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At least 145 records · Page 8Linked to original sources
PubMed2003

Changes in nitric oxide levels and antioxidant enzyme activities may have a role in the pathophysiological mechanisms involved in autism.

BACKGROUND: There is evidence that oxygen free radicals play an important role in the pathophysiology of many neuropsychiatric disorders. Although it has not been investigated yet, several recent studies proposed that nitric oxide (NO) and other parameters related to oxidative stress may have a pathophysiological role in autism. METHODS: We assessed the changes in superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and thiobarbituric acid-reactive substances (TBARS) levels in plasma as well as NO levels in red blood cells (RBC) in patients with autism (n=27) compared to age- and sex-matched normal controls (n=30). RESULTS: In the autistic group, increased RBC NO levels (p<0.0001) and plasma GSH-Px activity (p<0.0001) and unchanged plasma TBARS levels and SOD activity were detected. CONCLUSIONS: These findings indicate a possible role of increased oxidative stress and altered enzymatic antioxidants, both of which may be relevant to the pathophysiology of autism.

Autistic Disorder↗
PubMed1997

Injury by electrical forces: pathophysiology, manifestations, and therapy.

The pathogenesis and pathophysiologic features of electrical injury are more complex than once thought. The relative contributions of thermal and pure electrical damage depend on the duration of electric current passage, the orientation of the cells in the current path, their location, and other factors. If the contact time is brief, nonthermal mechanisms of cell damage will be most important and the damage is relatively restricted to the cell membrane. When contact time is much longer, however, heat damage predominates and the whole cell is affected directly. These parameters also determine the anatomic tissue distribution of injury. Damage by Joule heating is not known to be dependent on cell size, whereas larger cells are more vulnerable to membrane breakdown by electroporation. Cells do survive transient plasma membrane rupture under appropriate circumstances or if therapy is instituted quickly. If membrane permeabilization is the primary cellular pathologic condition, then injured tissue may be salvageable and the challenge for the future is to identify a technique to reseal the damaged membranes promptly. Present standards of care for electrical injury require a fully staffed and well-equipped intensive care unit, available operating suites, and the availability of the full range of medical specialists. Major teaching hospitals with burn centers may be the ideal setting for the treatment of an electrical trauma victim. After the initial resuscitation, efforts are directed primarily towards preventing additional tissue loss mediated through the compartment syndrome, compressive neuropathies, or the presence of necrotic tissue. Renal and cardiac failure caused by the release of intracellular muscle contents into the circulation must be prevented. Attention can then be directed towards maximizing tissue salvage and preventing late skeletal and neuromuscular complications. Reconstructive procedures that transfer healthy tissue from a distance are necessary to optimize the functional value of the remaining tissue. Finally, unless the patient is rehabilitated psychologically, the real benefit from other sophisticated care will not be fully realized. These goals are important throughout the acute care of the patient. In the future, new guidelines for treating electrical trauma will be based on a clearer understanding of the relevant pathophysiologic features. These strategies will rely on improved diagnostic imaging and on reversing the fundamental problem of cell membrane damage. Moreover, complex biochemical and organ system pathophysiologic interactions will require careful management. If successful, research efforts presently underway should improve the prognosis of victims after electrical trauma.

Burns, Electric↗
PubMedDate not supplied

Development, disease and degeneration in schizophrenia: a unitary pathophysiological model.

In recent years, several pathophysiological models of schizophrenia, i.e. the early and late brain neurodevelopmental and post-illness onset neurodegenerative models, have been proposed and theorists have often argued as if these explanations are mutually exclusive. We propose that all these mechanisms may interact cumulatively during successive critical 'windows of vulnerability' during brain development and during the early course of the illness to lead to the clinical manifestations of the illness. Early brain insults may lead to dysplasia of selective neural networks that account for the premorbid cognitive and psychosocial dysfunction seen in many patients. The onset of psychosis in adolescence may be related to an excessive elimination of synapses and secondarily, phasic dopaminergic overactivity. Following illness onset, these neurochemical alterations in relation to continuing untreated psychosis may lead to further neurodegenerative processes. A reduction in tonic glutamatergic neurotransmission and a phasic glutamatergic excess can potentially predispose to these processes and may have considerable explanatory power. This hypothesis is consistent with central characteristics of schizophrenia such as premorbid manifestations, adolescent onset, functional decline early in this illness, cognitive impairments, the role of dopamine and the role of genes and environment in pathophysiology. This 'three hit' model extends similar integrative conceptualization by other investigators and generates testable predictions of relevance to future pathophysiology and treatment research in schizophrenia.

