ABSTRACT
La hipertensión arterial pulmonar (HAP) es una grave enfermedad cuyo resultado final de la interacción entre el tono vascular y la alteración progresiva de la remodelación de las arterias pulmonares provoca insuficiencia cardíaca derecha y muerte. El remodelado vascular pulmonar es la alteración estructural clave en la hipertensión pulmonar. Este proceso implica cambios en la íntima, media, adventicia y espacio perivascular, a menudo con la interacción de células inflamatorias. Los mecanismos fisiopatológicos de la HAP abarcan una serie de modificaciones vasculares que producen un aumento de la resistencia vascular pulmonar. Las modificaciones vasculares que se producen en la HAP incluyen: la vasoconstricción, la proliferación del músculo liso, la inflamación, la apoptosis endotelial, la proliferación endotelial resistente a la apoptosis, la fibrosis, la trombosis in-situ, y finalmente, las lesiones plexiformes. Hasta hace poco, la HAP se consideraba una enfermedad restringida a la circulación pulmonar. Sin embargo, existe una creciente evidencia de que los pacientes con HAP también exhiben disfunción vascular sistémica, como lo demuestra la alteración de la dilatación mediada por el flujo de la arteria braquial, el flujo sanguíneo cerebral anormal, la miopatía esquelética y la enfermedad renal intrínseca. Los datos recientes apoyan un vínculo con los eventos genéticos y moleculares detrás de la patogénesis de la HAP. Esta revisión sirve de introducción a los principales hallazgos sistémicos en la HAP y la evidencia que apoya un vínculo común con la fisiopatología de la HAP. Sobre la base de la evidencia disponible, proponemos un paradigma en el que las anomalías metabólicas, la lesión genética y la disfunción vascular sistémica contribuyen a las manifestaciones sistémicas de la HAP. Este concepto no sólo abre interesantes posibilidades de investigación, sino que también anima a considerar las manifestaciones extrapulmonares en el tratamiento de los pacientes con HAP, pues la disfunción vascular sistémica contribuiría a las manifestaciones sistémicas de la HAP.
Pulmonary arterial hypertension (PAH) is a serious disease whose end result of the interaction between vascular tone and the progressive alteration of the remodeling of the pulmonary arteries causes right heart failure and death. Pulmonary vascular remodeling is the key structural alteration in pulmonary hypertension. This process involves changes in the intima, media, adventitia, and perivascular space, often with the interaction of inflammatory cells. The pathophysiological mechanisms of PAH include a series of vascular modifications that produce an increase in pulmonary vascular resistance. Vascular modifications that occur in PAH include: vasoconstriction, proliferation of smooth muscle, inflammation, Endothelial apoptosis, apoptosis-resistant endothelial proliferation, fibrosis, in-situ thrombosis, and finally, plexiform lesions. Until recently, PAH was considered a disease restricted to the pulmonary circulation. However, there is growing evidence that patients with PAH also exhibit systemic vascular dysfunction, as evidenced by impaired brachial artery flow-mediated dilation, abnormal cerebral blood flow, skeletal myopathy, and intrinsic kidney disease. Recent data support a link to the genetic and molecular events behind the pathogenesis of PAH. This review serves as an introduction to the main systemic findings in PAH and the evidence supporting a common link with the pathophysiology of PAH. Based on the available evidence, we propose a paradigm in which metabolic abnormalities, genetic injury, and systemic vascular dysfunction contribute to the systemic manifestations of PAH. This concept not only opens up interesting research possibilities, but also encourages consideration of extrapulmonary manifestations in the treatment of patients with PAH, since systemic vascular dysfunction would contribute to the systemic manifestations of PAH.
A hipertensão arterial pulmonar (HAP) é uma doença grave cujo resultado final da interação entre o tônus vascular e a alteração progressiva da remodelação das artérias pulmonares causa insuficiência cardíaca direita e morte. A remodelação vascular pulmonar é a principal alteração estrutural na hipertensão pulmonar. Esse processo envolve mudanças na íntima, média, adventícia e espaço perivascular, muitas vezes com a interação de células inflamatórias. Os mecanismos fisiopatológicos da HAP incluem uma série de modificações vasculares que produzem um aumento na resistência vascular pulmonar. As modificações vasculares que ocorrem na HAP incluem: vasoconstrição, proliferação do músculo liso, inflamação, apoptose endotelial, proliferação endotelial resistente à apoptose, fibrose, trombose in situ e, finalmente, lesões plexiformes. Até recentemente, a HAP era considerada uma doença restrita à circulação pulmonar. No entanto, há evidências crescentes de que os pacientes com HAP também apresentam disfunção vascular sistêmica, conforme evidenciado pela dilatação prejudicada mediada pelo fluxo da artéria braquial, fluxo sanguíneo cerebral anormal, miopatia esquelética e doença renal intrínseca. Dados recentes suportam uma ligação com os eventos genéticos e moleculares por trás da patogênese da HAP. Esta revisão serve como uma introdução aos principais achados sistêmicos em HAP e as evidências que apoiam uma ligação comum com a fisiopatologia da HAP. Com base nas evidências disponíveis, propomos um paradigma em que anormalidades metabólicas, lesão genética e disfunção vascular sistêmica contribuem para as manifestações sistêmicas da HAP. Esse conceito não apenas abre possibilidades interessantes de pesquisa, mas também incentiva a consideração das manifestações extrapulmonares no tratamento de pacientes com HAP, uma vez que a disfunção vascular sistêmica contribuiria para as manifestações sistêmicas da HAP.
