Non-respiratory Functions Of Lung Research Articles

Features of the course and treatment of bronchial asthma combined with arterial hypertension: a review

Bronchial asthma (BA) is a serious medical and social problem. Many patients with asthma have various concomitant chronic diseases, among which the pathology of the cardiovascular system occupies an important place. Most often, asthma occurs with arterial hypertension (AH). This concurrence can lead to mutual aggravation and progression of these diseases and may negatively affect the prognosis. Usually, difficulties appear when choosing the most effective therapy for BA along with hypertension. This review aimed to analyse the available publications on the problem of the combination of BA and hypertension. A review of the literature presents the summary, examines data on prevalence and indicates risk factors for the development of hypertension among patients with asthma. The coexistence of these diseases is more typical in older people. The review includes questions regarding the pathophysiology of this comorbidity. The role of impaired gas exchange and hypoxia, endothelial dysfunction, participation of the nitric oxide system and obesity in the development of hypertension in combination with asthma are highlighted. The significance of impaired nonrespiratory lung function is shown, and the inflammation features in this comorbid pathology are indicated, as well as the contribution of numerous genes to the development of asthma along with hypertension. In the literature, 330 common genes have been identified that may be involved in the molecular mechanisms of asthma and hypertension. This study shows the effect of concomitant hypertension on the course, asthma control and quality of life of the patients. In addition, the article shows modern approaches to effective therapy with the main groups of drugs used to treat these diseases. To date, studies have demonstrated the prevalence of the combination of asthma and hypertension in the structure of comorbidity, mutual influence and aggravation of these pathologies. Coexistence of BA and hypertension increases the severity of clinical symptoms. This article shows the important aspects of the treatment of a combination of diseases. The need for a thorough assessment of the safety of pharmacological therapy for BA along with hypertension has been demonstrated.

Evaluation of the hypocoagulatory role of the lungs using thromboelastography in postpartum women with multiple organ failure

Aim. To evaluate the hypocoagulatory role of the lungs in postpartum women with multiple organ failure using thromboelastography.Materials and methods. Sixty-six postpartum women aged 19 to 45 with multiple organ failure were examined. Postpartum women were divided into three groups depending on the nonrespiratory lung function impairment stage.The first group included 23 (34.8%) postpartum women with compensated nonrespiratory pulmonary function; the second group included 24 (36.4%) postpartum women with subcompensated stage of nonrespiratory pulmonary function disorder; the third group included 19 (28.8%) postpartum women with a decompensated form of nonrespiratory pulmonary function disorder.Results and discussion. When analyzing the results of studies in healthy individuals noted TEG constant R reflecting the rate of thromboplastin formation. Thrombin constant K, nonspecific coagulation constant R+K, prothrombin use constant R/K, T - total clotting, syneresis (compaction) C are prolonged in the arterial blood flowing from the lungs compared to the mixed venous blood.Conclusions. In healthy humans, the lungs act as a coagulation filter, reducing the hemostatic potential of the blood. The hypocoagulatory function of the lungs in postpartum women with multiple organ failure is impaired in stages. The thromboelastographic hemostasis study allows rapid and complete assessment of the hypocoagulatory role of the lungs in parturient women with multiple organ failure.

Treatment of Acute Lung Abscesses Considering their Non-Respiratory Function in Patients with Diabetes

During the examination and treatment of 465 patients with acute lung abscesses on the background ofdiabetes mellitus, a preoperative preparation program was developed that takes into account the phase of theprocess (group 1 - septic course of the process, group 2 - stabilization, group 3 - remission), the severity ofendotoxemia and non-respiratory lung function. Patients of the 1st group against the background of basiclong-term intra-arterial catheter therapy used the scheme of correction of non-respiratory function of thelungs that we developed, sanitized purulent foci with an electrolyzed solution of sodium hypochlorite. In202 (79.9%) of 254 patients of the 1st group, it was effective that allowed to refuse the operation, while only52 (40.6%) were not operated on in the 2nd, and 26 in the 3rd (31.3%) patients. In parallel, a pronouncednormalizing effect was achieved in correcting the degree of violation of non-respiratory lung functionagainst the background of delimitation and stabilization of the process. This allowed in 109 (60.9%) of 179operated patients to confine themselves to lung resection with 8.7% of postoperative complications in the 1stgroup versus 18.4% in the 2nd and 24.6% in the 3rd, which emphasizes the effectiveness of our preoperativepreparation.

