Bronchial Blood Flow Research Articles

Effect of Bronchial Blood Flow on Respiratory Heat Exchange: A Mathematical Analysis for Infectious Diseases

Abstract The present study aims to mathematically analyze the role of bronchial blood flow on heat transfer in respiratory infections. In general, the exchange of heat transfer in various infectious diseases like COVID-19 caused by SARS-CoV-2 has adversely affected respiration by reducing the physiological efficiency of the human respiratory tract. The mechanism of heat exchange through airway walls with the bronchial blood circulation still needs to be thoroughly studied for infectious diseases. In this article, a three-dimensional (3D) spatio-temporal theoretical model is developed to estimate the possible role of bronchial blood on heat exchange during breathing. The local description of the model is presented in a comprehensive and consistent dimensionless framework to explicitly state the actual physiological background. The global description is framed by a multicompartment-based approach, and the algorithm is solved using an advanced numerical scheme to ensure computational tractability. The numerical study elucidates the role of inhalation air temperature, breathing cycles, blood perfusion rate, and mucosal hydration. The outcomes of the algorithm estimate the parameters of the isothermal saturation boundary (ISB), which is defined as the position in the respiratory tract where the temperature of inhaled air comes in equilibrium with the body core saturation temperature. The derived results help to understand the pathophysiological threshold limits and recommend the values to evaluate respiratory distress. With the variations of inspiratory flow conditions, it is observed that the ISB position shifts to the distal branches with the increment in inhalation temperature, breathing rate and virus infection, and decrement in blood perfusion rate. The two antiparallel effects are observed: inhalation of cold air transmits the viral infection, and inhalation of warm air produces thermal injury. However, both can be well controlled by suitable ventilation rates. The observed threshold values may be helpful in clinical trials to correlate the anatomic configuration with pathophysiology.

Left ventricular venting in veno-arterial extracorporeal membrane oxygenation: A computer simulation study.

Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) is the fastest way to restore circulation in refractory cardiogenic shock, however it cannot unload the failing left ventricle. There is a lack of consensus regarding optimal approach to left ventricular venting in V-A ECMO patients with severely depressed or absent left ventricular function. A computer model was developed in Matlab Simulink R20016b (MathWorks, Inc., Natick, MA, USA) to analyze different venting options as well as atrial septostomy in the setting of cardiogenic shock and V-A ECMO. The model has shown an inverse linear relationship between left atrial pressure and either vent, Impella or atrial septum defect flow rate. The minimum vent flow required to prevent pulmonary edema in complete loss of left ventricular function needed to be higher than the bronchial blood flow. Atrial septostomy restored normal pulmonary blood flow with low left atrial pressure but induced stasis in the left ventricle. Venting the pulmonary artery induced stasis in the entire pulmonary circulation as well as left atrium and left ventricle. Venting the left ventricle directly with a cannula or Impella device avoided blood stasis. Our data suggest that reduction of left atrial pressure is linearly related to the vent, Impella or atrial septal defect flow rate. The preferred vent location is the left ventricle as it avoids stasis in the pulmonary circulation and cardiac chambers.

Prevention at Full Steam ‐ Can Steam Inhalation Stop the Contagion of Sars‐Cov 2?

Covid‐19 vaccination and social barrier efforts worldwide have deescalated the death and morbidity toll due to Sars CoV‐2 infection in most countries. However, intramuscular vaccination leads to a variable antibody response insufficient to provide airway mucosal immunity that prevents contagion and reinfection in asymptomatic carriers. Nasal vaccines could provide this missing piece and are currently being tested with encouraging results, but large‐scale availability and efficacy in humans are unknown. Moreover, previous exposure to the virus would render nasal spray vaccines less effective. Past literature on upper airway infections has shown that water steam inhalation therapy (WSIT) may modulate airway mucosa immunity responses. Airway mucosal immunity in COVID‐19 infection is a critical aspect to consider with WSIT. Based on a small but slowly growing body of evidence, we propose that WSIT may be a relevant home remedy worth revisiting to help halt mass contagion. Here, we review current and past studies on WSIT use in upper respiratory infections (URI). Previous studies reported mixed results on the efficacy of steam therapy on viral respiratory diseases. Safety concerns with steam therapy include possible nosocomial infections associated and burns. There is a paucity of studies with high methodological quality exploring the outcomes of this ancient therapy. Upper airway blood flow increases substantially after 15‐min of steam inhalation with temperatures of 42 ℃. Still, methods to measure bronchial blood flow are lacking, and this may be an essential variable for the analysis of how steam may impact mucosal immune responses. Studies with better methodologies demonstrate that nebulized steam at 80°C for 20 min reduces neutrophils compared to controls in COPD patients indicating an anti‐inflammatory effect. The best evidence for using WSIT for upper airway viral disease shows that 60% of asymptomatic carriers increased viral shedding immediately post steam inhalation, and Rt‐PCR testing confirmed viral negativity at 10‐days post‐treatment. Subjects used steam for a total of 20 minutes per hour with steam temperatures ranging from 55 to 65℃. Efficacy rates decline with research methodologies that use WSIT for less than 20 minutes. In summary, more recent studies using WSIT for URI show encouraging results and may help to disentangle former controversies. Lessons emerging from previous studies indicate that exposure of WSIT less than 20 minutes may be ineffective. Adopting WSIT as an inexpensive public health measure may lead to secondary prevention of airway viral infections, especially in new viral strands that have the potential to become pandemic.

