside: pathophysiology of acute coronary syndromes and implications for therapy.

Our understanding of the pathophysiology of unstable angina (UA) and non-ST-segment elevation (NSTE) myocardial infarction (MI) [commonly referred to as NSTE acute coronary syndrome(s) (ACS)] has evolved considerably over the years, with atherothrombosis playing a pivotal role. This review discusses the molecular interactions in coronary thrombosis that may serve as therapeutic targets for more effective management of these syndromes. The purposes of this review are: 1) to discuss current understanding of the pathophysiology of NSTE ACS; 2) to describe recent studies with novel antithrombotic agents [e.g., low-molecular-weight heparin, thienopyridines, glycoprotein (GP) IIb-IIIa inhibitors] in patients with NSTE ACS; and 3) to highlight recommendations for management of patients with NSTE ACS in the recently updated American College of Cardiology (ACC)/ American Heart Association (AHA) guidelines, including the appropriate use of antithrombotic therapies.

Acute Disease↗
PubMed2006

Bowel dysfunction in patients with motor complete spinal cord injury: clinical, neurological, and pathophysiological associations.

BACKGROUND: Abnormal bowel function is a key problem in patients with spinal cord injury (SCI). Previous works provided only partial information on colonic transit time (CTT) or anal dysfunction but did not identified a comprehensive neurogenic bowel pattern. AIM: To evaluate clinical, neurological, and pathophysiological counterparts of neurogenic bowel in patients with motor complete SCI. METHODS: Fifty-four patients (56% men, mean age 35 yr) with chronic motor complete SCI (mean evolution time 6 yr) were evaluated: 41% with injuries above T7 (> T7) and 59% with injuries below T7 (< T7); patients were also classified according to the presence or not of sacral spinal reflexes. Clinical assessment, total and segmental CTT quantification, anorectal function evaluation by manometry, intrarectal balloon distension, and surface electromyography were performed. RESULTS: Three different neuropathophysiological patterns were observed: Pattern A, present in > T7 injuries, characterized by very frequent constipation (86%) with significant defecatory difficulty and not very severe incontinence (Mean Wexner score 4.5); it was related to moderate delay in CTT (mainly in the left colon and recto-sigma), incapacity to increase the intra-abdominal pressure, and the absence of anal relaxation during the defecatory maneuvre; Pattern B, present in < T7 injuries with preserved sacral reflexes, characterized by not so frequent constipation (50%) but very significant defecatory difficulty and not very severe incontinence (Wexner 4.8); the pathophysiological counterpart was a moderate delay in CTT, capacity to increase intra-abdominal pressure, increased anal resistance during the defecatory maneuver, and presence of external anal sphincter (EAS) contraction when intra-abdominal pressure increased and during rectal distension; Pattern C, present in < T7 injuries without sacral reflexes, characterized by not very frequent constipation (56%) with less defecatory difficulty and greater severity of incontinence (Wexner 7.2); this was associated with severe delay in CTT (mainly in the left colon), capacity to increase intra-abdominal pressure, absence of anal resistance during the defecatory maneuver, and absence of EAS contraction when intra-abdominal pressure increased and during rectal distension. CONCLUSION: In patients with motor complete SCI, we were able to define three different neuropathophysiological patterns that are associated with bowel function abnormalities and clinical complaints; this might be of help when designing therapeutic strategies.

Adult↗
PubMed2006

Is functional dyspepsia of particular concern in women? A review of gender differences in epidemiology, pathophysiologic mechanisms, clinical presentation, and management.

Dyspepsia is a remarkably common symptom in the general population. Although multiple definitions have been used to describe the symptom, the most common explanation is that of chronic or recurrent pain or discomfort (a subjective negative feeling that may be associated with early satiety, fullness, bloating, or nausea) centered in the upper abdomen. When a thorough evaluation of a dyspeptic patient fails to identify a cause for her symptoms, the label of nonulcer or functional dyspepsia is applied. Functional dyspepsia is a heterogeneous disorder characterized by relapsing and remitting symptoms. Treatment strategies should focus on alleviating the most bothersome symptom and can be based on the proposed underlying pathophysiology. The effect of gender on mechanisms of disease, symptom presentation, and treatment response is an area of increasing interest and study. As with other functional gastrointestinal disorders, there appear to be some gender-specific features of functional dyspepsia. Specifically, gender-related differences have been observed in some studies of both the prevalence of individual dyspepsia symptoms, and in gastric emptying and proximal gastric motor function. There also appear to be gender differences in the psychosocial realm, with dyspeptic women experiencing a lesser sense of well-being than dyspeptic men, as well as an association of an abuse history with functional dyspepsia. This review will highlight specific gender differences related to the symptom presentation, pathophysiology, and approach to treatment of functional dyspepsia, while noting where differences have not been found and where further investigation is warranted.