Analysis of the current state of the postoperative pulmonary complications issue in abdominal surgery

Purpose: based on the analysis of the scientific literature data, to determine the relevance of postoperative pulmonary complications (PPCs) issue in abdominal surgery, as well as to examine the causes and modern methods of their development prevention in patients with unaffected lungs.Conclusions. Indicators of PPCs in abdominal surgery range from 17 % to 88 %, and their development leads to an increase in lethality, the cost of treatment, and the length of stay in a medical institution. Mechanical ventilation (MV) is non-physiological and can cause ventilator-associated lung injury (VALI), adversely affects the respiratory muscles, as well as non-respiratory lung function. The above factors are prominent in PPCs development causing an increase in morbidity and mortality in the postoperative period. Extensive open abdominal operations, especially upper abdominal surgical procedures, increase the risk of PPCs development. In the analysis of modern studies, there has been a clear “paradigm shift” from the prevention of death and complications of lung damage to the prevention of respiratory complications development itself. To date, the risk factors have been identified and scales have been developed that allow predicting PPCs development in a timely and reliable manner, one of which is the ARISCAT scale. There are various measures to prevent VALI and PPCs development and the main ones include low respiratory volume, the use of positive end-expiratory pressure (PEEP) and alveolar recruitment maneuvers. The combination of these measures has been termed “protective ventilation”. It has been proved that protective MV during abdominal surgery in patients with unaffected lungs can reduce the risk of PPCs development.

РОЛЬ ЛЕГКИХ В ПОДДЕРЖАНИИ БАЛАНСА СИСТЕМЫ ГЕМОСТАЗА НА ФОНЕ ХРОНИЧЕСКОГО ВОЗДЕЙСТВИЯ ВОЗДУШНЫХ ПОЛЛЮТАНТОВ

The aim of the study is to determine the nature of the consequences of non-respiratory lung function disorders and their influence on the hemostatic system in chronic inhalation of industrial hydrogen sulfide gas (HS). There were studied the parameters of hemostasis system (the number and function of platelet, total clotting time, level of soluble fibrin-monomer complex and D-dimer, speed of XIIa-dependent euglobulin lysis, the activity of Willebrand factor and factors VIII, protein C and inhibitor of tissue plasminogen activator-1 (TPA-1), the content of antithrombin III and plasminogen) in 146 white laboratory male rats taking into account the artery-venous difference. Blood collection was carried out from the abdominal aorta (pars abdominalis aortae) ("after the lungs") and from the posterior vena cava (vena cava caudalis) ("to the lungs", that excludes the influence of the liver). The rats were divided into 9 groups: four groups were experimental, which were exposed to HS for one month (20 animals), two months (20 animals), three months (19 animals) and four months (19 animals). HS was fed into chambers at a concentration of 70±2.34 mg/m3 by static method (once). Inhalation of rats with gas lasted for 4 hours a day, 5 days a week. The control groups were rats placed in cells with a normal air composition in a similar mode for a period of one, two, three and four months (12 individuals each). The reference parameters of the hemostatic system were determined before the experiment in a group of 20 rats. It was found that the artery-venous difference in the indicators of soluble fibrin-monomer complex (p<0.05), the content of antithrombin III (p<0.05), the activity of protein C (p<0.01) is more pronounced in the groups of the 1st month of exposure to HS. Increased activity of platelets (p<0.05), of Willebrand factor (p<0.05) and TPA-1 (p<0.001), as well as slowing of fibrinolysis (p<0.05) indicates the damage to the endothelium of pulmonary capillaries by the 4th month of HS inhalation and the decrease of ability of the lungs to regulate hemostasiological balance.

Adipokine signaling in bronchial asthma in combination with overweight

We examined 173 overweight patients with bronchial asthma (BA) using ELISA method, identifying leptin, adiponectin and resistin from samples of plasma and sputum. The idea that BA is heterogeneous in relation to adipokines signaling dependant on the variant of BA, severity of disease, sex and age of patients has been advanced. The imbalance of proinflammatory (leptin, resistin) and antiinflammatory (adiponectin) signaling molecules, at the system level, organ level (in sputum) and target cells (mononuclear cells peripheral blood) was revealed. The identification of the phenomenon of presence of adipokines (leptin and resistin) in the sputum is considered as one of mechanisms of adipokines elimination during exacerbation of BA, which allows to extend the understanding nonrespiratory lung function in BA. Refs 15. Figs 5. Tabl. 11.

Optimal Positive End-Expiratory Pressure Fails to Preserve Nonrespiratory Lung Function in Acute Lung Injury

Optimal Positive End-Expiratory Pressure Fails to Preserve Nonrespiratory Lung Function in Acute Lung Injury

HEALTH EFFECTS OF SULFUR-RELATED ENVIRONMENTAL AIR POLLUTION. II. Cellular and Molecular Parameters of Injury