ABSTRACT
Objective To systematically review the effects of exercise on systemic inflammation of chronic obstructive pulmonary disease (COPD) and skeletal muscle dysfunction. Methods The literature about the effect of exercise on COPD systemic inflammation and skeletal muscle dysfunction were retrieved from PubMed, Web of Science, CNKI, VIP and Wanfang data, until June, 2021, supplemented by reference review and manual retrieval. Results A total of 192 literatures were retrieved and eight were included, involving 245 subjects. The comprehensive results showed that exercise could decrease the level of pro-inflammatory factors and increase the level of anti-inflammatory factors. Exercise can improve the motor ability and skeletal muscle structure of patients with COPD. Exercise can improve systemic inflammation of COPD, which is related to the mode, intensity and duration of exercise. Exercise may affect ubiquitin-protease, insulin-like growth factors -1/phosphatidylinositol 3 kinase/Akt and other pathways by regulating the inflammatory response, and improve skeletal muscle dysfunction. Conclusion Exercise has certain effect on reducing systemic inflammation and improving skeletal muscle dysfunction.
ABSTRACT
Objective To systematically review the effects of exercise on systemic inflammation of chronic obstructive pulmonary disease (COPD) and skeletal muscle dysfunction. Methods The literature about the effect of exercise on COPD systemic inflammation and skeletal muscle dysfunction were retrieved from PubMed, Web of Science, CNKI, VIP and Wanfang data, until June, 2021, supplemented by reference review and manual retrieval. Results A total of 192 literatures were retrieved and eight were included, involving 245 subjects. The comprehensive results showed that exercise could decrease the level of pro-inflammatory factors and increase the level of anti-inflammatory factors. Exercise can improve the motor ability and skeletal muscle structure of patients with COPD. Exercise can improve systemic inflammation of COPD, which is related to the mode, intensity and duration of exercise. Exercise may affect ubiquitin-protease, insulin-like growth factors -1/phosphatidylinositol 3 kinase/Akt and other pathways by regulating the inflammatory response, and improve skeletal muscle dysfunction. Conclusion Exercise has certain effect on reducing systemic inflammation and improving skeletal muscle dysfunction.
ABSTRACT
Doxorubicin(DOX) is a widely used clinical anti-tumor drug for cancer. Unfortunately, DOX can also cause skeletal muscle dysfunction in a dose-dependent manner, leading to a significant decline in the quality of life of cancer patients. In this paper, we summarize the toxic effects of DOX, the characteristics of DOX-induced skeletal muscle dysfunction and its related mechanisms. We focus on pathological mechanisms, including oxidative stress, Ca2+overload, mitochondrial energy metabolism disorder, autophagy and apoptosis, nitric oxide concentration and amino acid metabolism and myogenic regulatory factor expression. Research prospects are outlined. It is expected to provide a theoretical basis for the clinical study of DOX toxicity.