Adolescent↗
PubMed2001

Pathophysiological aspects of frontotemporal dementia--emphasis on cytoskeleton proteins and autoimmunity.

The aim of this study was to investigate two putative pathophysiological aspects of the common neurodegenerative disorder frontotemporal dementia (FTD). To this end, cerebrospinal fluid (CSF) levels of tau (total tau) and the light subtype of the neurofilament proteins (NFL) were studied in patients with FTD (n=16) and in age-matched controls (n=16). In addition, serum was analysed for IgG and IgM antibodies to the most common gangliosides and sulfatide in FTD patients (n=13) and in age-matched controls (n=20). The CSF-NFL levels were increased in FTD (1606+/-1151 pg/ml, mean+/-S.D.; P<0.001) compared with controls (308+/-203 pg/ml), whereas the CSF-tau levels were normal. In serum, autoantibody IgG-GA1 was significantly increased in FTD (P<0.05) compared with controls. No correlations were found between the effect parameters and demographic variables in any group. The results of this study suggest that cytoskeleton proteins other than tau are also involved in the pathophysiology of FTD and that autoimmunity may be part of the pathophysiological processes in FTD, as it is believed to be in Alzheimer's disease.

Aged↗
PubMed1997

Chronic pain states: pathophysiology and medical therapy.

OBJECTIVE: The pathophysiology and management of chronic pain are reviewed in this two-part article, with an emphasis on pharmacological therapies and surgical interventions. DATA SOURCES: A thorough literature review of published articles available in Medline from 1966 to 1996 on the topic of pain management, including diagnosis, pathophysiology, interventions, and treatment. CONCLUSIONS: Despite the development of new instruments and treatments to assess and manage pain, chronic pain is often poorly understood and inadequately addressed. Caregivers often lack sufficient skills to intervene promptly and effectively. Traditionally, drug therapy has relied on the nonsteroidal antiinflammatory drugs (NSAIDs) and opioid analgesics for chronic nociceptive pain. A newer analgesic choice for moderate to moderately severe pain is tramadol, a centrally acting agent with at least two complementary mechanisms of action and minimal gastrointestinal or renal toxicity. Adjuvant agents, including tricyclic antidepressants (TCAs), anticonvulsants, and local anesthetics, also help manage chronic neuropathic pain. Although significant advances in the understanding of chronic pain and its pathophysiological mechanisms and newer techniques (noninvasive and invasive) for chronic pain management have become available, reduced patient morbidity and improved quality of life may only be realized with an improved understanding of available resources.

Analgesics↗
PubMed1998

Epidemiology, pathophysiology, and evaluation of urinary incontinence and overactive bladder.

OBJECTIVES: To present an overview of current knowledge regarding the epidemiology, pathophysiology, and evaluation of urinary incontinence (UI) with a focus on the problem of the overactive bladder. METHODS: The most recent data on the epidemiology of UI are presented. The literature on the pathophysiology of urinary urge incontinence (UUI) is reviewed, and key concepts related to patient evaluation are summarized. RESULTS: The prevalence of UI depends on the population being surveyed. The overactive bladder constitutes a substantial percentage of the overall problem, ranging from > 50% of incontinent men to only 10% to 15% of incontinent younger women. Few data are available on the incidence of the disorder or on racial/ethnic trends. Overactive bladder or urge incontinence is called detrusor hyperreflexia when a neurologic cause is known and detrusor instability when there is no neurologic abnormality. Although the pathophysiology of idiopathic instability is not well understood, some evidence suggests that this condition may result from subclinical neurologic disease or primary smooth muscle disease. Most patients with UUI can be adequately evaluated with a history, physical examination, determination of postvoid residual volume, and urinalysis. When neurologic disease or other complicating factors are present, or if initial treatment fails, sophisticated urodynamic testing is appropriate. CONCLUSIONS: Urinary incontinence is prevalent in all strata of the population, although it affects women and the elderly disproportionately. With the exception of cases in which a neurologic lesion can be demonstrated, the etiology of UUI remains elusive. A thorough history, physical examination, determination of postvoid residual, and urinalysis will be adequate to classify and treat the majority of patients.

