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Pulmonary Edema [keywords]
- Alpha-Klotho protects against oxidative damage in pulmonary epithelia. [JOURNAL ARTICLE]
- Am J Physiol Lung Cell Mol Physiol 2014 Jul 25.
Alpha-Klotho (αKlotho) exerts pleiotropic biologic actions. Heterozygous αKlotho haplo-insufficient mice (kl/+) appear normal at baseline except for age-related changes in the lung, suggesting heightened pulmonary susceptibility to αKlotho deficiency. We used in vivo and in vitro models to test whether αKlotho protects lung epithelia against injury. Normally, αKlotho is not expressed in the lung but circulating αKlotho levels are reduced ~40% in kl/+ mice and undetectable in homozygous αKlotho-deficient mice (kl/kl). kl/+ mice show distal air space enlargement at a given airway pressure with elevated lung oxidative damage marker (8-hydroxydeoxyguanosine; 8-OHdG); these abnormalities are exacerbated in kl/kl mice. Studies were performed in A549 lung epithelial cells and/or primary culture of alveolar epithelial cells. Hyperoxia (95% O2) and high inorganic phosphate concentrations (Pi, 3-5 mM) additively caused cell injury (lactate dehydrogenase release), oxidative DNA damage (8-OHdG), lipid oxidation (8-isoprostane), protein oxidation (carbonyl), and apoptosis (caspase-8 activity and TUNEL stain). Transfection of transmembrane or soluble αKlotho, or addition of soluble αKlotho-containing conditioned media, increased cellular antioxidant capacity (Cu- and Fe-based assays) via increased nrf1/2 transcriptional activity, and ameliorated hyperoxic and phosphotoxic injury. To validate the findings in vivo, we injected αKlotho-containing conditioned media into rat peritoneum before and during hyperoxia exposure, and found reduced alveolar interstitial edema and oxidative damage. We conclude that circulating αKlotho protects the lung against oxidative damage and apoptosis partly via increasing endogenous antioxidative capacity in pulmonary epithelia. Cytoprotection by αKlotho may play an important role in degenerative diseases of the lung.
- Protective effect of hesperidin against lung injury induced by intestinal ischemia/reperfusion in adult albino rats: Histological, immunohistochemical and biochemical study. [JOURNAL ARTICLE]
- Tissue Cell 2014 Jul 1.
Hesperidin is a naturally common flavonoid. It is an abundant and cheap by-product of citrus cultivation. It is reported to have antioxidative, anti-inflammatory and anticarcinogenic effects. This work was performed to investigate the possible protective role of hesperidin in ameliorating the effect of experimentally induced intestinal ischemia/reperfusion injury (I/R) on lung tissue, histologically, immunohistochemically and biochemically. Thirty male Wistar adult albino rats were randomized into three groups named: group I (control group); group II (I/R); and group III (I/R with hesperidin). Intestinal I/R was induced by occluding the superior mesenteric artery for 60min, followed by 120min of reperfusion period. Animals were given hesperidin orally 1h before the onset of ischemia. At the end of the reperfusion period the lung tissues were extracted for histopathological examination and immunohistochemical detection of the distribution of inducible nitric oxide synthase (iNOS). Pulmonary edema was evaluated by lung tissue wet/dry weight ratios. The levels of malondialdehyde (MDA, a biomarker of oxidative damage), myeloperoxidase (MPO, an index of the degree of neutrophil accumulation) and glutathione (GSH, a biomarker of protective oxidative injury) were also determined in all dissected tissues. Pretreatment with hesperidin (in group III) alleviated lung morphological changes noticed in I/R group and the levels of MDA and MPO were significantly decreased whereas those of GSH were significantly increased. Immunohistochemical study revealed a significant decrease in the iNOS. Hesperidin also significantly alleviated the formation of pulmonary edema as evidenced by the decreased organ wet/dry weight ratios. Hesperidin exerts a protective effect against lung damage induced by intestinal I/R injury in rats by reducing oxidative stress.
- Anaesthetic management of cytoreductive surgery followed by hyperthermic intrathoracic chemotherapy perfusion. [JOURNAL ARTICLE]
- J Cardiothorac Surg 2014 Jul 25; 9(1):125.