ABSTRACT
PURPOSE: To investigate the clinical features associated with hypertropia and report the surgical outcomes of hypertropia coexisting with exotropia. METHODS: We reviewed the medical records of 148 patients with intermittent exotropia coexisting with hypertropia over 4 PD who received exotropia surgery. The cases accompanied by apparent paralytic strabismus such as superior oblique palsy were excluded. Patients were divided into group I(clinically diagnosed hypertropia) and group II (non-specific hypertropia) and the clinical features of coexisting hypertropia and surgical outcomes were analyzed. RESULTS: Among the 148 patients, group Iconsisted of 38 patients (26%) and group II of 110 patients (74%). The average amount of preoperative hypertropia angle in primary gaze was 9.58 +/- 3.89 PD and 6.62 +/- 2.69 PD in group I and II, respectively. Group I included 12 patients with dissociated vertical deviation (DVD), 10 patients with unilateral inferior oblique overaction, 13 patients with asymmetric bilateral inferior oblique overaction and 3 patients with superior oblique overaction. Group II included 19 patients with comitant hypertropia (17%), head tilt positive pattern (simulated superior oblique palsy) was found in 84 patients (76.3%) and variable incomitance was observed. In group I, 29 patients received simultaneous horizontal muscle with hypertropia surgery. Postoperative hypertropia angle in group I was 1.41 +/- 2.93 PD and 4 cases were considered surgical failure. In group II, hypertropia was resolved with horizontal muscle surgery only and the amount of postoperative hypertropia was 0.45 +/- 1.60 PD. CONCLUSIONS: In this study, vertical deviations in intermittent exotropia with concomitant hypertropia related to obvious oblique muscle dysfunction or DVD were corrected effectively by oblique or vertical rectus muscle surgery. Nonspecific hypertropia can be resolved after horizontal muscle surgery alone, however, for precise differential diagnosis, careful examination for variable clinical features is necessary before determining surgery.
Subject(s)
Humans , Diagnosis, Differential , Exotropia , Head , Medical Records , Paralysis , StrabismusABSTRACT
Objective To study the relationship between ischemic mitral regurgitation and geometric angles of the mitral valve leaflets in patients with coronary artery disease and papillary muscle dysfunction by transesophageal echocardiography(TEE) ,and to evaluate anatomy and pathophysiology mechanicm of the ischemic mitral regurgitation with left ventricular papillary muscle dysfunction .Methods A total of 84 subjects were enrolled in this study .All of the subjects were divided into group A (healthy volunteers constituted the control group ,n =40) ,group B (chronic inferior or posterior myocardial infarction patients with papillary muscle dysfunction group ,n =44) ,group C(patients from group B after mitral valvuloplasty surgery ,n = 20) .The relationship between mitral regurgitation and geometric angles of the mitral valve leaflets and mitral annulus were studied by TEE .Results Geometric angle between the mitral valve leaflets and mitral annulus were significantly larger in group B ,and geometric angles of the mitral valve leaflets and mitral annulus was positive correlated with degree of mitral regurgitation .Degree of mitral regurgitation significantly reduced in group C ,no significant difference was found at the geometric angles of the mitral valve leaflets and mitral valve annular compared with group A .Conclusions The degree of mitral regurgitation were highly correlated with geometric angles of the mitral valve leaflets and mitral valve annular in patients with left ventricular papillary muscle dysfunction caused by coronary heart disease .Repair of the mitral valve leaflets surgery can significantly reduce geometric angles of the mitral valve leaflets and mitral valve annular ,and reduce the degree of mitral regurgitation significantly .
ABSTRACT
@#Respiratory dysfunction is the primary cause of death early after cervical spinal cord injury, and it can be restored by electrical stimulation, magnetic stimulation, nerve transfer surgery, and cell transplantation. This paper reviewed the anatomy, clinical manifestations,and associated restoration techniques of respiratory muscle dysfunction after cervical spinal cord injury.
ABSTRACT
Background & objectives: There are very few studies that have investigated the muscle strength and endurance of upper limbs (UL) in chronic obstructive pulmonary disease (COPD). We undertook this study to measure and compare the skeletal muscle strength and endurance of UL in COPD patients and age matched healthy controls and to study the association between lung function parameters and UL muscle strength and endurance. Methods: Forty one COPD patients and 45 height and weight matched healthy subjects of the same age group were studied. UL skeletal muscle strength and endurance were measured using the hand grip dynamometer test. Forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), forced expiratory flow during 25-75% FVC (FEF25-75%) and peak expiratory flow rate (PEFR) were measured. The handgrip muscle strength and endurance between the two groups were compared and correlations between FVC and FEV1 with muscle strength and endurance were analyzed. Results: The mean handgrip strength and mean muscle endurance in COPD patients were significantly lesser than the normal subjects in both males and females (P<0.001). There was significant positive correlation between muscle strength and FVC in males (r2=0.32, P<0.05); and between muscle strength and FEV1 in females (r2=0.20, P<0.05). Interpretation & conclusion: The study showed that the handgrip muscle strength decreases as the FVC and FEV1 decrease in patients with COPD. Identifying those patients who have reduced strength and endurance will allow early interventions targeted at improving the quality of life of the patient.