Towards a Quantitative Mechanistic Understanding of Localized Pulmonary Tissue Retention-A Combined In Vivo/In Silico Approach Based on Four Model Drugs.

Increasing affinity to lung tissue is an important strategy to achieve pulmonary retention and to prolong the duration of effect in the lung. As the lung is a very heterogeneous organ, differences in structure and blood flow may influence local pulmonary disposition. Here, a novel lung preparation technique was employed to investigate regional lung distribution of four drugs (salmeterol, fluticasone propionate, linezolid, and indomethacin) after intravenous administration in rats. A semi-mechanistic model was used to describe the observed drug concentrations in the trachea, bronchi, and the alveolar parenchyma based on tissue specific affinities (Kp) and blood flows. The model-based analysis was able to explain the pulmonary pharmacokinetics (PK) of the two neutral and one basic model drugs, suggesting up to six-fold differences in Kp between trachea and alveolar parenchyma for salmeterol. Applying the same principles, it was not possible to predict the pulmonary PK of indomethacin, indicating that acidic drugs might show different pulmonary PK characteristics. The separate estimates for local Kp, tracheal and bronchial blood flow were reported for the first time. This work highlights the importance of lung physiology- and drug-specific parameters for regional pulmonary tissue retention. Its understanding is key to optimize inhaled drugs for lung diseases.

EP1.17-23 Omentopexy for Post-Pneumonectomy Bronchopleural Fistula in Patients with Non-Small Cell Lung Cancer After Salvage Radiotherapy

Preoperative chemotherapy or radiotherapy could affect bronchial mucosa blood flow and also the normal healing process of bronchial stump after surgical resection. Otherwise, bronchopleural fistula (BPF) is the worst and time consuming complication in lung cancer surgery. Pneumonectomy is reported as a high risk surgery of BPF. Here, we report our successful treatment experience of BPF using omentum after salvage radiotherapy in NSCLC patient. Retrospective medical chart review A sixty-four years old male patient who had a history of chronic obstructive pulmonary disease diagnosed as squamous carcinoma in left upper lobe, clinical stage of T2aN1M0. Because interlobar artery invasion was suspicious, the patient was treated with radical radiotherapy. After 6600cGy of radiotherapy, the lesion showed marked response. Thus we decided to perform curative surgical resection, pneumonectomy. The patient had discharged in postoperative day 11 and the pathologic report was ypT1aN0M0. But after 1 week from discharge, the patient readmitted and complained of dyspnea and profound sputum. In bronchoscopy, fistula was seen. We performed the second operation. Due to hard fibrosis, direct closure of bronchial stump was not possible. Thus, we covered the stump site with omental flap in multilayers. The patient discharged uneventfully and now in disease free status almost after 2 years from initial operation.View Large Image Figure ViewerDownload Hi-res image Download (PPT) Neoadjuvant radiation therapy and pneumonectomy are risk factors for post-operative BPF. Direct closure with buttressing biocompatible flap is the treatment of choice. But if direct closure is not possible, double-layered omentopexy could be an alternative treatment strategy.