Dyspepsia↗
PubMed1988

Pathophysiological aspects of acute experimental allergic encephalomyelitis.

Traditionally, research in experimental allergic encephalomyelitis (EAE) has focussed on immunological and histopathological aspects. The present review introduces a physiological approach to EAE. As EAE is characterized by many small, focal lesions in the central nervous system (CNS), methods with a high spatial resolution should be used to conduct studies on regional pathophysiology in the condition. Quantitative autoradiography seems an ideal method as it offers, 1) high regional resolution (approximately 50 um), 2) precise quantitation and, 3) a direct correlation between regional histopathology and pathophysiology. By the use of this method, the author has performed studies on 1) regional blood-brain barrier (BBB) permeability, and 2) regional metabolism of energy substrate and related subjects, (i.e. regional cerebral blood flow, regional cerebral glucose metabolic rate and regional pH). Corresponding to the EAE lesions (lymphocytic accumulations), there is a considerable increase in BBB permeability. Metabolism of energy substrate at the lesion sites is severely deranged, which is expressed in a CBF/CMR ratio of 3 ml/mumol compared to the normal 1.5 ml/mumol. No changes in regional pH are seen in the lesions. Unrelated to the lesion sites there is a 50% decrease in blood flow in cerebral cortex. This observation probably reflects a functional decrease in cortical flow due to sensory motor impairment.

Animals↗
PubMed1979

Delirium tremens and related clinical states. Aetiology, pathophysiology and treatment.

Definitions of Delirium Tremens (DT) and related clinical states are discussed together with the concepts of aetiology and pathogenesis in relation to psychiatric disease. The withdrawal theory which considers reduction or cessation of alcohol intake as an important precipitating factor in DT is discussed; this theory is supported by experimental studies of ethanol withdrawal in man and by studies indicating cross dependence between ethanol and several other CNS depressors; the arguments in the literature for and against the withdrawal theory are discussed. Other possible aetiological factors such as type of liquor, hypovitaminosis, liver disease, dysfunction of the adrenals and fat emboli are reviewed, and it is concluded that these factors are unimportant as precipitating or specific aetiological factors in DT. Possible pathophysiological mechanisms are discussed, especially concerning electrolyte metabolism and cerebral blood flow and oxygen consumption. It is concluded that the pathophysiology of the disease is poorly understood, and some possibilities for future research are indicated. The discussion about treatment of DT is concentrated on drug treatment, and the literature concerning antipsychotics and sedatives is reviewed. It is concluded that barbital, a long-acting barbiturate, is the most effective treatment; diazepam can be recommended as an acceptable alternative. Finally, practical recommendations concerning treatment are given.

Adrenal Insufficiency↗
PubMed2004

Possible pathophysiological roles of mitogen-activated protein kinases (MAPKs) in endometriosis.

