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Pulmonary Circulation (pulmonary + circulation)
Selected AbstractsA Novel Model for Post-Transplant Obliterative Airway Disease Reveals Angiogenesis from the Pulmonary CirculationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 2 2005Andre E. Dutly We present a novel animal model for post-transplant obliterative airway disease in which the donor trachea is implanted into the recipient's lung parenchyma. Although this procedure is technically more challenging than the heterotopic model of implantation into a subcutaneous pouch, it has several important advantages some of which are the appropriate local environment and the possibility of local immunosuppressive therapy after transtracheal gene, cell or drug delivery. This model has revealed new insights into angiogenic potential of the pulmonary circulation. [source] Responses of the bronchial and pulmonary circulations to short-term nitric oxide inhalation before and after endotoxaemia in the pigACTA PHYSIOLOGICA, Issue 1 2002R. J. M. Middelveld ABSTRACT The physiological responses of the bronchial circulation to acute lung injury and endotoxin shock are largely unexplored territory. This study was carried out to study the responsiveness of the bronchial circulation to nitric oxide (NO) inhalation before and after endotoxaemia, in comparison with the pulmonary circulation, as well as to study changes in bronchial blood flow during endotoxaemia. Six anaesthetized pigs (pre-treated with the cortisol-synthesis inhibitor metyrapone) received an infusion of 10 µg/kg endotoxin during 2 h. Absolute bronchial blood flow was measured via an ultrasonic flow probe around the bronchial artery. The pigs received increasing doses of inhaled NO over 5 min each (0, 0.2, 2 and 20 ppm) before and after 4 h of endotoxaemia. The increase in bronchial vascular conductance during 5 min of inhalation of 20 ppm NO before endotoxin shock was significantly higher (area under curve (AUC) 474.2 ± 84.5% change) than after endotoxin shock (AUC 118.2 ± 40.4%, P < 0.05 Mann,Whitney U -test). The reduction of the pulmonary arterial pressure by 20 ppm NO was not different. A short rebound effect of the pulmonary arterial pressure occurred after discontinuation of inhaled NO before endotoxaemia (AUC values above baseline 54.4 ± 19.7% change), and was virtually abolished after endotoxaemia (AUC 6.1 ± 4.0%, P = 0.052, Mann,Whitney U -test). Our results indicate that the responsiveness of the bronchial circulation to inhalation of increasing doses of inhaled NO during endotoxin shock clearly differ from the responsiveness of the pulmonary circulation. The reduced responsiveness of the bronchial circulation is probably related to decreased driving pressure for the bronchial blood flow. The absence of the short rebound effect on pulmonary arterial pressure (PAP) after induction of shock could be related to maximum constriction of the pulmonary vessels at 4 h. [source] Dual ETA/ETB vs. selective ETA endothelin receptor antagonism in patients with pulmonary hypertensionEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2006C. F. Opitz Abstract Since the identification of endothelin as a key mediator in the pathogenesis of several diseases, including pulmonary arterial hypertension (PAH), the pharmacologic control of the activated endothelin system with endothelin receptor antagonists (ETRA) has been a major therapeutic achievement for the treatment of patients with PAH. To date, dual ETA/ETB and selective ETA receptor antagonists have clinically been evaluated. To answer the question of whether selective or dual ETRA is preferable in patients with PAH, experimental and clinical data with relevance to the pulmonary circulation are reviewed in this article. Whereas experimental and clinical data provide unambiguous evidence that ETA receptors mediate the detrimental effects of ET-1, such as vasoconstriction and cell proliferation, the elucidation of the role of ETB receptors has been more complex. It has been shown that there is a subpopulation of ETB receptors on smooth muscle cells and fibroblasts mediating vasoconstriction and proliferation. On the contrary, there is clear evidence that endothelial ETB receptors continue to mediate vasodilation, vasoprotection and ET-1 clearance despite the pathology associated with pulmonary hypertension. More difficult to assess is the net effect of these mechanisms in patients to be treated with ETRA. When considering the available data from controlled clinical trials, nonselectivity does not appear to carry a relevant clinical benefit for the treatment of patients with PAH when compared with selective ETA receptor antagonism. [source] Cerebral