Bronchial Blood Flow

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Daniel L. Traber - One of the best experts on this subject based on the ideXlab platform.

  • Direct delivery of low-dose 7-Nitroindazole into the Bronchial artery attenuates pulmonary pathophysiology after smoke inhalation and burn injury in an ovine model
    Shock (Augusta Ga.), 2011
    Co-Authors: Atsumori Hamahata, Hiroyuki Sakurai, Lillian D. Traber, Perenlei Enkhbaatar, Hal K. Hawkins, Robert A. Cox, Matthias Lange, Daniel L. Traber
    Abstract:

    ABSTRACTBronchial circulation plays a critical role in the pathophysiology of burn and smoke inhalation–induced acute lung injury. A 10-fold increase in Bronchial Blood Flow is associated with excessive production of nitric oxide (NO) following smoke inhalation and cutaneous burn. Because an increas

  • Impact of Bronchial circulation on Bronchial exudates following combined burn and smoke inhalation injury in sheep.
    Burns : journal of the International Society for Burn Injuries, 2010
    Co-Authors: Naoki Morita, Lillian D. Traber, Perenlei Enkhbaatar, Martin Westphal, Marc O. Maybauer, Dirk M. Maybauer, Kazunori Murakami, Hal K. Hawkins, Robert A. Cox, Daniel L. Traber
    Abstract:

    Abstract We previously reported Bronchial circulation contributes to pulmonary edema and increases shunt fraction following smoke inhalation, and Bronchial Blood Flow significantly increases in inhalation injury. We hypothesized reduction of Bronchial Blood Flow reduces exudation to the airway and ameliorates lung injury from combined burn and smoke insults (BS (2) Bronchial artery left intact and injured (injury + no ligation group); (3) Bronchial artery ligated but not injured (no injury + ligation group) were subjected to a flame burn and inhalation injury under halothane anesthesia. Parameters were analyzed using Scheffe's post hoc test ( P Results Pulmonary gas exchange (PaO 2 /FiO 2 ) improved in injury + ligation group. Further, obstruction score, an index of airway cast formation, significantly changed between injury + no ligation group compared to both ligation groups. Conclusion Bronchial circulation plays a significant role in lung injury after B&S injury, and reduction of Bronchial Blood Flow by Bronchial artery ligation reduces Bronchial exudates, resulting in improved gas exchange.

  • Sclerosis therapy of Bronchial artery attenuates acute lung injury induced by burn and smoke inhalation injury in ovine model
    Burns : journal of the International Society for Burn Injuries, 2010
    Co-Authors: Atsumori Hamahata, Hiroyuki Sakurai, Perenlei Enkhbaatar, Motohiro Nozaki, Daniel L. Traber
    Abstract:

    Abstract Introduction In burned sheep, we showed more than a 10-fold increase in Bronchial Blood Flow following smoke inhalation. It was previously reported that sclerosis of the Bronchial artery prior to smoke exposure reduces the pathophysiology of the inhalation insult. We hypothesized that sclerosis of the Bronchial artery after insult attenuates smoke/burn-induced acute lung injury. Methods Through an incision at the 4th intercostal space, a catheter was placed via the esophageal artery into the Bronchial artery such that the Bronchial Blood Flow remained intact. Acute lung injury was induced by a 40% total body surface area, 3rd degree cutaneous burn and smoke inhalation. Adult female sheep ( n  = 18, 35.6 ± 1.0 kg) were divided into three groups following the injury: (1) sclerosis group: 1 h after injury, 4 mL of 70% ethanol was injected into Bronchial artery via Bronchial catheter, n  = 6; (2) control group: 1 h after injury, an equal dose of saline was injected into Bronchial artery via the Bronchial catheter, n  = 6; (3) sham group: no injury and no treatment, n  = 6. The experiment was conducted in awake animals for 24 h. Results Bronchial Blood Flow, measured by microspheres, was significantly reduced after ethanol injection in the sclerosis group. Pulmonary function, evaluated by measurement of Blood gas analysis, pulmonary mechanics, and pulmonary transvascular fluid flux, was severely impaired in the control group. However, pulmonary function was significantly improved by Bronchial artery sclerosis. Conclusion The results of our study clearly demonstrate a crucial role of enhanced Bronchial circulation in thermal injury-related morbidity. Decreasing Bronchial circulation using pharmacological agents may be an effective strategy in management of burn patients with concomitant smoke inhalation injury.