PROBLEM: Endometriosis accompanies local inflammatory reactions in the peritoneal cavity. We examined the phosphorylation of mitogen-activated protein kinases (MAPKs), i.e. extracellular signal-regulated kinase (ERK), p38 MAPK (p38) and c-Jun N-terminal kinase (JNK) in endometriotic stromal cells, and their possible pathophysiological roles in endometriosis in relation to proinflammatory substances. METHOD OF STUDY: Endometriotic stromal cells were isolated from endometriomas and were cultured for the experiments. Phosphorylation of MAPKs in endometriotic stromal cells treated with interleukin (IL)-1beta, tumor necrosis factor (TNF)alpha and H(2)O(2) were examined by Western blot analysis. Effects of PD98059, SB202190 and SP600125 (inhibitors of ERK, p38 and JNK, respectively) on IL-1beta-induced secretion of IL-6 and IL-8, and on IL-1beta-induced expression of cyclo-oxygenase-2 (COX-2) in endometriotic cells were studied. In addition, eutopic endometrial tissues were collected, and the phosphorylation rate of p38 in eutopic endometrial tissues and endometriotic tissues were determined. RESULTS: IL-1beta, TNFalpha and H(2)O(2) stimulated the phosphorylation of ERK, p38 and JNK, while the total amounts of proteins of the respective MAPKs were virtually the same compared with those in the unstimulated controls. Both SB202190 and SP600125 suppressed IL-1beta-induced secretion of IL-6 and IL-8, and PD98059 suppressed IL-1beta-induced secretion of IL-8. Both SB202190 and PD98059 suppressed IL-1beta-induced expression of COX-2 in endometriotic cells. The p38 phosphorylation rates in the endometriotic tissues were significantly higher than those in the eutopic endometrial tissues of the same patients. CONCLUSIONS: Given the current theory that inflammatory changes are involved in the progression of endometriosis, MAPKs could play as pivotal intracellular signal transducers in endometriotic cells, and thus have a pathophysiological role in the disease.

Anthracenes↗
PubMed2005

Pathophysiology of erectile dysfunction.

INTRODUCTION: Multiple regulatory systems are involved in normal erectile function. Disruption of psychological, neurological, hormonal, vascular, and cavernosal factors, individually, or in combination, can induced erectile dysfunction (ED). The contribution of neurogenic, vascular, and cavernosal factors was thoroughly reviewed by our committee, while psychological and hormonal factors contributing to ED were evaluated by other committees. AIM: To provide state of the art knowledge on the physiology of ED. METHODS: An international consultation in collaboration with the major urology and sexual medicine associations assembled over 200 multidisciplinary experts from 60 countries into 17 committees. Committee members established specific objectives and scopes for various male and female sexual medicine topics. The recommendations concerning state-of-the-art knowledge in the respective sexual medicine topic represent the opinion of experts from five different continents developed in a process over a 2-year period. Concerning the pathophysiology of ED committee, there were seven experts from five different countries. MAIN OUTCOME MEASURE: Expert opinion was based on the grading of evidence-based medical literature, widespread internal committee discussion, public presentation, and debate. RESULTS: The epidemiology and classification of neurogenic ED was reviewed. The evidence for the association between vascular ED and atherosclerosis/hypercholesterolemia, hypertension and diabetes was evaluated. In addition, the pathophysiological mechanisms implicated in vascular ED were defined, including: arterial remodeling, increased vasoconstriction, impaired neurogenic vasodilatation, and impaired endothelium-dependent vasodilatation. The possible mechanisms underlying the association between chronic renal failure and ED were also evaluated as well as the evidence supporting the association of ED with various classes of medications. CONCLUSIONS: A better understanding of how diseases interfere with the physiological mechanisms that regulate penile erection has been achieved over the last few years, which helps establish a strategy for the prevention and treatment of ED.

Cardiovascular Agents↗
PubMedDate not supplied

Pediatric short bowel syndrome: pathophysiology, nursing care, and management issues.

ISSUES AND PURPOSE: A comprehensive overview of the etiology, pathophysiology, nursing care, and medical and surgical management of the child with short bowel syndrome (SBS), which follows massive anatomical or functional loss of the small intestine. CONCLUSIONS: The outlook for children with SBS has improved due to recent advances in parenteral and enteral nutrition, pharmacologic interventions, and surgical options. PRACTICE IMPLICATIONS: Nurses whose practice reflects an in-depth knowledge of the etiology, pathophysiology, medical and surgical management, nursing interventions, and complications of SBS will be equipped to provide quality care for children and families affected by SBS.

Enteral Nutrition↗
PubMed2002

Asthma: a case study, review of pathophysiology, and management strategies.