Value of dual-input perfusion of 320 row CT on the efficacy evaluation of small cell lung cancer

Objective To discuss the value of dual-input perfusion of 320 row CT on the efficacy evaluation of small cell lung cancer (SCLC). Methods A total of 18 patients with SCLC confirmed by pathology who received cisplatin plus etoposide chemotherapy between June 2016 and June 2018 in the 8th Medical Center of Chinese PLA General Hospital were collected. All patients received 320 row CT perfusion scan at 3 time points before chemotherapy, after 2 cycles and 4 cycles of chemotherapy. Tumor size, perfusion pseudo color map and bronchial arterial blood flow (BF), pulmonary flow (PF) and perfusion index (PI) were obtained. The efficacy and adverse reactions were evaluated. The single factor analysis was used to make the group comparison. Pearson test was used to make correlation analysis. Results Two patients after 2 cycles of chemotherapy had complete remission (CR), another 2 patients after 4 cycles of chemotherapy had CR, and 3 patients of the above 4 cases with CR had abundant BF; after 4 cycles of chemotherapy, 7 cases had partial remission (PR), 6 cases had stable disease (SD), 1 patient had progression of disease (PD). Dual-input perfusion of 320 row CT showed that 10 cases had the tumor area 15 cm2 before the treatment. There was a negative correlation between PI and the tumor area (r=-0.694, P = 0.026) on patients with the tumor area 15 cm2 (P > 0.05). One case had Ⅳ degree of bone marrow suppression, and obvious adverse reactions were not seen in the rest of the patients. Conclusion Dual-input perfusion of 320 row CT based on the simple imaging can make an accurate quantitative judgement of the effect of SCLC according to perfusion parameter, which provides a new basis for curative effect evaluation on SCLC. Key words: Small cell lung carcinoma; Pulmonary perfusion imaging; Dual-input perfusion CT; Treatment outcome

Inhalation Injury in the Burned Patient.

Inhalation injury causes a heterogeneous cascade of insults that increase morbidity and mortality among the burn population. Despite major advancements in burn care for the past several decades, there remains a significant burden of disease attributable to inhalation injury. For this reason, effort has been devoted to finding new therapeutic approaches to improve outcomes for patients who sustain inhalation injuries.The three major injury classes are the following: supraglottic, subglottic, and systemic. Treatment options for these three subtypes differ based on the pathophysiologic changes that each one elicits.Currently, no consensus exists for diagnosis or grading of the injury, and there are large variations in treatment worldwide, ranging from observation and conservative management to advanced therapies with nebulization of different pharmacologic agents.The main pathophysiologic change after a subglottic inhalation injury is an increase in the bronchial blood flow. An induced mucosal hyperemia leads to edema, increases mucus secretion and plasma transudation into the airways, disables the mucociliary escalator, and inactivates hypoxic vasocontriction. Collectively, these insults potentiate airway obstruction with casts formed from epithelial debris, fibrin clots, and inspissated mucus, resulting in impaired ventilation. Prompt bronchoscopic diagnosis and multimodal treatment improve outcomes. Despite the lack of globally accepted standard treatments, data exist to support the use of bronchoscopy and suctioning to remove debris, nebulized heparin for fibrin casts, nebulized N-acetylcysteine for mucus casts, and bronchodilators.Systemic effects of inhalation injury occur both indirectly from hypoxia or hypercapnia resulting from loss of pulmonary function and systemic effects of proinflammatory cytokines, as well as directly from metabolic poisons such as carbon monoxide and cyanide. Both present with nonspecific clinical symptoms including cardiovascular collapse. Carbon monoxide intoxication should be treated with oxygen and cyanide with hydroxocobalamin.Inhalation injury remains a great challenge for clinicians and an area of opportunity for scientists. Management of this concomitant injury lags behind other aspects of burn care. More clinical research is required to improve the outcome of inhalation injury.The goal of this review is to comprehensively summarize the diagnoses, treatment options, and current research.

Athletes Do Not Condition Inspired Air More Effectively than Nonathletes during Hyperpnea.