emboli and paradoxical embolisation in dementia: a pilot studyINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 1 2005Nitin Purandare Abstract Background The causes of the common dementias remain unknown. Paradoxical embolisation of the cerebral circulation by venous thrombi passing through venous to arterial shunts (v-aCS) in the heart or pulmonary circulation is known to occur in cryptogenic stroke and post-operative confusion following hip replacement. Objectives To explore the role of paradoxical embolisation in dementia by investigating for cerebral emboli, venous to arterial circulation shunt (v-aCS) and carotid artery disease. Methods Forty-one patients with dementia (24 Alzheimer's AD and 17 vascular VaD) diagnosed using DSM-IV criteria and 16 controls underwent transcranial Doppler (TCD) detection of spontaneous cerebral emboli in both middle cerebral arteries. A v-aCS was detected by intravenous injection of an air/saline ultrasound contrast at rest and after provocation by coughing and Valsalva's manoeuvre. Carotid artery disease was assessed by duplex imaging. Results Cerebral emboli were detected in 11 (27.5%) dementia patients compared with one (7%) control (p,=,0.15) with emboli being most frequent in VaD (41%) compared to controls [OR (95% CI): 10.5 (1.1, 98.9), p,=,0.04]. A v-aCS was detected in 25 (61%) patients and seven (44%) controls (p,=,0.24). In dementia patients with cerebral emboli; v-aCS was detected in seven (64%) and moderate to severe carotid stenosis was present in three (30%). Conclusion Cerebral emboli and v-aCS may be more frequent in patients with both VaD and AD than in controls, which suggest paradoxical embolisation as a potential mechanism for cerebral damage. This pilot study justifies a definitive case-control study. Copyright © 2004 John Wiley & Sons, Ltd. [source] Pulmonary Venous Wedge Pressure Provides an Accurate Assessment of Pulmonary Artery Pressure in Children with a Bidirectional Glenn ShuntJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 5 2003DANIEL H. GRUENSTEIN M.D. Purpose: In circulations with pulsatile pulmonary artery flow the pulmonary venous wedge pressure (PVWp) has been validated as a good estimate of pulmonary artery pressure (PAp), when PAp is low. The purpose of this study was to validate PVWp estimates of PAp in the less-pulsatile pulmonary circulation of children after bidirectional Glenn shunts. Methods: A retrospective study was performed of 22 simultaneous measurements of PVWp and PAp made during 20 catheterizations in 19 children who had undergone bidirectional Glenn procedures. The PAp was measured directly from the branch PA ipsilateral to the side of the PVWp, or in the SVC. Pulmonary resistance (Rp) was calculated with both PAp and PVWp, to assess the impact of PAp estimates on Rp determinations. Results: Patients ranged in age from 5 months to 10.7 years. There were a variety of univentricular cardiac malformations in the study group. Two children had antegrade pulmonary blood flow in addition to a bidirectional Glenn shunt. The mean PAp ranged from 4 to 14 mmHg, while mean PVWp ranged from 3 to 15 mmHg. Mean PVWp never differed from mean PAp by more than 3 mmHg. There was a significant linear relation between mean PAp and PVWp: PAp = 0.86 (PVWp) + 2.0 (R2= 0.89; P < 0.0001). PVWp provided a good approximation of PAp regardless of the presence (n = 2) or absence (n = 19) of antegrade pulmonary flow. There was a good linear correlation between the Rp calculated by both methods (RpPAp = 0.9 (RpVWp) + 0.5; R2= 0.74; P < 0.0001). Conclusion: The mean PVWp provides a close approximation of mean PAp in children with a bidirectional Glenn shunt and provides valuable hemodynamic information in cases where direct PAp measurements are unavailable. (J Interven Cardiol 2003;16:367,370) [source] Functional morphology and patterns of blood flow in the heart of Python regius,JOURNAL OF MORPHOLOGY, Issue 6 2009J. Matthias Starck Abstract Brightness-modulated ultrasonography, continuous-wave Doppler, and pulsed-wave Doppler-echocardiography were used to analyze the functional morphology of the undisturbed heart of ball pythons. In particular, the action of the muscular ridge and the atrio-ventricular valves are key features to understand how patterns of blood flow emerge from structures directing blood into the various chambers of the heart. A step-by-step image analysis of echocardiographs shows that during ventricular diastole, the atrio-ventricular valves block the interventricular canals so that blood from the right atrium first fills the cavum venosum, and blood from the left atrium fills the cavum arteriosum. During diastole, blood from the cavum venosum crosses the muscular