PURPOSE: To review the pathophysiology of asthma, present a case study, and provide management strategies for treating this common, yet complex disorder in children and adults. DATA SOURCES: Selected clinical guidelines, clinical articles, and research studies. CONCLUSIONS: Asthma is a chronic inflammatory airway disorder with acute exacerbations that currently affects approximately 14 million-15 million children and adults in the United States. Costs for asthma are staggering and nurse practitioners (NPs) are frequently presented with management decisions for the acute treatment and chronic management of this disorder. Disparities exist with the occurrence of asthma between race and gender. Additionally, there is an increased incidence in acute exacerbations resulting from poor long-term control and follow-up care among the socioeconomically disadvantaged. IMPLICATIONS FOR PRACTICE: Standards of care, along with new and emerging treatment strategies, guide NPs in providing the most comprehensive care to those affected with this chronic disorder. Knowledge about the pathophysiology of asthma and correlated to the case presentation enhances understanding treatment strategies for NPs who are often faced with providing care for patients with this chronic disorder that may sometimes present in an acute exacerbation.

Adult↗
PubMed1998

Pathophysiologic and somatic investigations of hypothalamic-pituitary-adrenal axis activation in patients with depression.

Preclinical studies of inflammatory and autoimmune illnesses have demonstrated the importance of central components of the HPA axis in disease pathophysiology. The implications of these data for human illness are poorly understood. We have studied the pathophysiology of the hypercortisolism seen in two human illnesses involving the central nervous system, multiple sclerosis (MS) and depression, and looked for demonstrable somatic changes that may be associated with such hypercortisolism. Data from a study of medication-free patients with multiple sclerosis not in acute exacerbation suggest that compared with depression, MS is associated with increased prominence of hypothalamic vasopressin secretion (p < 0.05). Data from studies of depressed patients with mild to moderate hypercorticolism (assessed by 24-hour urinary free cortisol excretion) demonstrate marked reductions in bone mineral density compared to healthy, carefully matched controls (p < 0.001), as well as changes in markers of bone metabolic activity similar to those seen in patients with Cushing's disease or exogenous glucocorticoid treatment (p < 0.05). Taken together, these studies suggest HPA axis dysregulations demonstrated in preclinical models of autoimmune and inflammatory illness also occur in human illness and may have important and lasting somatic sequelae.

Adrenocorticotropic Hormone↗
PubMed2003

Xanthine oxidoreductase and cardiovascular disease: molecular mechanisms and pathophysiological implications.

There is substantial evidence that oxidative stress participates in the pathophysiology of cardiovascular disease. Biochemical, molecular and pharmacological studies further implicate xanthine oxidoreductase (XOR) as a source of reactive oxygen species in the cardiovascular system. XOR is a member of the molybdoenzyme family and is best known for its catalytic role in purine degradation, metabolizing hypoxanthine and xanthine to uric acid with concomitant generation of superoxide. Gene expression of XOR is regulated by oxygen tension, cytokines and glucocorticoids. XOR requires molybdopterin, iron-sulphur centres, and FAD as cofactors and has two interconvertible forms, xanthine oxidase and xanthine dehydrogenase, which transfer electrons from xanthine to oxygen and NAD(+), respectively, yielding superoxide, hydrogen peroxide and NADH. Additionally, XOR can generate superoxide via NADH oxidase activity and can produce nitric oxide via nitrate and nitrite reductase activities. While a role for XOR beyond purine metabolism was first suggested in ischaemia-reperfusion injury, there is growing awareness that it also participates in endothelial dysfunction, hypertension and heart failure. Importantly, the XOR inhibitors allopurinol and oxypurinol attenuate dysfunction caused by XOR in these disease states. Attention to the broader range of XOR bioactivity in the cardiovascular system has prompted initiation of several randomised clinical outcome trials, particularly for congestive heart failure. Here we review XOR gene structure and regulation, protein structure, enzymology, tissue distribution and pathophysiological role in cardiovascular disease with an emphasis on heart failure.

Animals↗
PubMed2005

Pathophysiological manifestations in mice exposed to anthrax lethal toxin.

Pathophysiological changes associated with anthrax lethal toxin included loss of plasma proteins, decreased platelet count, slower clotting times, fibrin deposits in tissue sections, and gross and histopathological evidence of hemorrhage. These findings suggest that blood vessel leakage and hemorrhage lead to disseminating intravascular coagulation and/or circulatory shock as an underlying pathophysiological mechanism.

Animals↗
PubMed1996

Use of Wigglesworth pathophysiological classification for perinatal mortality in Malaysia.