Twenty-three endurance athletes from various sports, 12 with airway hyperresponsiveness (AHR) and/or exercise-induced bronchoconstriction (EIB) (A+), 11 without AHR and/or EIB (A-), 12 nonathletes with AHR and/or EIB (C+), and 11 nonathletes without AHR and/or EIB (C-) were recruited. All subjects attended the laboratory on three occasions, twice for baseline characterization, including questionnaires, pulmonary function, methacholine bronchoprovocation, allergy skin prick tests, exhaled nitric oxide measurement, and a standard EVH, and once to perform a modified EVH to assess ΔT. Inspired and expired air temperatures were measured with a high-precision probe during EVH and at regular intervals until 30 min after the end of the test. The global ΔT during the EVH was +5.8°C ± 1.5°C and +4.7°C ± 1.5°C during the 30 min after the EVH. No difference was found between groups for either the ΔT or the slope of ΔT, during and after the EVH. This study shows no evidence of improved capacity to condition inspired air in endurance athletes, which could have suggested an increased bronchial blood flow or another adaptive mechanism. The absence of an adaptive mechanism could therefore contribute to airway damage observed in athletes in allowing colder but mainly dryer air to penetrate deeper in the lung.

Beta-blocker management of refractory hemoptysis in cystic fibrosis: a novel treatment approach

/objective: Recurrent hemoptysis is a debilitating complication of cystic fibrosis (CF) and likely results from mucosal erosions into abnormal bronchial blood vessels due to chronic respiratory infection. We hypothesize that the use of beta-blockade will decrease mean arterial pressure resulting in lower bronchial artery blood flow and, subsequently, decrease the frequency and severity of hemoptysis, rate of hospitalizations, and usage of intravenous antibiotics. Retrospective chart review was performed on 12 CF patients with recurrent hemoptysis, aged 13-40 years old, along with a follow-up telephone survey to assess the effectiveness of beta-blockade for hemoptysis, tolerance of inhaled respiratory medications, activity tolerance, and potential adverse effects. A beta-blocker, specifically atenolol, was initiated in all subjects within 24 hours after experiencing recurrent hemoptysis episodes. A majority of patients (72.7%) had complete cessation of hemoptysis. There were significant decreases in the frequency of hemoptysis (p = 0.02) and the amount of hemoptysis (p = 0.004). The rate of hospitalizations significantly decreased from 1.33 to 0.67 (p = 0.05) after initiation of atenolol. There was a trend toward statistical significance in the reduction of intravenous antibiotics use (p = 0.08). No statistical difference was found when comparing the pre- and post-treatment means of forced expiratory volume in 1-second (p = 0.59). Very minimal adverse effects were observed with only one patient reporting intermittent facial flushing. Beta-blockade, particularly with atenolol, appears to successfully treat, if not resolve, recurrent hemoptysis refractory to conservative therapy in CF. Beta-blocker therapy appears to maintain an effective safety profile in CF.

Editorial Comment: Safety of bronchovascular reconstructions after induction therapy

trolled trial. Lancet 2009;374:379–86. [7] Stupp R, Mayer M, Kann R, Weder W, Zouhair A, Betticher DC et al. Neoadjuvant chemotherapy and radiotherapy followed by surgery in selected patients with stage IIIB non-small-cell lung cancer: a multicentre phase II trial. Lancet Oncol 2009;10:785–93. [8] Rusch VW, Giroux DJ, Kraut MJ, Crowley J, Hazuka M, Winton T et al. Induction chemoradiation and surgical resection for superior sulcus non-small-cell lung carcinomas: long-term results of Southwest Oncology Group Trial 9416 (Intergroup Trial 0160). J Clin Oncol 2007;25: 313–8. [9] Kunitoh H, Kato H, Tsuboi M, Shibata T, Asamura H, Ichinose Y et al. Phase II trial of preoperative chemoradiotherapy followed by surgical resection in patients with superior sulcus non-small-cell lung cancers: report of Japan Clinical Oncology Group trial 9806. J Clin Oncol 2008;26:644–9. [10] Yamamoto R, Tada H, Kishi A, Tojo T. Effects of preoperative chemotherapy and radiation therapy on human bronchial blood flow. J Thorac Cardiovasc Surg 2000;119:939–45. [11] Rendina EA, Venuta F, De Giacomo T, Flaishman I, Fazi P, Ricci C. Safety and efficacy of bronchovascular reconstruction after induction chemotherapy for lung cancer. J Thorac Cardiovasc Surg 1997;114:830–5; discussion 835–837. [12] Milman S, Kim AW, Warren WH, Liptay MJ, Miller C, Basu S et al. The incidence of perioperative anastomotic complications after sleeve lobectomy is not increased after neoadjuvant chemoradiotherapy. Ann Thorac Surg 2009;88:945–50. discussion 950–941. [13] Katayama H, Ueoka H, Kiura K, Tabata M, Kozuki T, Tanimoto M et al. Preoperative concurrent chemoradiotherapy with cisplatin and docetaxel in patients with locally advanced non-small-cell lung cancer. Br J Cancer 2004;90:979–84. [14] Toyooka S, Kiura K, Takemoto M, Oto T, Takigawa N, Fujiwara T et al. Long-term outcome of induction chemoradiotherapy with docetaxel and cisplatin followed by surgery for non-small-cell lung cancer with mediastinal lymph node metastasis. Interact CardioVasc Thorac Surg 2012;14:565–9. [15] Goldstraw P, Crowley J, Chansky K, Giroux DJ, Groome PA, Rami-Porta R et al. The IASLC Lung Cancer Staging Project: proposals for the revision of the TNM stage groupings in the forthcoming (seventh) edition of the TNM Classification of malignant tumours. J Thorac Oncol 2007;2: 706–14. [16] Oken MM, Creech RH, Tormey DC, Horton J, Davis TE, McFadden ET et al. Toxicity and response criteria of the Eastern Cooperative Oncology Group. Am J Clin Oncol 1982;5:649–55. [17] Roswit B, White DC. Severe radiation injuries of the lung. Am J Roentgenol 1977;129:127–36. [18] Davis SD, Yankelevitz DF, Henschke CI. Radiation effects on the lung: clinical features, pathology, and imaging findings. Am J Roentgenol 1992; 159:1157–64.