Female↗
PubMedDate not supplied

Pathophysiology of nitric oxide and related species: free radical reactions and modification of biomolecules.

Since its initial discovery as an endogenously produced bioactive mediator, nitric oxide (.NO) has been found to play a critical role in the cellular function of nearly all organ systems. Furthermore, aberrant production of .NO or reactive nitrogen species (RNS) derived from .NO, has been implicated in a number of pathological conditions, such as acute lung disease, atherosclerosis and septic shock. While .NO itself is fairly non-toxic, secondary RNS are oxidants and nitrating agents that can modify both the structure and function of numerous biomolecules both in vitro, and in vivo. The mechanisms by which RNS mediate toxicity are largely dictated by its unique reactivity. The study of how reactive nitrogen species (RNS) derived from .NO interact with biomolecules such as proteins, carbohydrates and lipids, to modify both their structure and function is an area of active research, which is lending major new insights into the mechanisms underlying their pathophysiological role in human disease. In the context of .NO-dependent pathophysiology, these biochemical reactions will play a major role since they: (i) lead to removal of .NO and decreased efficiency of .NO as an endothelial-derived relaxation factor (e.g. in hypertension, atherosclerosis) and (ii) lead to production of other intermediate species and covalently modified biomolecules that cause injury and cellular dysfunction during inflammation. Although the physical and chemical properties of .NO and .NO-derived RNS are well characterised, extrapolating this fundamental knowledge to a complicated biological environment is a current challenge for researchers in the field of .NO and free radical research. In this review, we describe the impact of .NO and .NO-derived RNS on biological processes primarily from a biochemical standpoint. In this way, it is our intention to outline the most pertinent and relevant reactions of RNS, as they apply to a diverse array of pathophysiological states. Since reactions of RNS in vivo are likely to be vast and complex, our aim in this review is threefold: (i) address the major sources and reactions of .NO-derived RNS in biological systems, (ii) describe current knowledge regarding the functional consequences underlying .NO-dependent covalent modification of specific biomolecules, and (iii) to summarise and critically evaluate the available evidence implicating these reactions in human pathology. To this end, three areas of special interest have been chosen for detailed description, namely, formation and role of S-nitrosothiols, modulation of lipid oxidation/nitration by RNS, and tyrosine nitration mechanisms and consequences.

Animals↗
PubMed2006

Kidney stones: pathophysiology and medical management.

The formation of stones in the urinary tract stems from a wide range of underlying disorders. That clinicians look for the underlying causes for nephrolithiasis is imperative to direct management. There are many advances in genetics, pathophysiology, diagnostic imaging, medical treatment, medical prevention, and surgical intervention of nephrolithiasis. Here, I provide a brief general background and focus mainly on pathophysiology and medical treatment of kidney stones. Although important advances have been made in understanding nephrolithiasis from single gene defects, the understanding of polygenetic causes of kidney stones is still largely elusive. A substantial proportion of data that resulted in new methods of treatment and prevention, which can be empirical or definitive, has focused on urinary luminal chemical composition of the precipitating solutes. Manipulation of inhibitors and epithelial factors is important and needs further investigation. Advances in the management of nephrolithiasis depend on combined efforts of clinicians and scientists to understand the pathophysiology.

Diet↗
PubMed2002

Pathophysiology, signs, and symptoms of acute tumor lysis syndrome.

OBJECTIVES: To provide a review of the pathophysiology and corresponding signs and symptoms of tumor lysis syndrome (TLS); to review clinical and laboratory monitoring parameters. DATA SOURCES: Primary and tertiary literature and clinical experience. CONCLUSIONS: An understanding of the pathophysiology of TLS, meticulous assessment for signs and symptoms and monitoring of laboratory data, as well as early recognition of problems are essential for optimal patient outcomes. IMPLICATIONS FOR NURSING PRACTICE: Knowledge of the pathophysiology of TLS will assist the oncology nurse in better understanding the overall syndrome and allow improved patient care management through close clinical and laboratory monitoring of signs and symptoms, and, ideally, promote a proactive approach to managing TLS.

Acute Disease↗
PubMed1997

Neurochemical sensitization in the pathophysiology of schizophrenia: deficits and dysfunction in neuronal regulation and plasticity.