ridge into the cavum pulmonale. During middle to late systole the muscular ridge closes, thus prohibiting further blood flow into the cavum pulmonale. At the same time, the atrio-ventricular valves open the interventricular canal and allow blood from the cavum arteriosum to flow into the cavum venosum. In the late phase of ventricular systole, all blood from the cavum pulmonale is pressed into the pulmonary trunk; all blood from the cavum venosum is pressed into both aortas. Quantitative measures of blood flow volume showed that resting snakes bypass the pulmonary circulation and shunt about twice the blood volume into the systemic circulation as into the pulmonary circulation. When digesting, the oxygen demand of snakes increased tremendously. This is associated with shunting more blood into the pulmonary circulation. The results of this study allow the presentation of a detailed functional model of the python heart. They are also the basis for a functional hypothesis of how shunting is achieved. Further, it was shown that shunting is an active regulation process in response to changing demands of the organism (here, oxygen demand). Finally, the results of this study support earlier reports about a dual pressure circulation in Python regius. J. Morphol., 2009. © 2008 Wiley-Liss, Inc. [source] Retrospective Evaluation of Sildenafil Citrate as a Therapy for Pulmonary Hypertension in DogsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2006Jonathan F. Bach DACVIM (SA-IM) Pulmonary arterial hypertension (PH) is a pathologic condition in dogs characterized by abnormally high pressures in the pulmonary circulation and has been associated with a poor outcome. Sildenafil is a type V phosphodiesterase inhibitor that produces nitric oxide-mediated vasodilatation. Sildenafil treatment decreases pulmonary arterial pressure and pulmonary vascular resistance in people with PH. The purpose of this study was to describe the clinical characteristics and outcome of dogs with PH treated with sildenafil. The cardiology database was searched for dogs with PH treated with sildenafil. PH was defined as systolic pulmonary arterial pressure (PAPS) 25 mmHg at rest. Medical records were reviewed for the following information: signalment, duration and type of clinical signs before treatment, underlying disease, estimated or measured PAPS, dosage and dosing interval of sildenafil, and the effect of treatment on clinical signs and pulmonary arterial pressure and survival time. Thirteen affected dogs were identified. Clinical signs included collapse, syncope, respiratory distress, and cough. Duration of clinical signs before presentation ranged from 3 days to 5 months. An underlying cause was identified in 8 dogs. The median sildenafil dosage was 1.9 mg/kg. Ten dogs received concurrent medications. Median PAPS was 90 mmHg; 8 dogs were reevaluated after therapy, and the median decrease in PAPS was 16.5 mmHg. The median survival time of all dogs was 91 days. Sildenafil appeared to be well tolerated in dogs with PH and was associated with decreased PAPS and amelioration of clinical signs in most. Sildenafil represents a reasonable treatment option for dogs with pulmonary hypertension. [source] The Role of K+ Channels in Determining Pulmonary Vascular Tone, Oxygen Sensing, Cell Proliferation, and Apoptosis: Implications in Hypoxic Pulmonary Vasoconstriction and Pulmonary Arterial HypertensionMICROCIRCULATION, Issue 8 2006ROHIT MOUDGIL ABSTRACT Potassium channels are tetrameric, membrane-spanning proteins that selectively conduct K+ at near diffusion-limited rates. Their remarkable ionic selectivity results from a highly-conserved K+ recognition sequence in the pore. The classical function of K+ channels is regulation of membrane potential (EM) and thence vascular tone. In pulmonary artery smooth muscle cells (PASMC), tonic K+ egress, driven by a 145/5 mM intracellular/extracellular concentration gradient, contributes to a EM of about ,60 mV. It has been recently discovered that K+ channels also participate in vascular remodeling by regulating cell proliferation and apoptosis. PASMC express voltage-gated (Kv), inward rectifier (Kir), calcium-sensitive (KCa), and two-pore (K2P) channels. Certain K+ channels are subject to rapid redox regulation by reactive oxygen species (ROS) derived from the PASMC's oxygen-sensor (mitochondria and/or NADPH oxidase). Acute hypoxic inhibition of ROS production inhibits Kv1.5, which depolarizes EM, opens voltage-sensitive, L-type calcium channels, elevates cytosolic calcium, and initiates hypoxic pulmonary vasoconstriction (HPV). Hypoxia-inhibited K+ currents are not seen in systemic arterial SMCs. Kv expression is also transcriptionally regulated by