Differential effects of inhaled methacholine on circumferential wall and vascular smooth muscle of third-generation airways in awake sheep

Evolution and natural selection ensure that specific mechanisms exist for selective airway absorption of inhaled atmospheric molecules. Indeed, nebulized cholinoceptor agonists used in asthma-challenge tests may or may not enter the systemic circulation. We examined the hypothesis that inhaled cholinoceptor agonists have selective access. Six sheep were instrumented under general anesthesia (propofol 5 mg/kg iv, 2-3% isoflurane-oxygen), each with pulsed-Doppler blood flow transducers mounted on the single bronchial artery and sonomicrometer probes mounted on the intrapulmonary third-generation lingula lobe bronchus. Continuous measurements were made of bronchial blood flow (Q(br)), Q(br) conductance (C(br)), bronchial hemicircumference (CIRC(br)), and bronchial wall thickness (WALL TH(br)) in recovered, standing, awake sheep. Methacholine (MCh; 0.125-2.0 μg/kg iv), at the highest dose, caused a 233% rise in Q(br) (P < 0.05) and a 286% rise in C(br) (P < 0.05). CIRC(br) fell to 90% (P < 0.05); WALL TH(br) did not change. In contrast, nebulized MCh (1-32 mg/ml), inhaled through a mask at the highest dose, caused a rise in ventilation and a rise in Q(br) proportional to aortic pressure without change in C(br). CIRC(br) fell to 91% (P < 0.01), and WALL TH(br) did not change. Thus inhaled MCh has access to cholinoceptors of bronchial circumferential smooth muscle to cause airway lumen narrowing but effectively not to those of the systemic bronchovascular circulation. It is speculated that the mechanism is selective neuroparacrine inhibition of muscarinic acetylcholine receptors (M3 bronchovascular cholinoceptors) by prostanoids released by intense MCh activation of epithelial and mucosal cells lining the airway.

Tissue hypoxaemia causes oedema, inflammation and fibrosis in porcine bronchial transsection

Objectives. Bronchial artery revascularization in lung transplantation is disputed. This study examined the physiological consequences of porcine bronchial transsection and reanastomosis with and without bronchial artery blood supply with relation to lung transplantation. Design. Translational, controlled animal study. Twelve pigs were operated through a left lateral thoracotomy. The left bronchus was transsected and reanastomosed. In the control group (n = 6), the bronchial arteries were preserved and in the study group (n = 6) they were severed. Bronchial mucosa blood flow (BMBF) was measured with laser-Doppler velocimetry and bronchial mucosa haemoglobin saturation and concentration with diffuse reflectance spectrophotometry. Measurements were made preoperatively, postoperatively and after 1 week. Results. In the study group, left postoperative BMBF was significantly lower than preoperatively (115 vs. 210 PU/s, p = 0.0001) and lower than in the control group (115 vs. 205 PU/s, p = 0.002). Repeated measurement ANOVA showed a significant treatment effect depending on time (p = 0.0034). The left mucosal haemoglobin saturation in the study group was significantly reduced postoperatively, 92% versus 61%, with a treatment effect depending on time (p = 0.0080). The reduction in left/right ratio of the mucosal haemoglobin concentration 1 week postoperatively in the study group was insignificant. Conclusion. Bronchial transsection and reanastomosis without bronchial artery blood supply was followed by significant decrease in mucosal blood flow and saturation postoperatively, and also in tissue haemoglobin concentration at section, and provides a physiologic explanation of histological changes.