Existing pathophysiological models of schizophrenia are limited in their ability to account for all the clinical dimensions of the disorder. The purpose of this article is to describe a comprehensive hypothesis of the pathophysiology of schizophrenia and specifically how a deficit in neural regulation of developmental origin can lead to a pathologic form of neuroplasticity, i.e., neurochemical sensitization, which causes the onset and psychotic symptoms of the illness. We propose that the symptoms of schizophrenia may be caused by deficits in neural regulation resulting in a pathologic condition of neurochemical sensitization analogous to the preclinical model of pharmacologically-induced behavioral sensitization. This condition, if sustained, can lead to potential neurotoxic effects which produce structural neuronal alterations and persistent morbidity. Several lines of indirect and direct clinical evidence are consistent with this hypothesis. These include the ability of stimulant and psychotomimetic drugs to induce psychosis in normal subjects, the development of apparent sensitization to psychosis-inducing effects of stimulants in chronic stimulant abusers and the increased susceptibility of patients with schizophrenia to the psychotogenic effects of Dopamine (DA) agonists. This hypothesis integrates and extends the work of other investigators and is consistent with specific aspects of the longitudinal course of schizophrenia. The association of longer duration and more episodes of psychosis, with poor treatment response and outcome, are also consistent with this model. Form this hypothesis, specific predictions about the illness course, treatment interventions, and pathophysiologic features of schizophrenia can be derived and tested through clinical investigation.

Brain Chemistry↗
PubMed1998

Role of intestinal mast cells in modulating gastrointestinal pathophysiology.

OBJECTIVE: This article reviews the current understanding of the pathophysiologic role of intestinal mast cells. DATA SOURCE: Up to date English language publications on mast cell characteristics, heterogeneity and functions were used. Recent articles were used to develop and extend novel concepts about the role of intestinal mast cells. STUDY SELECTION: Reference sources were selected because of their pertinence to the pathophysiological effects of mast cells in intestinal hypersensitivity. Recent publications on the following topics were emphasized: mast cell proteases in intestinal anaphylaxis; effects of nitric oxide in gastrointestinal pathophysiology; involvement of cytokines derived from mast cells in tissue damage and repair. RESULTS: Mast cells are clearly implicated in the pathology of intestinal disease. Growing evidence suggests physiological roles for mast cells in the protection of tissues from inflammatory damage, and in intestinal maturation. Mast cells can release cytokines, such as tumour necrosis factor-alpha and interleukin-10, which were originally thought to contribute to inflammatory damage, but which may also have anti-inflammatory properties. Interestingly, mast cell function can be regulated by nitric oxide, and mast cells themselves are sources of this important mediator. Nitric oxide has protective as well as detrimental effects in the intestine. CONCLUSIONS: Intestinal mast cells have physiologic regulatory effects in addition to their pathologic effects. However, relatively little is known about the mechanisms of these regulatory effects. Mast cells are likely in an ongoing fluctuating balance between physiological functions and pathological effects in normal individuals. Poorly known factors can create an imbalance and lead to pathologic reactions.

Anaphylaxis↗
PubMed2000

Apoptosis in hepatic pathophysiology.

Apoptosis is a fundamental biologic process that is important in many physiologic and pathophysiologic processes in the liver. Although dysregulation of apoptosis may contribute to a wide range of diseases, the role of this process in liver disease and pathophysiology has only recently begun to be recognized and remains to be fully defined. Several important questions remain unanswered: How does excessive apoptosis in response to injury contribute to inflammation and fibrogenesis in the liver? How does control of apoptosis contribute to the regulation of hepatic structure following injury? What is the role of death receptors in hepatic disease? Can an understanding of apoptosis be helpful in therapeutic modulation of specific liver diseases or liver cancer? The identification of target molecules involved in apoptosis raises the prospect of pharmacologic modulation that may result in better treatment options for patients with liver diseases. Inhibition of apoptosis is likely to be useful in treating fulminant hepatic failure or in organ preservation before transplantation. In these situations, treatment is for a limited period, and the potential hazards of nonselective long-term inhibition of apoptosis are minimized. Safe and organ-specific inhibitors of apoptosis would be required for prolonged treatment of chronic liver diseases. For treatment of liver tumors, the goal is to induce apoptosis selectively in cancer cells. Drugs that decrease the apoptotic threshold by modulating the intracellular regulatory mechanisms and drugs that enhance the susceptibility of cancer cells to undergo immune-mediated apoptosis will be useful in the treatment of liver cancers. The rapid advances in the understanding of the intracellular mechanisms and the regulation of apoptosis will ultimately result in a better understanding of the role of apoptosis in the pathophysiology of liver diseases and may allow therapeutic modulation of this process.