Macroscopic cytoreductive surgery and hyperthermic intrathoracic chemotherapy perfusion (HITHOC) is a new multimodal approach for selected patients with primary and secondary pleural tumors, which may provide the patient with better local tumor control and increased overall survival rate.We present a single-center study including 20 patients undergoing cytoreductive surgery and HITHOC between September 2008 and April 2013 at the University Medical Center Regensburg, Germany. Objective of the study was to describe the perioperative, anaesthetic management with special respect to pain and complication management.Anaesthesia during this procedure is characterized by increased intrathoracic airway and central venous pressure, hemodynamic alterations and the risk of systemic hypo- and hyperthermia. Securing an adequate intravascular volume is one of the primary goals to prevent decreased cardiac output as well as pulmonary edema. Transfusion of packed red blood cells (PRBC) was necessary in seven of 20 (35%) patients. Only two patients (10%) showed an impairment of coagulation in postoperative laboratory analysis. Perioperative forced diuresis is recommended to prevent postoperative renal insufficiency. Supplementary thoracic epidural analgesia in 13 patients (65%) showed a significant reduction of post-operative pain compared with peroral administration of opioid and non-opioid analgesics.This article summarizes important experiences of the anaesthesiological and intensive care management in patients undergoing HITHOC.
- Characterization of oleic acid-induced acute respiratory distress syndrome model in rat. [Journal Article, Research Support, Non-U.S. Gov't]
- Indian J Exp Biol 2014 Jul; 52(7):712-9.
Animal studies using oleic acid (OA) model to produce acute respiratory distress syndrome (ARDS) have been inconsistent. Therefore, the present study was undertaken to establish an acute model of ARDS in rats using OA and to characterize its effect on cardio-respiratory parameters and lethality. The trachea, jugular vein and femoral artery of anesthetized adult rats were cannulated. A dose of OA (30-90 microL; iv) was injected in each animal and changes in respiratory frequency (RF), heart rate (HR) and mean arterial pressure (MAP) were recorded. Minute ventilation and PaO2/FiO2 (P/F) ratio were also determined. At the end, lungs were excised for determination of pulmonary water content and histological examination. At all doses of OA, there was immediate decrease followed by increase in RF, however at 75 and 90 microL of OA, RF decreased abruptly and the animals died by 63 +/- 8.2 min and 19 +/- 6.3 min; respectively. In all the groups, HR and MAP changes followed the respiratory changes. The minute ventilation increased in a dose-dependent manner while the values of P/F ratio decreased correspondingly. Pulmonary edema was induced at all doses. Histological examination of the lung showed alveolar damage, microvascular congestion, microvascular injury, infiltration of inflammatory cells, pulmonary edema and necrosis in a dose-dependent manner. With these results, OA can be used to induce different grades of ARDS in rats and OA doses of 50, 60 and 75 microL resemble mild, moderate and severe forms of ARDS respectively. Hence, OA model serves as a useful tool to study the pathophysiology of ARDS.
- The clinical and integrated management of COPD. An official document of AIMAR (Interdisciplinary Association for Research in Lung Disease), AIPO (Italian Association of Hospital Pulmonologists), SIMER (Italian Society of Respiratory Medicine), SIMG (Italian Society of General Medicine). [Journal Article]
- Multidiscip Respir Med 2014; 9(1):25.