Selective effects of inhaled methacholine on 3rd generation bronchial blood flow and airway dimensions in awake sheep

Evolution and natural selection in mammals has ensured mechanisms for preventing absorption of inhaled molecules from lung airways. The postulate that inhaled cholinergic compounds selectively access airway wall structures was examined in six sheep instrumented at left thoracotomy under general anaesthesia (i.v. propofol 5 mg.kg−1, 3% isoflurane‐oxygen) each with pulsed‐ Doppler blood flow transducers mounted on bronchial artery, and sonomicrometer probes (Bishop et al, Pulm Pharmacol Ther 20, 178–189, 2007) on high air‐flow resistance 3rd generation lingular lobe bronchus. Continuous measurements of bronchial blood flow (Qbr) and conductance (Cbr), plus bronchial hemi‐circumference (CIRCbr) and wall thickness (THbr) were made in recovered, standing, awake sheep. Dose‐response studies were performed using i.v. methacholine (MCh: 0.125–2.0 μg.kg−1), or nebulised MCh (1–32 mg.kg−1) inhaled by mask. MCh i.v. at the highest dose caused 233% rise in Qbr (P&lt; 0.05), and 286% in Cbr (P&lt; 0.05). CIRCbr fell to 90% of control (P&lt; 0.05); THbr did not change. Inhaled MCh at highest dose caused rise in ventilation, and proportional rise in aortic pressure and Qbr; CIRCbr fell to 91% (P&lt; 0.05); Cbr and THbr did not change. Thus cholinoceptor agonists penetrate the airway wall ex‐ or endogenously to maximally contract the bronchial wall, but by unknown selective mechanisms do not penetrate the systemic vascular bed.

EComment. Thromboendarterectomy and aortic occlusion: the good, the bad and the ugly

The article by Poullis [1] brings home an important problem of operative field flooding while performing thromboendarterectomy. The novel idea from Poullis [1] of intra-aortic balloon deployment at the level of the origin of the bronchial arteries seems like an attractive simple option that may significantly reduce bronchial artery blood flow and flooding of the pulmonary vascular system while maintaining organ perfusion and avoiding circulatory arrest. Although Poullis briefly mentioned the risks of aortic and vascular injury and embolization during intra-aortic balloon deployment, we would like to emphasize that these are real risks that are not to be neglected. From a recent large series of endovascular stenting for descending thoracic aortic pathology, 5.7% had complication from vascular access injury requiring emergency rescue iliac-femoral artery bypass and 1.9% had cerebral embolic event [2]. Elderly patients, those with atherosclerotic and calcified aortas, and peripheral vascular disease are particularly at risk. Therefore, careful patient selection may be the key to minimizing morbidity from this intra-aortic balloon approach. In terms of spinal cord ischemia during intra-aortic balloon deployment, apart from the utilization of motor and sensory evoked potential monitoring and CSF drainage to minimize cord ischemic injury, the administration of perioperative steroids such as methylprednisolone, can also be considered to help reduce spinal cord inflammation and ischemic injury, in order to reduce incidence of paraplegia [3]. In order to prevent spinal cord ischemia, an alternative bronchial artery occlusion strategy would be to place highly selective small balloon occluders within the bronchial arteries, totally avoiding any thoracic aortic flow occlusion, further limiting the risks to the spinal cord. Furthermore, latest innovations in intra-vascular occlusion polymers such as LeGoo?, which is a reverse thermo-sensitive polymer that provides temporary internal vessel occlusion may be injected inside the bronchial arteries via a catheter obviating the need for any balloon deployment [4]. Bronchial artery occlusion by intra-aortic balloon under moderate hypothermia may have additional consequences in terms of lung ischemia reperfusion injury [5]. The lung is dependent on the pulmonary artery, bronchial artery, and alveolar ventilation to oxygenate lung tissue to prevent ischemia. Variable systemic collaterals to the lungs may have a minor role in contributing to lung perfusion. The status during circulatory arrest for thromboendarterectomy is that of no pulmonary artery, no bronchial artery and no systemic collateral lung perfusion but with lung protection from hypothermia, whereas Poullis's approach will result in some systemic collateral lung perfusion under the lesser protection of moderate hypothermia. The effects of these techniques on lung ischemia reperfusion injury will need further evaluation[5]. Furthermore, perhaps worth studying would be the potential protective role of pulmonary ischemic preconditioning with a short duration of intra-aortic balloon inflation prior to the prolonged deployment to reduce the effects of lung ischemia-reperfusion injury [5]. We applaud the novel idea by Poullis of intra-aortic balloon bronchial artery occlusion during pulmonary endarterectomy to reduce operative field flooding while avoiding circulatory arrest, nevertheless, the good, the bad and the ugly of these strategies will require further investigations. Conflict of Interest: None declared