  • Effect of ablated Bronchial Blood Flow on survival rate and pulmonary function after burn and smoke inhalation in sheep
    Burns : journal of the International Society for Burn Injuries, 2009
    Co-Authors: Atsumori Hamahata, Perenlei Enkhbaatar, Sakurai Hiroyuki, Motohiro Nozaki, Daniel L. Traber
    Abstract:

    Summary The Bronchial circulation plays a significant role in the pathophysiological changes of burn and smoke-inhalation injury. Bronchial Blood Flow markedly increases immediately after inhalational injury. This study examines whether the ablation of the Bronchial artery attenuates pathophysiological changes and improves survival after burn and smoke-inhalational injury in an ovine model. Acute lung injury was induced by 40% total body surface-area third-degree cutaneous burn and cotton smoke inhalation (48 breaths of cotton smoke, n  = 6); (2) ablation (injured, ablated Bronchial artery, n  = 6). Ablation of the Bronchial artery was performed 72 h before the injury. The experiment was continued for 96 h. Burn and smoke-inhalation injury significantly increased regional Blood Flow in the bronchi. Ablation of the Bronchial artery significantly reduced acute regional Blood Flow increases in the proximal and distal bronchi. All animals in the ablation group survived to 96 h. Four of these were successfully weaned off the ventilator. Three animals of the sham group met standardised euthanasia criteria at 60 h, while another met the criteria at 78 h. The lung wet-to-dry weight ratio, histology score and myeloperoxidase (MPO) activity were significantly increased by the insult, but ablation of the Bronchial artery attenuated these changes. Burn and smoke-inhalation injury induced a significant increase in Bronchial Blood Flow and accelerated airway obstruction, pulmonary vascular changes, pulmonary oedema and pulmonary dysfunction. Ablated Bronchial circulation attenuated these pathophysiological changes.

  • Pathophysiological Basis of Smoke Inhalation
    2003
    Co-Authors: Daniel L. Traber
    Abstract:

    moke inhalation injury is a serious health threat to victims of house fires, explosions, and other disasters involving fire and smoke. The clinical symptoms and prognosis of smoke inhalation injury are often exacerbated by additional burn injury or bacterial infection (such as pneumonia). From our experience using an ovine model of inhalation injury, we have found that the acute lung injury (ALI) resulting from a combination injury of smoke inhalation and burn injury or pneumonia is more severe than that resulting from smoke inhalation injury alone. We have also observed that a combination of smoke inhalation and pneumonia results in a severe septic response in sheep. We will review the pathophysiological aspects of smoke inhalation injury and note the various treatment strategies being currently investigated. Because of space limitations, this review will not discuss the pathophysiology of toxic gas inhalation or oropharyngeal and/or tracheoBronchial thermal injury. These topics are important issues to be considered elsewhere. Bronchial Blood Flow The lungs have two separate Blood supplies (the systemic and the pulmonary), each of which can contribute to lung edema. Under normal conditions, the pulmonary Blood supply is equivalent to the cardiac output, whereas the Bronchial Blood Flow is ~1% of the cardiac output. After inhalation injury, there is a marked increase in Bronchial Blood Flow, which results in pulmonary edema. In an ovine smoke inhalation model, airway Blood Flow increases eightfold or more in the main stem bronchi after the injury, whereas cardiac output, and thus Blood Flow to the peripheral tissues, remains relatively unchanged (1). Bronchial Blood Flow enters into the pulmonary vasculature through various bronchopulmonary anastomoses. It has been suggested that the Bronchial circulation plays a significant role in the spread of injury from the airway to the parenchyma. We have investigated the effect of Bronchial artery ligation or ethanol injection after inhalation injury in sheep (11) and have found that the decrease in gas exchange [PaO 2 /FiO 2 (P/F) ratio], the increase in lung lymph Flow, and the lung wet/dry weight ratio were all improved by these Bronchial artery occlusion techniques. Therefore, we have concluded that the Bronchial circulation contributes to edema formation in the lung that occurs after ALI caused by smoke inhalation injury. This phenomenon has been confirmed by other investigators (4). There are several mediators involved in the regulation of Bronchial circulation, including nitric oxide (NO), a potent vasodilator. It has been reported that NO synthase (NOS) inhibitors reduce the increase in Bronchial Blood Flow. There may be other factors, such as neurotransmitters, involved in this phenomenon, but they are still under investigation.