Apoptosis↗
PubMed2001

The pathophysiologic basis for the treatment of cirrhotic ascites.

Advances in the understanding of the pathophysiology of sodium retention and ascites formation in cirrhosis has helped improve the treatment of ascites in these patients. It is likely that further unraveling of these pathophysiologic changes will lead to the development of novel and better treatment options. For example, the development of aquaretic agents for the management of hyponatremia in cirrhosis may allow more effective use of diuretic therapy. The ultimate challenge is to use the understanding of the pathophysiology to develop new strategies to prevent the development of ascites in cirrhosis.

Ascites↗
PubMed2003

Role of cytochrome P450-dependent arachidonic acid metabolites in liver physiology and pathophysiology.

Arachidonic acid (AA) can undergo monooxygenation or epoxidation by enzymes in the cytochrome P450 (CYP) family in the brain, kidney, lung, vasculature, and the liver. CYP-AA metabolites, 19- and 20-hydroxyeicosatetraenoic acids (HETEs), epoxyeicosatrienoic acids (EETs) and diHETEs have different biological properties based on sites of production and can be stored in tissue lipids and released in response to hormonal stimuli. 20-HETE is a vasoconstrictor, causing blockade of Ca(++)-activated K(+) (KCa) channels. Inhibition of the formation of nitric oxide (NO) by 20-HETE mediates most of the cGMP-independent component of the vasodilator response to NO. 20-HETE elicits a potent dilator response in human and rabbit pulmonary vascular and bronchiole rings that is dependent on an intact endothelium and COX. 20-HETE is also a vascular oxygen sensor, inhibits Na(+)/K(+)-ATPase activity, is an endogenous inhibitor of the Na(+)-K(+)-2Cl(-)cotransporter, mediates the mitogenic actions of vasoactive agents and growth factors in many tissues and plays a significant role in angiogenesis. EETs, produced by the vascular endothelium, are potent dilators. EETs hyperpolarize VSM cells by activating KCa channels. Several investigators have proposed that one or more EETs may serve as endothelial-derived hyperpolarizing factors (EDHF). EETs constrict human and rabbit bronchioles, are potent mediators of insulin and glucagon release in isolated rat pancreatic islets, and have anti-inflammatory activity. Compared with other organs, the liver has the highest total CYP content and contains the highest levels of individual CYP enzymes involved in the metabolism of fatty acids. In humans, 50-75% of CYP-dependent AA metabolites formed by liver microsomes are omega/omega-OH-AA, mainly w-OH-AA, i.e. 20HETE, and 13-28% are EETs. Very little information is available on the role of 19- and 20-HETE and EETs in liver function. EETs are involved in vasopressin-induced glycogenolysis, probably via the activation of phosphorylase. In the portal vein, inhibition of EETs exerts profound effects on a variety of K-channel activities in smooth muscles of this vessel. 20-HETE is a weak, COX-dependent, vasoconstrictor of the portal circulation. EETs, particularly 11,12-EET, cause vasoconstriction of the porto-sinusoidal circulation. Increased synthesis of EETs in portal vessels and/or sinusoids or increased levels in blood from the meseneric circulation may participate in the pathophysiology of portal hypertension of cirrhosis. CYP-dependent AA metabolites are involved in the pathophysiology of portal hypertension, not only by increasing resistance in the porto-sinusoidal circulation, but also by increasing portal inflow through mesenteric vasodilatation. In patients with cirrhosis, urinary 20-HETE is several-fold higher than PGs and TxB2, whereas in normal subjects, 20-HETE and PGs are excreted at similar rates. Thus, 20-HETE is probably produced in increased amounts in the preglomerular microcirculation accounting for the functional decrease of flow and increase in sodium reabsorption. In conclusion, CYP-AA metabolites represent a group of compounds that participate in the regulation of liver metabolic activity and hemodynamics. They appear to be deeply involved in abnormalities related to liver diseases, particularly cirrhosis, and play a key role in the pathophysiology of portal hypertension and renal failure.

Animals↗
PubMed1987

Pathophysiology of parasitic infections.