Measurement of exhaled breath temperature in science and clinical practice

Educational aims To review the link between inflammation and increased vascularity and blood flow of the airways, and exhaled breath temperature. To position exhaled breath temperature (EBT) as a physiological characteristic differing from core temperature measured at other body sites. To review the existing experience about measuring EBT in different disease states of the respiratory system. To emphasise the influence of airway remodeling/destruction in modulating EBT. Summary Evaluation of the exhaled breath temperature (EBT) has been suggested as a new method to detect and monitor pathological processes in the respiratory system. The putative mechanism of this approach is based upon changes in the blood flow in the conducting airways that are characteristic of different disease states, which influence the temperature of the exhaled gases. The first attempts to prove this concept were made in conjunction with measurement of exhaled nitric oxide fraction ( F eNO ) about a decade ago. They made use of an open-circuit, single-breath method in a closed indoor environment, and demonstrated associations between EBT on the one hand, and bronchial blood flow, F eNO and sputum cellular content on the other. These findings have been further extended to practical applicability with the introduction of multiple-breath, portable hand-held devices. Measurement of EBT using these is less dependent on the ambient environment and easier to perform. Studies have been conducted to explore the relationship between EBT and different physiological characteristics, and to assess possible confounding influences in the process of measurement. The value of the method has been explored in the diagnosis and monitoring of asthma, chronic obstructive pulmonary disease and other respiratory diseases. While initially, emphasis focused on airway inflammation as the primary process to be captured by this method, it was subsequently realised that destructive and other remodelling processes reducing the integral contact surface of the conducting airways and/or damaging their vasculature would also affect the end result by shifting EBT downwards. As obstructive airway disease is, in most cases, a combination of airway inflammation and remodelling/destruction, EBT should be viewed as an individual characteristic indicating fluctuating changes in the balance of these processes. Hence, an important potential application of the method is in monitoring airway diseases. EBT measurement has emerged as an attractive noninvasive new approach in respiratory and, possibly, other diseases. Systematic research will determine its place in clinical practice.

Direct Delivery of Low-Dose 7-Nitroindazole Into the Bronchial Artery Attenuates Pulmonary Pathophysiology After Smoke Inhalation and Burn Injury in an Ovine Model

Bronchial 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 increased release of neuropeptides from the airway has been implicated in smoke inhalation injury, we hypothesized that direct delivery into the bronchial artery of low-dose 7-nitroindazole (7-NI), a specific neuronal NO synthase inhibitor, would attenuate smoke/burn-induced acute lung injury. Eighteen adult female sheep were instrumented for chronic hemodynamic monitoring 5 to 7 days before the injury. The bronchial artery was cannulated via intercostal thoracotomy, while blood flow was preserved. Acute lung injury was induced by 40% total body surface area third-degree cutaneous burn and smoke inhalation (48 breaths of cotton smoke, <40°C) under deep anesthesia. Following injury, animals (35.4 ± 1.1 kg) were divided into three groups: (a) 7-NI group: 1 h after injury, 7-NI (0.01 mg · kg · h, 2 mL · h) was continuously infused into the bronchial artery, n = 6; (b) control group: 1 h after injury, same amount of saline was injected into the bronchial artery, n = 6; (c) sham group: no injury, no treatment, same operation and anesthesia, n = 6. After injury, all animals were ventilated and fluid resuscitated according to an established protocol. The experiment was conducted for 24 h. Injury induced severe pulmonary dysfunction, which was associated with increases in lung edema formation, airway obstruction, malondialdehyde, and nitrate/nitrite. 7-Nitroindazole injection into the bronchial artery reduced the degree of lung edema formation and improved pulmonary gas exchange. The increase in malondialdehyde and nitrate/nitrite in lung tissue was attenuated by treatment. Our data strongly suggest that local airway production of NO contributes to pulmonary dysfunction following smoke inhalation and burn injury. Most mechanisms that drive this pathophysiology reside in the airway.