HIF-1, and NFAT. Loss of PASMC Kv1.5 and Kv2.1 contributes to the pathogenesis of pulmonary arterial hypertension (PAH) by causing a sustained depolarization, which increases intracellular calcium and K+, thereby stimulating cell proliferation and inhibiting apoptosis, respectively. Restoring Kv expression (via Kv1.5 gene therapy, dichloroacetate, or anti-survivin therapy) reduces experimental PAH. Electrophysiological diversity exists within the pulmonary circulation. Resistance PASMC have a homogeneous Kv current (including an oxygen-sensitive component), whereas conduit PASMC current is a Kv/KCa mosaic. This reflects regional differences in expression of channel isoforms, heterotetramers, splice variants, and regulatory subunits as well as mitochondrial diversity. In conclusion, K+ channels regulate pulmonary vascular tone and remodeling and constitute potential therapeutic targets in the regression of PAH. [source] Combining low inspired oxygen and carbon dioxide during mechanical ventilation for the Norwood procedurePEDIATRIC ANESTHESIA, Issue 1 2003Ilan Keidan MD Summary Background: Staged reconstruction has become the preferred approach for treating neonates with hypoplastic left heart syndrome (HLHS). The haemodynamic instability of a single ventricle providing blood flow in parallel to the systemic and the pulmonary circulation, combined with the effects of cardiopulmonary bypass (CPB), results in precarious perioperative conditions. The two ventilatory manoeuvres commonly used for increasing pulmonary vascular resistance are (i) decreasing the fraction of inspired oxygen to <,0.21 and (ii) adding carbon dioxide (CO2) to the ventilatory circuit. Whether molecular nitrogen (N2) or CO2 is used in these situations is a matter of physician and institutional preference. The effect of the two modalities in combination has not been studied in depth. Methods: This prospective observational study was designed to look at the effects of adding inhaled CO2 to children with HLHS who were already on a hypoxic mixture during the immediate perioperative period. Results: Twelve suitable neonates were enrolled in the study. Combining the two ventilatory modalities had an additive effect. The effect was more significant in the prebypass (83% of patients) compared with the postbypass period (25% of patients). Conclusions: Low inspired oxygen and CO2 have an additive vasoconstrictive effect on the pulmonary vessels. The use of both of these ventilatory manoeuveres is less effective postoperatively compared with the prebypass period. [source] The bronchial circulation,worth a closer look: A review of the relationship between the bronchial vasculature and airway inflammationPEDIATRIC PULMONOLOGY, Issue 1 2010Angela McCullagh MBBS Abstract Until recently, the bronchial circulation has been relatively ignored in the research and clinical arenas, perhaps because of its small volume and seeming dispensability relative to the pulmonary circulation. Although the bronchial circulation only receives around 1% of the cardiac output in health, it serves functions that are critical to maintaining airway and lung function. The bronchial circulation also plays an important role in many lung and airway diseases; through its ability to increase in size, the bronchial circulation is able to provide lung parenchymal perfusion when the pulmonary circulation is compromised, and more recently the role of the bronchial circulation in the pathogenesis of inflammatory airway disease has been explored. Due to the anatomic variability and small volume of the bronchial circulation, much of the research to date has necessitated the use of animal models and invasive procedures. More recently, non-invasive techniques for measuring bronchial blood flow in the mucosal microvascular network have been developed and offer a new avenue for the study of this circulation in humans. In conjunction with molecular research, measurement of airway blood flow (Qaw) may help elucidate the role of the bronchial circulation in inflammatory airway disease and become a useful tool for monitoring therapy. Pediatr Pulmonol. 