S. Lakshminarayan - One of the best experts on this subject based on the ideXlab platform.

Peter J. Barnes - One of the best experts on this subject based on the ideXlab platform.

  • Autonomic Control of the Lower Airways
    Primer on the Autonomic Nervous System, 2012
    Co-Authors: Peter J. Barnes
    Abstract:

    Publisher Summary This chapter focuses on autonomic control of the lower airways and airway innervation. There is a close interrelationship between inflammation and neural responses in the airways, since inflammatory mediators may influence the release of neurotransmitters via activation of sensory nerves leading to reflex effects and via stimulation of prejunctional receptors that influence the release of neurotransmitters. Cough is an important defense reflex that may be triggered from either laryngeal or lower airway afferents. Sympathetic innervation of human airways is sparse and there is no functional evidence for direct innervation of airway smooth muscle, although sympathetic nerves regulate Bronchial Blood Flow and to a lesser extent mucus secretion. The bronchodilator nerves in human airways are nonadrenergic noncholinergic (NANC) and the major neurotransmitter is nitric oxide (NO). Neuronal NO synthase is expressed mainly in cholinergic neurons. Multiple neuropeptides have been localized to nerves in the respiratory tract and function as cotransmitters of classical autonomic nerves to fine-tune airway function.

  • The airway vasculature: recent advances and clinical implications
    Thorax, 2009
    Co-Authors: Paolo Paredi, Peter J. Barnes
    Abstract:

    It is increasingly recognised that the airway circulation plays an important role in airway diseases, either through a change in Blood Flow or through microvascular leakage. Most of the information available regarding the anatomy and physiology of Bronchial Blood Flow and its regulation has necessarily derived from animal studies. However, there have recently been important advances in understanding airway Blood Flow in airway disease in humans through the development of non-invasive methods and in the quantification of microvascular leakage using plasma markers. These studies have shown that Bronchial Blood Flow is increased in patients with asthma but not in those with chronic obstructive pulmonary disease, confirming previous pathology investigations. Changes in Bronchial Blood Flow may in part reflect the generation of new vascular vessels, a process known as "angiogenesis" which is caused by airway inflammation. Angiogenesis and the resulting plasma leak affect airway physiology, drug clearance and its bioavailability. This review discusses the anatomy, physiology and regulation of Bronchial Blood Flow in the normal and diseased lung, In addition, it analyses the effect of current medical treatment and discusses the potential use of new anti-angiogenesis medications. The development of non-invasive assessment of Bronchial Blood Flow and the study of angiogenesis have provided a tool to investigate airway physiology in vivo; these advances will contribute to a better understanding of inflammatory airway diseases as well as the implication of these findings to management.

  • Normal Bronchial Blood Flow in COPD Is Unaffected by Inhaled Corticosteroids and Correlates With Exhaled Nitric Oxide
    Chest, 2007
    Co-Authors: Paolo Paredi, Peter J. Barnes, Simon Ward, Derek Cramer, Sergei A. Kharitonov
    Abstract:

    Background In COPD patients, there is reduced vascularity and inflammation of the bronchi, which may have opposite effects on Bronchial Blood Flow (QAW). We studied the relationship of QAW with the fraction of exhaled nitric oxide (FENO), which is a potent vasodilator. We also investigated the vascular response to budesonide and a β 2 -agonist. Methods We measured QAW in 17 patients with COPD (mean [± SEM] age, 67 ± 3 years; 10 male patients; mean FEV 1 , 57 ± 3% predicted; mean FEV 1 /FVC ratio, 54 ± 4%), all of whom were ex-smokers, and in 16 age-matched nonsmoking volunteers (mean age, 64 ± 4 years) and compared this to FENO. QAW was measured using the acetylene dilution method. Results Mean QAW was similar in patients with COPD (34.29 ± 1.09 μL/mL/min) compared to healthy subjects (35.50 ± 1.74 μL/mL/min; p > 0.05) and was not affected by long-term treatment (35.89 ± 1.63 μL/mL/min) or short-term treatment (32.50 ± 1.24 μL/mL/min; p ie , carbon monoxide transfer coefficient: r = 0.74; p r = 0.6; p Conclusions QAW is normal in COPD patients and is not affected by therapy with inhaled corticosteroids or β 2 -agonists. In addition, QAW correlates with levels of FENO, which may have a regulatory role.

  • Correlation of exhaled breath temperature with Bronchial Blood Flow in asthma
    Respiratory research, 2005
    Co-Authors: Paolo Paredi, Sergei A. Kharitonov, Peter J. Barnes
    Abstract:

    In asthma elevated rates of exhaled breath temperature changes (Δe°T) and Bronchial Blood Flow (Qaw) may be due to increased vascularity of the airway mucosa as a result of inflammation.

  • Correlation of exhaled breath temperature with Bronchial Blood Flow in asthma
    Respiratory Research, 2005
    Co-Authors: Paolo Paredi, Sergei A. Kharitonov, Peter J. Barnes
    Abstract:

    In asthma elevated rates of exhaled breath temperature changes (Δe°T) and Bronchial Blood Flow (Q_aw) may be due to increased vascularity of the airway mucosa as a result of inflammation. We investigated the relationship of Δe°T with Q_aw and airway inflammation as assessed by exhaled nitric oxide (NO). We also studied the anti-inflammatory and vasoactive effects of inhaled corticosteroid and β_2-agonist. Δe°T was confirmed to be elevated (7.27 ± 0.6 Δ°C/s) in 19 asthmatic subjects (mean age ± SEM, 40 ± 6 yr; 6 male, FEV_1 74 ± 6 % predicted) compared to 16 normal volunteers (4.23 ± 0.41 Δ°C/s, p < 0.01) (30 ± 2 yr) and was significantly increased after salbutamol inhalation in normal subjects (7.8 ± 0.6 Δ°C/ s, p < 0.05) but not in asthmatic patients. Q_aw, measured using an acetylene dilution method was also elevated in patients with asthma compared to normal subjects (49.47 ± 2.06 and 31.56 ± 1.6 μl/ml/min p < 0.01) and correlated with exhaled NO (r = 0.57, p < 0.05) and Δe°T (r = 0.525, p < 0.05). In asthma patients, Q_aw was reduced 30 minutes after the inhalation of budesonide 400 μg (21.0 ± 2.3 μl/ml/min, p < 0.05) but was not affected by salbutamol. Δe°T correlates with Q_aw and exhaled NO in asthmatic patients and therefore may reflect airway inflammation, as confirmed by the rapid response to steroids.

Piergiuseppe Agostoni - One of the best experts on this subject based on the ideXlab platform.

  • Systemic to Pulmonary Bronchial Blood Flow in Heart Failure
    Chest, 1995
    Co-Authors: Piergiuseppe Agostoni, Elisabetta Doria, Carlo Antona, F. Bortone, Paolo Moruzzi
    Abstract:

    Study objective The aim of this study was to measure systemic to pulmonary Blood Flow from Bronchial circulation (Qbr[s-p]) in patients with heart failure. Design In the absence of pulmonary and coronary Flows, Qbr(s-p) is the volume of Blood accumulating in the left side of the heart; Qbr(s-p) was measured during total cardiopulmonary bypass for coronary artery surgery; Bronchial Blood was vented through a cannula introduced into the left side of the heart and its volume was measured. Patients Patients were subdivided according to the presence for more than 6 months (group I, n=6) or less than 2 months (group 2, n=7), or the absence of heart failure (group 2, n=15). Measurements and results Qbr(s-p) was 89 ± 18* mL/min, 27±3, 22±2, in groups 1, 2, and 3, respectively (*=p Conclusions During total cardiopulmonary bypass, Qbr(s-p) is increased in patients with chronic heart failure. Since with elevated pulmonary vascular pressure Blood Flow through Qbr(s-p) vessels is from the pulmonary to the systemic circulation, the lower resistance observed in group 1 suggests that Bronchial vessels might contribute to reduced lung fluid overload in patients with chronic heart failure.