What’s New in Shock, December 2011?

What’s New in Shock, December 2011?

Effect of supine posture on airway blood flow and pulmonary function in stable heart failure

The aim of this study was to determine the relationship between body position, pulmonary function (PF) and bronchial blood flow (Q(aw)) in a group of heart failure (HF) and control subjects. Thirty-six subjects were studied: 24 stable, ambulatory HF patients (HF: LVEF=27±6%, age=65±9 yr) and 12 age- and sex-matched controls (CTRL: LVEF=60±7%, age=62±8 yr). Measures of Q˙(aw) (soluble gas method) and PF were collected upright and following 30min in the supine position. Q˙(aw) was similar between groups and remained unchanged with body position. Declines in forced vital capacity (FVC) and forced expiratory volume in 1s (FEV1) with the supine position were observed in both groups; declines in forced expiratory flow 25-75% (FEF(25-75)) and FEF 75% (FEF75) with the supine position were observed in the HF group only. Changes in Q˙(aw) were related to changes in PF only in the HF patient groups (ΔFVC, % predicted, r = -0.45, p<0.04, ΔFEV1 r = -0.61, p<0.01, ΔFEV1% predicted, r = -0.45, p<0.04). These data demonstrate that relationships between postural changes in Q˙(aw) and PF exist only in the HF population and that the bronchial circulation may contribute to postural PF decline in HF.

Oparzenia dróg oddechowych

Respiratory tract burns are one of the most serious injuries of human organism. They often accompany severe skin burns, increasing morbidity and mortality. Pathologic events happening in the lungs in the course of inhalation injury consist of: edema and necrosis of bronchial mucosa, increase of bronchial blood flow and vascular permeability, recruitment of inflammatory mediators, and obturation of bronchial tract with the casts composed of mucus, tissue debris, neutrophils and fibrin. The above mentioned processes lead to progressive disturbances of pulmonary gas exchange and tissue hypoxia. Introduction of standardized bronchoscopic procedures resulted in the possibility of early diagnosis and treatment of inhalation injuries. There are many treatment options, some of them combined with early and late complications, the optimal treatment protocol is still lacking. Early hyperbaric oxygen therapy is one of the most promising methods of treatment leading to decrease of mortality due to inhalation injury.

Integration of baroreflex and autoregulation control of bronchial blood flow in awake dogs

Baroreflex control of the bronchial circulation is unresolved. Early studies suggested that baroreflexes dilate or have no effect, but recent studies in awake dogs suggested baroreflexes did not normally engage tonic vasoconstrictor efferents but during excitement systemic pressure rises may also trigger local sensory-motor dilator reflexes. We examined the postulate that bronchial flow is normally regulated at rest during controlled changes in pressure gradient (Pg) by integration of tonic autonomic activity with autoregulation. Twelve greyhounds were instrumented under general anaesthesia by surgical implantation of pulsed Doppler flow transducers on the right bronchial artery (BA). After recovery baroreflex effects were evoked by raising and lowering aortic pressure using a lower thoracic aortic balloon in 11 animals, and in six of these after cholinoceptor plus adrenoceptor blockade. The right BA bed showed pressure-passive responses and the time-dependent bronchial bed effects in the autonomically intact state (INT) were largely similar to those in the blocked state (TAB). When results were replotted as pressure-flow relationships and analysed using covariance, the regression line over the pressure range 70-135 mmHg for TAB demonstrated a significant slope (P < 0.05), a linear regression elevated 120% (P = 0.006) above and parallel to INT (Y(Q) = 0.034 + 0.00033(X(Pg) - 104.6). The regression fell on the line of equal proportional change. Baroreflexes do not functionally engage the autonomic outflow to the bronchial circulation. Under controlled conditions of systemic Pg change, the bronchial circulation is normally controlled by the integration of resting autonomic tone, myogenic autoregulation and pressure-passive effects.