2010; 45:1,13. © 2009 Wiley-Liss, Inc. [source] Effects of meconium aspiration in isolated perfused rat lungsPEDIATRIC PULMONOLOGY, Issue 4 2005Wlodzimierz M. Wisniewski MD Abstract Our objective was to study meconium-induced lung injury in isolated perfused rat lungs exposed to anoxia. Our working hypothesis was that meconium-induced lung injury is independent of preexisting hypoxia, and that hypoxia will increase severity of lung injury observed after meconium aspiration. We comparde five different groups of animals (n,=,5) for pulmonary arterial pressure (PAP), weight lung changes, and TNF, expression. Group I had lungs instilled with 4 ml of normal saline. Group II had lungs exposed to 5 min of anoxia. Group III had lungs instilled with 4 ml of 30% filtered human meconium. Group IV had lungs exposed to 5 min of anoxia and then instilled with 4 ml of 30% filtered human meconium. Group V had lungs instilled with 4 ml of 30% unfiltered human meconium. Our subjects were adult Sprague-Dawley rats. The isolated rat lung model was prepared according to Levey and Gast (J Appl Physiol 1966;21:313,316). Lungs were ventilated with room air. Anoxia was caused by the use of N2. The pulmonary artery was cannulated, and pulmonary arterial pressure and lung weight were measured. Lung weight and pulmonary arterial pressure were monitored for 120 min, and TNF, levels were measured in effluent at 15, 30, 60, and 120 min. Experiments were done at the Michael Reese Hospital (Chicago, IL). At the end of the experiment, PAP reached its highest values in group V (10.0,±,1.7 mmHg). Final PAPs in groups I,IV were: 4.85,±,0.3, 4.99,±,0.4, 5.93,±,0.3, and 7.25,±,0.51 mmHg, respectively). Lung wet weight increased significantly only in groups IV and V vs. group I; at 120 min, they were: 0.96,±,0.3 g, P,<,0.01, and 1.5 g,±,0.2 g, P,<,0.01, respectively. TNF, levels did not change significantly over time in group I. TNF, is a marker as well as proprietor of pulmonary inflammatory response. TNF, reached its highest levels in groups IV and V: 595 and 753 pg/ml at 120 min, respectively. In conclusion, a short episode of anoxia prior to meconium aspiration may increase lung sensitivity to meconium-induced lung injury. This effect may be moderated by the TNF, present in the pulmonary circulation. Pediatr Pulmonol. 2005; 39:368,373. © 2005 Wiley-Liss, Inc. [source] Blunted effect of the Kv channel inhibitor on pulmonary circulation in Tibetan sheep: A model for studying hypoxia and pulmonary artery pressure regulationRESPIROLOGY, Issue 1 2004Takeshi Ishizaki Objective: The aim of this study was to assess the effect of 4-aminopyridine, a Kv channel inhibitor, on the pulmonary circulation of Tibetan sheep. It has been reported that chronic hypoxia downregulates the 4-aminopyridine (4AP)-sensitive Kv channel (which governs the membrane potential (Em) of pulmonary vascular smooth muscle cells in pulmonary vessels) without a change in 4AP sensitivity. Methodology: Pulmonary haemodynamic indices and blood gas analyses were measured in six young male animals in an altitude chamber that was adjusted to simulated altitudes of 0 m, 2260 m, and 4500 m. Drip infusion of 4AP, 10 mg/h for 3 h, was started and continued during the study. Results: With the increase in altitude mean pulmonary artery pressure increased and mean Pao2 decreased. 4AP had no effect on the levels of mean PPA, mean pulmonary artery wedge pressure, cardiac output, and mean PaO2, mean PaCO2, and mean pH at any altitude but tended to alter heart rate and mean arterial pressure at altitudes of 2260 m and 4500 m. Conclusion: It is concluded that the 4AP-sensitive Kv channel does not play a role in pulmonary vascular tone in high-altitude active Tibetan sheep. Their pulmonary vascular oxygen sensing appears not to involve Kv channels. [source] Morphological Changes in the Chicken Ductus Arteriosi During Closure at HatchingTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 8 2008Candace Belanger Abstract The chicken embryo has two functioning ductus arteriosi (DA) during development. These blood vessels connect the pulmonary arteries to the descending aorta providing a right-to-left shunt of blood away from the nonrespiring lungs and to the systemic circuit and chorioallanotic membrane. The DA consists of two distinct tissue types along its length, a muscular proximal portion and an elastic distal portion. During hatching, the DA must close for proper separation of systemic and pulmonary circulation. We examined the morphological changes of the chicken DA before, during, and after hatching. Occlusion of the proximal DA began during external pipping and was complete at hatching. Anatomical remodeling began as early as external pipping with fragmentation of the internal elastic lamina and smooth muscle actin appearing in the neointimal zone. By day 2 posthatch, the proximal DA lumen was fully occluded by endothelial cells and smooth muscle actin positive cells. In contrast, the distal DA was not fully occluded by day 2 posthatch. Increases in Po2 of the blood serves as the main stimulus for closure of the mammalian DA. The responsiveness of the chicken proximal DA to oxygen increased during hatching, peaking during external pipping. This peak correlated with an increase in blood gas Po2 and the initial occlusion of