ABSTRACT
Several studies have shown that poor exercise tolerance in Chronic Obstructive Pulmonary Disease (COPD) patients is multifactorial in origin. However, a major exercise-limiting factor in COPD is peripheral muscle dysfunction, particularly the muscles of the lower extremities, characterized by atrophic muscles and reduced fatigue resistance due to morphological and metabolic alterations of peripheral muscles. This chapter therefore evaluated the scientific evidence regarding the beneficial effect of lower extremities exercise in the pulmonary rehabilitation in COPD patients. The technical characteristics of this exercise training were also reviewed. Exercise training of lower limbs was recommended in respiratory rehabilitation of COPD patients. The lower extremities muscle exercise training provides significant benefits to patients with COPD in terms of reduction of dyspnea and improvemet in exercise capacity and in quality of life (quality level of evidence = A, strong recommendation). Higher-intensity exercise training and with interval exercise of the lower extrmities produces greater physiological benefits.
Diversos estudios han demostrado que la pobre tolerancia al ejercicio de los pacientes con Enfermedad Pulmonar Obstructiva Crónica (EPOC) es de origen multifactorial. Sin embargo, un importante factor limitante del ejercicio en los pacientes con EPOC es la disfunción muscular periférica, sobre todo de los músculos de las extremidades inferiores, que se caracteriza por atrofia muscular y reducida resistencia a la fatiga dado por alteraciones morfológicas y metabólicas de los músculos periféricos. En este capitulo se evaluó la evidencia científica que existe en cuanto a los beneficios del entrenamiento muscular de extremidades inferiores (EEII) en la rehabilitación respiratoria en pacientes con EPOC. También se revisan las características técnicas de dicho entrenamiento. Se recomienda la realización de entrenamiento muscular de EEII en rehabilitación respiratoria de pacientes con EPOC. El entrenamiento muscular de extremidades inferiores otorga significativos beneficios a los pacientes con EPOC en cuanto a disminuir la disnea, mejorar la capacidad de ejercicio y la calidad de vida (calidad de la evidencia A, recomendación fuerte). El entrenamiento de EEII de alta intensidad y con intervalos produce significativos beneficios fisiológicos.
Subject(s)
Humans , Exercise Therapy , Pulmonary Disease, Chronic Obstructive/rehabilitation , Lower Extremity/physiology , Chile , Consensus , Dyspnea/therapy , Evidence-Based Medicine , Quality of LifeABSTRACT
OBJECTIVE: To evaluate vaginal cone therapy in two phases, passive and active, in women with stress urinary incontinence. METHODS: A prospective study was conducted at the Department of Obstetrics and Gynecology, São Paulo University, Brazil. Twenty-four women with a clinical and urodynamic diagnosis of stress urinary incontinence were treated with vaginal cones in a passive phase (without voluntary contractions of the pelvic floor) and an active phase (with voluntary contractions), each of which lasted three months. Clinical complaints, a functional evaluation of the pelvic floor, a pad test, and bladder neck mobility were analyzed before and after each phase. RESULTS: Twenty-one patients completed the treatment. The reduction in absolute risk with the pad test was 0.38 (p<0.034) at the end of the passive phase and 0.67 (p<0.0001) at the end of the active phase. The reduction in absolute risk with the pelvic floor evaluation was 0.62 (p<0.0001) at the end of the passive phase and 0.77 (p<0.0001) at the end of the active phase. The reduction in absolute risk of bladder neck mobility was 0.38 (p<0.0089) at the end of the passive phase and 0.52 (p<0.0005) at the end of the active phase. Complete reversal of symptomatology was observed in 12 (57.1 percent) patients, and satisfaction was expressed by 19 (90.4 percent). CONCLUSION: Using vaginal cones in the passive phase, as other researchers did, was effective. Inclusion of the active phase led to additional improvement in all of the study parameters evaluated in women with stress urinary incontinence. Randomized studies are needed, however, to confirm these results.
Subject(s)
Adult , Female , Humans , Exercise Therapy/instrumentation , Muscle Contraction/physiology , Pessaries , Pelvic Floor/physiopathology , Urinary Incontinence, Stress/therapy , Exercise Therapy/methods , Patient Satisfaction , Prospective Studies , Treatment Outcome , Urinary Incontinence, Stress/physiopathologyABSTRACT
The electromyogram(EMG) of lateral pterygoid muscle (LP) in 43 patients with LP dysfunction was measured before, when and after the use of occlusal splint. The postural and clenching activity of superior LP decreased dramatically when patients were wearing the occlusal splint. Normal EMG was observed in patients with normal arthrograra when the symptoms and signs were eliminated or reduced by occlusal splint. The EMG of dysfunctional LP in some patients with anteriorly displaced disk recovered to that with normal function as the incoordinated condyle -disk rektion was corrected. However, LP dysfunction was still present in most patients with irreversible anterior disk displacement and disk perforation after splint therapy.