A one year prospective study of perinatal deaths was conducted to test the feasibility of using the Wigglesworth pathophysiological classification in the Malaysian health service. Four regions with high perinatal mortality rates were selected. Deaths were actively identified. Nursing staff were trained to use the classification and every death was reviewed by a clinician. A total of 26,198 births and 482 perinatal deaths were reported. The perinatal mortality rate was 18.4. Only 14 (2.9%) deaths had their Wigglesworth category reclassified. Most deaths were in the normally formed macerated stillbirths (34.4%), asphyxial conditions (26.8%), and immaturity (20.1%) subgroups. The results were compared with data from other countries that used this classification. This study has shown that the Wigglesworth pathophysiological classification can be applied to perinatal deaths in the existing Malaysian health service.

Cause of Death↗
PubMed1987

Multiple duodenal ulcer: natural history and pathophysiology.

It has not been established whether multiple duodenal ulcer is associated with a different natural history, pathophysiology, and therapeutic response than a single duodenal ulcer. A consecutive series of 96 patients with two or more duodenal ulcers at endoscopy, representing 9.6% of the total number of new patients with duodenal ulcer seen during the period 1980-1985, were compared with a random series of 200 patients with single duodenal ulcer seen in the middle years of this period. Multiple duodenal ulcer was associated with higher (p less than 0.02) male to female ratio, more (p less than 0.05) late onset patients (those with ulcer symptoms starting after age 30 years, more (p less than 0.05) chronic cigarette smokers, and more frequent (p less than 0.05) moderate to severe deformity of the duodenal bulb. More (p less than 0.05) patients with multiple duodenal ulcer had abnormally low D50 derived from pentagastrin dose response tests, indicating that they were more sensitive to gastrin stimulation. Furthermore, their mean fasting and meal stimulated serum gastrin concentrations were significantly higher than those of patients with single ulcer (p less than 0.005), or of controls (p less than 0.05). Compared with single duodenal ulcer, multiple ulcer had significantly lower placebo healing rate, and required a higher dose of misoprostol (1200 v 800 micrograms/day) to achieve a similar healing efficacy at four weeks. We conclude that multiple duodenal ulcer is associated with different clinical features, pathophysiology, and possibly therapeutic response from single duodenal ulcer, and appears to represent the more aggressive side of the ulcer spectrum.

Adult↗
PubMed1998

Enantiomers of flurbiprofen can distinguish key pathophysiological steps of NSAID enteropathy in the rat.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal damage by a non-prostaglandin (PG) dependent "topical" action and by inhibiting cyclooxygenase. AIMS: To discriminate between these two effects by studying some key pathophysiological steps in NSAID enteropathy following administration of (R)- and (S)-flurbiprofen, the racemic mixture, and an uncoupler, dinitrophenol. METHODS: The effects of dinitrophenol, racemic, (R)-, and (S)-flurbiprofen on mitochondria were assessed in vitro and on key pathophysiological features of small intestinal damage in vivo (ultrastructure by electron microscopy, mucosal prostanoid concentrations, intestinal permeability, inflammation, and ulcer count) in rats. RESULTS: All the drugs uncoupled mitochondrial oxidative phosphorylation in vitro, caused mitochondrial damage in vivo, and increased intestinal permeability. Dinitrophenol and (R)-flurbiprofen caused no significant decreases in mucosal prostanoid concentrations (apart from a decrease in thromboxane (TX) B2 concentrations following (R)-flurbiprofen) while racemic and (S)- flurbiprofen reduced mucosal prostanoids significantly (PGE, TXB2, and 6-keto-PGF1alpha concentrations by 73-95%). Intestinal inflammation was significantly greater following administration of (S)-flurbiprofen and racemate than with dinitrophenol and (R)-flurbiprofen. No small intestinal ulcers were found following dinitrophenol or (R)-flurbiprofen while both racemic and (S)-flurbiprofen caused numerous ulcers. CONCLUSIONS: Dinitrophenol and (R)-flurbiprofen show similarities in their actions to uncouple mitochondrial oxidative phosphorylation in vitro, alter mitochondrial morphology in vivo, increase intestinal permeability, and cause mild inflammation without ulcers. Concurrent severe decreases in mucosal prostanoids seem to be the driving force for the development of severe inflammation and ulcers.

Animals↗