COPD is a chronic pathological condition of the respiratory system characterized by persistent and partially reversible airflow obstruction, to which variably contribute remodeling of bronchi (chronic bronchitis), bronchioles (small airway disease) and lung parenchyma (pulmonary emphysema). COPD can cause important systemic effects and be associated with complications and comorbidities. The diagnosis of COPD is based on the presence of respiratory symptoms and/or a history of exposure to risk factors, and the demonstration of airflow obstruction by spirometry. GARD of WHO has defined COPD "a preventable and treatable disease". The integration among general practitioner, chest physician as well as other specialists, whenever required, assures the best management of the COPD person, when specific targets to be achieved are well defined in a diagnostic and therapeutic route, previously designed and shared with appropriateness. The first-line pharmacologic treatment of COPD is represented by inhaled long-acting bronchodilators. In symptomatic patients, with pre-bronchodilator FEV1 < 60% predicted and ≥ 2 exacerbations/year, ICS may be added to LABA. The use of fixed-dose, single-inhaler combination may improve the adherence to treatment. Long term oxygen therapy (LTOT) is indicated in stable patients, at rest while receiving the best possible treatment, and exhibiting a PaO2 ≤ 55 mmHg (SO2 < 88%) or PaO2 values between 56 and 59 mmHg (SO2 < 89%) associated with pulmonary arterial hypertension, cor pulmonale, or edema of the lower limbs or hematocrit > 55%. Respiratory rehabilitation is addressed to patients with chronic respiratory disease in all stages of severity who report symptoms and limitation of their daily activity. It must be integrated in an individual patient tailored treatment as it improves dyspnea, exercise performance, and quality of life. Acute exacerbation of COPD is a sudden worsening of usual symptoms in a person with COPD, over and beyond normal daily variability that requires treatment modification. The pharmacologic therapy can be applied at home and includes the administration of drugs used during the stable phase by increasing the dose or modifying the route, and adding, whenever required, drugs as antibiotics or systemic corticosteroids. In case of patients who because of COPD severity and/or of exacerbations do not respond promptly to treatment at home hospital admission should be considered. Patients with "severe" or "very severe" COPD who experience exacerbations should be carried out in respiratory unit, based on the severity of acute respiratory failure. An integrated system is required in the community in order to ensure adequate treatments also outside acute care hospital settings and rehabilitation centers. This article is being simultaneously published in Sarcoidosis Vasc Diffuse Lung Dis 2014, 31(Suppl. 1);3-21.
- Extracorporeal membrane oxygenation saved a mother and her son from fulminant peripartum cardiomyopathy. [Journal Article]
- J Obstet Gynaecol Res 2014 Jul; 40(7):1940-3.
A 34-year-old full-term pregnant woman presented with abruptly aggravating dyspnea. A chest X-ray showed pulmonary edema, and an echocardiogram revealed a left ventricular ejection fraction of 39%. Despite conventional medical treatment for acute heart failure and mechanical ventilation, hypoxia and metabolic acidosis were aggravated, and the fetal heart rate decreased to 90 b.p.m., suggestive of fetal distress. We decided to initiate extracorporeal membrane oxygenation (ECMO) and perform a cesarean section. The infant was successfully delivered without hypoxic brain damage. The patient was weaned from ECMO 6 days after delivery and was extubated 1 day after discontinuation of ECMO. Left ventricular systolic function had completely recovered at this time. This is the first report of a patient with peripartum cardiomyopathy who had a successful delivery with the support of ECMO, demonstrating that ECMO can serve as a rescue therapy, not only treating peripartum cardiomyopathy but also permitting a safe delivery.
- Consecutive transcatheter valve-in-valve implantations: the first in the aortic position, the second in the mitral position, in a patient with failing aortic and mitral bioprostheses. [Journal Article]
- BMJ Case Rep 2014.
A 69-year-old man with a failing aortic valve homograft and failing mitral valve xenograft was admitted with an inability to complete full sentences and pulmonary oedema with right ventricular overload. Severe aortic and mitral regurgitation, severe biventricular impairment and pulmonary hypertension were confirmed on transthoracic and transoesophageal echocardiography. An urgent transfemoral valve-in-valve transcatheter valve implantation (TAVI) was performed within the aortic valve homograft with full resolution of aortic regurgitation. Three months later, a semielective trans-apical valve-in-valve procedure was performed in the mitral position, under cardiopulmonary bypass, with full resolution of mitral regurgitation. His exercise tolerance increased from 5 yards to half a mile. This case report summarises a staged double valve-in-valve procedure in a patient who had three previous sternotomies and who had severe heart failure due to failing aortic and mitral bioprostheses. We report two different delivery approaches, using two different transcatheter devices, and describe valve-in-valve techniques, including cardiopulmonary bypass, in the catheter laboratory.
- Acclimatization to Long-Term Hypoxia: Gene Expression in Ovine Carotid Arteries. [JOURNAL ARTICLE]
- Physiol Genomics 2014 Jul 22.