  • Effects of Positive End-Expiratory Pressure (PEEP) on Bronchial Blood Flow
    Current Topics in Rehabilitation, 1991
    Co-Authors: Piergiuseppe Agostoni, Elisabetta Doria, Mauro Pepi, Gloria Tamborini
    Abstract:

    The Bronchial circulation is the source of systemic Blood to the lung. The drainage of Bronchial Blood Flow to structures outside the lung (trachea, main bronchi, esophagus, etc.) is into the right heart.1–3 Conversely, the drainage of Bronchial Blood Flow to the lung (lung parenchyma and intrapulmonary bronchi) is via the broncho-pulmonary anastomoses into the pulmonary circulation.1–3 Therefore, this portion of Bronchial Blood Flow is named systemic to pulmonary Bronchial Blood Flow [Qbr(s-p)].4

  • Systemic to pulmonary Bronchial Blood Flow in mitral stenosis.
    Chest, 1991
    Co-Authors: Piergiuseppe Agostoni, Elisabetta Doria, Vincenzo Arena, Andrea Sala, Marco Agrifoglio, G. Susini
    Abstract:

    We measured systemic to pulmonary Bronchial Blood Flow [ Q ˙ br(s − p) ] during total cardiopulmonary bypass in 15 patients with mitral stenosis and elevated pulmonary venous pressure (group A, mean pulmonary wedge pressure=22.2 ± 5.4 mm Hg, mean ± SD) and in 15 patients with coronary artery diseases and normal pulmonary venous pressure (group B). Q ˙ br(s − p) is the volume of Blood accumulating in the left side of the heart in the absence of pulmonary and coronary Flows. This Blood was vented through a cannula introduced into the left atrium and measured. Q ˙ br(s − p) was 76.3 ± 13.9 ml/min (2.18 ± 0.37 percent of extracorporeal circulation pump Flow) and 22.3 ± 2.1 (0.63 ± 0.15) in group A and B, respectively (p

G.a. Patterson - One of the best experts on this subject based on the ideXlab platform.

  • The effect of pulmonary arterial Flow and positive end-expiratory pressure on retrograde Bronchial mucosal Blood Flow.
    The Journal of thoracic and cardiovascular surgery, 1991
    Co-Authors: Hiroyasu Yokomise, Paulo Francisco Guerreiro Cardoso, H. Kato, Shaf Keshavjee, Hironobu Wada, A. S. Slutsky, G.a. Patterson
    Abstract:

    Bronchial viability within the first few days after lung transplantation depends on collateral Blood Flow from the pulmonary to the Bronchial circulation. In the present study the relationship between pulmonary arterial Flow and retrograde Bronchial Blood Flow, and the effect of positive end-expiratory pressure on Bronchial Blood Flow were evaluated by laser Doppler velocimetry in an isolated in situ lung perfusion model. Nine adult mongrel dogs were exsanguinated by way of a left atrial cannula. Blood was pumped by a roller pump into the main pulmonary artery. Lungs were perfused at random Flow (in 0.5 L/min increments) at rates of 1 to 3 L/min. Steady-state laser Doppler velocimetric measurements at each level of Flow were made at the tracheal carina and both Bronchial carinae. Pump Flow was then set at baseline cardiac output and positive end-expiratory pressure was applied. Steady-state laser Doppler velocimetric measurements were obtained at each level of positive end-expiratory pressure (5 cm H2O and 10 cm H2O). Bronchial Blood Flow correlated well with pulmonary arterial Flow (for the tracheal carina; rs = 0.912 and p

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