Recently, concern has been raised about effects related to environmental sulfur and/ or acidic aerosols. To assess long-term effects on nonrespiratory lung function, 8 beagle dogs were exposed over a period of 13 mo for 16.5 h/day to a neutral sulfite aerosol at a sulfur(IV) concentration of 0.32 mg m-3 and for 6 h/day to an acidic sulfate aerosol providing a hydrogen concentration of 15.2 mumol m-3 for inhalation. Prior to exposure the dogs were kept under clean air conditions for 16 mo to establish physiological baseline values for each animal. A second group of eight dogs (control) was kept for the entire study under clean air conditions. No clinical symptoms were identified that could be related to the combined exposure. Biochemical and cellular parameters were analyzed in sequential bronchoalveolar lavage (BAL) fluids. The permeability of the alveolocapillary membrane and diethylenetriaminepentaacetic acid (DTPA) clearance was not affected. Similarly, oxidant burden of the epithelial lining fluid evaluated by levels of oxidation products in the BAL fluid protein fraction remained unchanged. Both the lysosomal enzyme- N -acetylglucosaminidase and the alpha-1-AT were increased (p < .05). In contrast, the cytoplasmic marker lactate dehydrogenase remained unchanged, indicating the absence of severe damages to epithelial cells or phagocytes. Various surfactant functions were not altered during exposure. Three animals showed elevated levels of the type II cell-associated alkaline phosphatase (AP), indicating a nonuniform response of type II cells. Significant correlations were found between AP and total BAL protein, but not between AP and lactate dehydrogenase, suggesting proliferation of alveolar type II cells. Absolute and relative cell counts in the BAL fluid were not influenced by exposure. Alveolar macrophages showed no alterations with regard to their respiratory burst upon stimulation with opsonized zymosan. The percentage of alveolar macrophages capable of phagocytozing latex particles was significantly decreased (p < .05), while the phagocytosis index was not altered. In view of the results of this and previous studies, we conclude that there is no synergism of effects of these two air pollutants on nonrespiratory lung functions. It is hypothesized that antagonistic effects of these air pollutants on phospholipase A2-dependent pathways account for compensatory physiological mechanisms. The results emphasize the complexity of health effects on lung functions in response to the complex mixture of air pollutants and disclose the precariousness in the risk assessment of air pollutants for humans.

Collagen Biosynthesis

Collagen is the major structural protein of the lung. At least five genetically distinct collagen types have been identified in lung tissue. However, the precise role of collagen in nonrespiratory lung function is not well understood, in part because of the difficulties inherent in studying lung collagen, regardless of the type of assay used. A major problem is the insolubility of lung collagen; generally less than 20% of total lung collagen can be solubilized as intact chains, even with harsh extraction procedures. Since such collagen may not be representative of total lung collagen, errors in quantitating collagen types, for example, may arise from using such material. Measurement of total lung collagen content may also pose problems, unless appropriate parameters of normalization are chosen. Biopsy dry weight, protein content, and DNA content, for example, may all change in certain disease states. Despite these difficulties, a number of changes in lung collagen have been documented in experimental pulmonary fibrosis, including increased collagen content, increased collagen synthesis rates, and changes in collagen type ratios. Many questions remain. For example, why do diverse toxic substances appear to cause essentially the same fibrotic response, even though initial sites of damage may vary? Conversely, why do similar toxic substances, such as ozone and NO2, cause diverse responses (fibrosis and emphysema, respectively)? Much work remains to be done to elucidate the mechanisms underlying the lung's choice of response.

Collagen biosynthesis.

Collagen is the major structural protein of the lung. At least five genetically distinct collagen types have been identified in lung tissue. However, the precise role of collagen in nonrespiratory lung function is not well understood, in part because of the difficulties inherent in studying lung collagen, regardless of the type of assay used. A major problem is the insolubility of lung collagen; generally less than 20% of total lung collagen can be solubilized as intact chains, even with harsh extraction procedures. Since such collagen may not be representative of total lung collagen, errors in quantitating collagen types, for example, may arise from using such material. Measurement of total lung collagen content may also pose problems, unless appropriate parameters of normalization are chosen. Biopsy dry weight, protein content, and DNA content, for example, may all change in certain disease states. Despite these difficulties, a number of changes in lung collagen have been documented in experimental pulmonary fibrosis, including increased collagen content, increased collagen synthesis rates, and changes in collagen type ratios. Many questions remain. For example, why do diverse toxic substances appear to cause essentially the same fibrotic response, even though initial sites of damage may vary? Conversely, why do similar toxic substances, such as ozone and NO2, cause diverse responses (fibrosis and emphysema, respectively)? Much work remains to be done to elucidate the mechanisms underlying the lung's choice of response.