Exposure to acute high altitude hypoxia is associated with an increase in cerebral blood flow (CBF) as a consequence of low arterial O2 tension. However, with acclimatization response to high altitude, CBF returns to levels similar to those at sea-level, and blood flow is maintained by increase in angiogenesis. Of consequence, dysregulation of the acclimatization responses and CBF can result in acute mountain sickness, acute cerebral and/or pulmonary edema. To elucidate the signal transduction pathways involved in successful acclimatization to high altitude, we tested the hypothesis that high-altitude associated long-term hypoxia (LTH) results in changes in gene expression of critical signaling pathways in ovine carotid arteries. We acclimatized non-pregnant adult sheep to 3801 m altitude for ∼ 110 days and conducted oligonucleotide microarray experiments on carotid arteries. Of total 118 regulated genes, 60 genes were significantly upregulated and 58 genes were significantly downregulated (each > 2-fold; P < 0.05). Major upregulated genes included suprabasin, myelin basic protein, apoliprotein B; whereas major downregulated genes included protein kinase C delta, endonucleas V, BCL6. Several of these genes are known to activate the ERK canonical signal transduction pathway and the process of angiogenesis. We conclude that the altered signal transduction molecules involved in high altitude acclimatization are associated ERK activation and angiogenesis.
- 4-Hydroxyphenylacetic Acid Attenuated Inflammation and Edema via Suppressing HIF-1α in Seawater Aspiration-Induced Lung Injury in Rats. [Journal Article]
- Int J Mol Sci 2014; 15(7):12861-84.
4-Hydroxyphenylacetic acid (4-HPA) is an active component of Chinese herb Aster tataricus which had been widely used in China for the treatment of pulmonary diseases. The aim of this study is to investigate the effect of 4-HPA on seawater aspiration-induced lung injury. Pulmonary inflammation and edema were assessed by enzyme-linked immunosorbent assay (ELISA), bronchoalveolar lavage fluid (BALF) white cell count, Evans blue dye analysis, wet to dry weight ratios, and histology study. Hypoxia-inducible factor-1α (HIF-1α) siRNA and permeability assay were used to study the effect of 4-HPA on the production of inflammatory cytokines and monolayer permeability in vitro. The results showed that 4-HPA reduced seawater instillation-induced mortality in rats. In lung tissues, 4-HPA attenuated hypoxia, inflammation, vascular leak, and edema, and decreased HIF-1α protein level. In primary rat alveolar epithelial cells (AEC), 4-HPA decreased hypertonicity- and hypoxia-induced HIF-1α protein levels through inhibiting the activations of protein translational regulators and via promoting HIF-1α protein degradation. In addition, 4-HPA lowered inflammatory cytokines levels through suppressing hypertonicity- and hypoxia-induced HIF-1α in NR8383 macrophages. Moreover, 4-HPA decreased monolayer permeability through suppressing hypertonicity and hypoxia-induced HIF-1α, which was mediated by inhibiting vascular endothelial growth factor (VEGF) in rat lung microvascular endothelial cell line (RLMVEC). In conclusion, 4-HPA attenuated inflammation and edema through suppressing hypertonic and hypoxic induction of HIF-1α in seawater aspiration-induced lung injury in rats.
- Complications in the clinical course of tako-tsubo cardiomyopathy. [JOURNAL ARTICLE]
- Int J Cardiol 2014 Jul 11.
This study evaluated the frequency, severity and outcome of complications in the clinical course of tako-tsubo cardiomyopathy (TTC).TTC is regarded as a benign disease since left ventricular (LV) function returns to normal within a short time. However, severe complications have been reported in selected patients.From 37 hospitals, 209 patients (189 female, age 69±12years) were prospectively included in a TTC registry.Complications developed in 108/209 patients (52%); 23 (11%) had >2 complications. Complications occurred median 1day after symptom onset, and 77% were seen within 3days. Arrhythmias were documented in 45/209 patients (22%) including atrial fibrillation in 32 (15%) and ventricular tachycardia in 17 (8%). Of 8 patients resuscitated (4%), 6 survived. Additional complications were right ventricular involvement (24%), pulmonary edema (13%), cardiogenic shock (7%), transient intraventricular pressure gradients (5%), LV thrombi (3%) and stroke (1%). During hospitalization, 5/209 patients (2.5%) died. Patients with complications were older (70±13 vs 67±10years, p=0.012), had a higher heart rate (91±26 vs 83±19/min, p=0.025), more frequently Q\ waves on the admission ECG (36% vs 21%, p=0.019) and a lower LV ejection fraction (47±15 vs 54±14%, p=0.002). Multivariate regression analysis identified Q-waves on admission (OR 2.49, 95% CI 1.23-5.05, p=0.021) and ejection fraction ≤30% (OR 4.03, 95% CI 1.04-15.67, p=0.022) as independent predictors for complications.TTC may be associated with severe complications in half of the patients. Since the majority of complications occur up to day 3, monitoring is advisable for this time period.