Parasites can have a wide range of pathophysiological effects on the host. This review describes those associated with some parasites of major importance in man and animals. Haemoprotozoan diseases such as trypanosomiasis and malaria are primarily associated with anaemia. Such anaemias have a complex aetiology involving various mechanisms responsible for red cell destruction as well as possible defects in red cell production. In addition to these haematological effects these diseases are associated with marked disturbances in heart function and the nervous, immune and urinary systems. The other major groups of parasitic diseases are those associated with the gastrointestinal tract. The most advanced studies have been conducted on the pathophysiology of gastrointestinal nematode parasites of sheep and have revealed significant effects on feed intake, gastrointestinal function, and protein and energy metabolism. Similar studies have yet to be conducted in other hosts and parasitic diseases. There is also a need to examine in greater detail the factors which can modulate pathophysiological responses by the host to parasitic infections.

Anemia↗
PubMed2006

Pathophysiology and therapy for haemoglobinopathies. Part I: sickle cell disease.

In sickle cell disease, a single base pair substitution in the gene encoding the beta-globin chain of the haemoglobin molecule gives rise to a surprisingly broad spectrum of pathophysiological and clinical manifestations. Inflammation, endothelial activation, red blood cell membrane abnormalities and altered availability of vasoactive factors characterise this disorder. Clinically, patients suffer from a host of seemingly unrelated maladies, from pain episodes to strokes, life-threatening infections and pulmonary hypertension. Deepened understanding of this complex disease now allows us to begin to turn away from simple supportive treatments, and move towards therapies aimed at specific pathophysiological targets. This article, the first of two reviews on the pathophysiology of haemoglobinopathies, discusses the molecular basis of sickle cell disease, and elaborates on the many factors that exacerbate or ameliorate the disease process. It then focuses on the promising targeted therapies currently in use or under investigation. An accompanying article on haemoglobinopathies (Part II) focuses on thalassaemias.

Anemia, Sickle Cell↗
PubMed2003

Cardiac expression of urocortin (Ucn) in diseased heart; preliminary results on possible involvement of Ucn in pathophysiology of cardiac diseases.

Recently, several studies reported that urocortin (Ucn) had beneficial effects on cardiovascular system and was expressed both in the normal heart and in the heart of dilated cardiomyopathy (DCM), yet the relationship between high expression of Ucn and pathophysiology of Ucn in diseased heart has been discussed. Thus, the present study was designed to elucidate the expression of Ucn in the diseased heart by immunohistochemical approach using endomyocardial biopsy specimens. The involvement of immunoreactive Ucn in pathophysiology of cardiac disease was evaluated using endomyocardial biopsy specimens obtained from the patients with some heart diseases, including DCM and hypertrophic cardiomyopathy (HCM). Ucn was detected in all endomyocardial biopsy specimens of ventricular tissue obtained from the patients with such cardiac diseases, a specimens of atrial tissue, and normal heart specimens obtained from autopsy cases. In DCM patients, left ventricular end-diastolic pressure significantly elevated in severely stained group. On the contrary, in HCM patients, left ventricular ejection fraction was higher in the severely stained group. Ucn was expressed more abundantly in the diseased heart, especially in HCM and DCM, than in the normal heart. In conclusion, such close relationship between Ucn expression in the heart and cardiac function indicated that clinical features of Ucn resembled those of norepinephrine and Ucn could play a certain pathophysiological roles in the cardiac diseases.

Aged↗
PubMed2006

[From understanding the pathophysiological mechanisms of dyspnea to the correct symptomatic treatment].

Breathing discomfort is one of the most common and distressing symptoms experienced by patients. Various pathophysiologic mechanisms underlie the symptom of dyspnea, and multiple mechanisms may be present in a given patient. The evaluation of the dyspneic patient must begin with a thorough history examining the key characteristics of the symptom, including quality, intensity, duration, frequency, and distress. The words utilized by patients to describe their breathing discomfort may provide insights into the underlying pathophysiology of their disease. Treatment for dyspnea should be selected based on the pathophysiologic mechanisms involved and not only according to the specific disease. Attempts are made to reduce mechanical impedance (by reducing lung hyperinflation by bronchodilators or surgical volume reduction), to reduce ventilatory demand (by exercise training), to improve inspiratory muscle function (by inspiratory muscle training), to alter breathing patterns, to begin supplemental oxygen therapy and to reduce central perception. It is often necessary to combine several treatment modalities in order to achieve a significant reduction in dyspnea.

Bronchodilator Agents↗