The surgical implications of nonrespiratory lung function

Interest in nonrespiratory lung function has increased with the realization that the injured lung might influence pathological processes in distant vascular beds. Alterations in the lung's ability to metabolize or release biologically active compounds (prostaglandins, kinins) may influence distant cellular metabolism, local blood flow, and vascular permeability. Fortunately, pharmacological manipulation of these systems which may contribute to systemic hypotension during sepsis, positive pressure ventilation, trauma, and anaphylaxis is feasible. Furthermore, since the lung is an important way station in the storage and metabolism of many drugs, the contribution of the lung must be recognized when attempting to unravel complex drug interactions. Indeed, an understanding of the lung's handling of airborne pollutants has led to the development of a simple blood test to identify individuals with increased risk of developing bronchogenic carcinoma. Acute respiratory insufficiency is a multifaceted malady from which 66,000 people died in 1977. Clearly, nonrespiratory pulmonary dysfunction contributes to respiratory disease and may exacerbate nonpulmonary disorders. The vulnerability of the lung to insult and the ability of the injured lung to influence distant organ function is now better appreciated. The systemic manifestations of altered pulmonary metabolism are manifested characteristically in acute injury and should therefore be appreciated and incorporated into a rational, surgical approach to therapy.

Distribution of blood flow in the lungs in acute pulmonary edema in dogs.

ArticleDistribution of blood flow in the lungs in acute pulmonary edema in dogs.A L Muir, D L Hall, P Despas, and J C HoggA L Muir, D L Hall, P Despas, and J C HoggPublished Online:01 Dec 1972https://doi.org/10.1152/jappl.1972.33.6.763MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByLung transplant after prolonged ex vivo lung perfusion: predictors of allograft function in swine31 July 2018 | Transplant International, Vol. 31, No. 12Pulmonary HemodynamicsPhosphoinositide 3-kinase, Src, and Akt modulate acute ventilation-induced vascular permeability increases in mouse lungsTakashige Miyahara, Kazutoshi Hamanaka, David S. Weber, Douglas A. Drake, Mircea Anghelescu, and James C. Parker1 July 2007 | American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol. 293, No. 1The spatial distribution of pulmonary lesions in severe ARDS An autopsy study of 35 casesPathology - Research and Practice, Vol. 194, No. 7Experimental Hydrostatic Pulmonary Edema in Rabbit Lungs: MorphologyAmerican Review of Respiratory Disease, Vol. 147, No. 4A quantitative correlation of extravascular lung water accumulation with vascular permeability and hydrostatic pressure measurements: a positron emission tomography studyJournal of Critical Care, Vol. 5, No. 3The effects of norepinephrine on gas exchange and regional blood flows after massive bead embolizationJournal of Critical Care, Vol. 5, No. 3Respiratory and non-respiratory lung function indices during the development and resolution ofO,S,S-trimethyl phosphorodithioate-induced lung damage in the rat. A chemical model of adult respiratory distress syndromeJournal of Applied Toxicology, Vol. 7, No. 6Effect of edema on segmental vascular resistance in isolated lamb lungs determined by micropuncture.Circulation Research, Vol. 61, No. 2Pulmonary interstitial resistanceAnnals of Biomedical Engineering, Vol. 15, No. 2Gas Exchange in Acute Lung InjuryCritical Care Clinics, Vol. 2, No. 3Pulmonary Interstitial Spaces and Lymphatics1 January 2011Pulmonary EdemaVeterinary Clinics of North America: Small Animal Practice, Vol. 15, No. 5Sepsis and Pulmonary EdemaClinics in Chest Medicine, Vol. 6, No. 3Adult respiratory distress syndrome--I. Aetiology and mechanisms.Postgraduate Medical Journal, Vol. 60, No. 706The Influence of Cardiovascular Function on Gas ExchangeClinics in Chest Medicine, Vol. 4, No. 2Mechanisms and consequences of pulmonary edema: Cardiac lung, shock lung, and principles of ventilatory therapy in adult respiratory distress syndromeAmerican Heart Journal, Vol. 103, No. 1GAS EXCHANGE IN THE ADULT RESPIRATORY DISTRESS SYNDROMEClinics in Chest Medicine, Vol. 3, No. 1Regional edema formation in isolated perfused dog lungs.Circulation Research, Vol. 48, No. 1Pulmonary OedemaBritish Journal of Diseases of the Chest, Vol. 74Ozone exposure, adaptation, and changes in lung elasticityEnvironmental Research, Vol. 19, No. 2Der Einfluß von Blut und parenteral zugeführter Flüssigkeit auf die Lungenstrombahn und Methoden zur quantitativen Erfassung statischer und dynamischer Flüssigkeitsvolumina in der LungeRelationship between colloid osmotic pressure and pulmonary artery wedge pressure in patients with acute cardiorespiratory failureThe American Journal of Medicine, Vol. 64, No. 4Ventilatory management in acute pulmonary edemaThe American Journal of Medicine, Vol. 54, No. 5Lung water balance More from this issue > Volume 33Issue 6December 1972Pages 763-9 https://doi.org/10.1152/jappl.1972.33.6.763PubMed4643854History Published online 1 December 1972 Published in print 1 December 1972 Metrics