the vessel. The distal portion remained unresponsive to oxygen throughout hatching. In conclusion, the chicken DA begins to close during external pipping when arterial Po2 increases and vessel tone is most sensitive to oxygen. Anat Rec, 291:1007,1015, 2008. © 2008 Wiley-Liss, Inc. [source] A Novel Model for Post-Transplant Obliterative Airway Disease Reveals Angiogenesis from the Pulmonary CirculationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 2 2005Andre E. Dutly We present a novel animal model for post-transplant obliterative airway disease in which the donor trachea is implanted into the recipient's lung parenchyma. Although this procedure is technically more challenging than the heterotopic model of implantation into a subcutaneous pouch, it has several important advantages some of which are the appropriate local environment and the possibility of local immunosuppressive therapy after transtracheal gene, cell or drug delivery. This model has revealed new insights into angiogenic potential of the pulmonary circulation. [source] Experimental Setup to Evaluate the Performance of Percutaneous Pulmonary Valved Stent in Different Outflow Tract MorphologiesARTIFICIAL ORGANS, Issue 1 2009Riccardo Vismara Abstract Percutaneous pulmonary valve implantation is a potential treatment for right ventricular outflow tract (RVOT) dysfunction. However, RVOT implantation site varies among subjects and the success of the procedure depends on RVOT morphology selection. The aim of this study was to use in vitro testing to establish percutaneous valve competency in different previously defined RVOT morphologies. Five simplified RVOT geometries (stenotic, enlarged, straight, convergent, and divergent) were manufactured by silicone dipping. A mock bench was developed to test the percutaneous valve in the five different RVOTs. The bench consists of a volumetric pulsatile pump and of a hydraulic afterload. The pump is made of a piston driven by a low inertia programmable motor. The hydraulic afterload mimics the pulmonary input impedance and its design is based on a three element model of the pulmonary circulation. The mock bench can replicate different physiological and pathological hemodynamic conditions of the pulmonary circulation. The mock bench is here used to test the five RVOTs under physiological-like conditions: stroke volume range 40,70 mL, frequency range 60,80 bpm. The valved stent was implanted into the five different RVOT geometries. Pressures upstream and downstream of the valved stent were monitored. Flow rates were measured with and without the valved stent in the five mock RVOTs, and regurgitant fraction compared between the different valved stent RVOTs. The percutaneous valved stent drastically reduced regurgitant flow if compared with the RVOT without the valve. RVOT geometry did not significantly influence the flow rate curves. Mean regurgitant fractions varied from 5% in the stenotic RVOT to 7.3% in the straight RVOT, highlighting the influence of the RVOT geometry on valve competency. The mock bench presented in this study showed the ability to investigate the influence of RVOT geometry on the competence of valved stent used for percutaneous pulmonary valve treatment. [source] Responses of the bronchial and pulmonary circulations to short-term nitric oxide inhalation before and after endotoxaemia in the pigACTA PHYSIOLOGICA, Issue 1 2002R. J. M. Middelveld ABSTRACT The physiological responses of the bronchial circulation to acute lung injury and endotoxin shock are largely unexplored territory. This study was carried out to study the responsiveness of the bronchial circulation to nitric oxide (NO) inhalation before and after endotoxaemia, in comparison with the pulmonary circulation, as well as to study changes in bronchial blood flow during endotoxaemia. Six anaesthetized pigs (pre-treated with the cortisol-synthesis inhibitor metyrapone) received an infusion of 10 µg/kg endotoxin during 2 h. Absolute bronchial blood flow was measured via an ultrasonic flow probe around the bronchial artery. The pigs received increasing doses of inhaled NO over 5 min each (0, 0.2, 2 and 20 ppm) before and after 4 h of endotoxaemia. The increase in bronchial vascular conductance during 5 min of inhalation of 20 ppm NO before endotoxin shock was significantly higher (area under curve (AUC) 474.2 ± 84.5% change) than after endotoxin shock (AUC 118.2 ± 40.4%, P < 0.05 Mann,Whitney U -test). The reduction of the pulmonary arterial pressure by 20 ppm NO was not different. A short rebound effect of the pulmonary arterial pressure occurred after discontinuation of inhaled NO before endotoxaemia (AUC values above baseline 54.4 ± 19.7% change), and was virtually abolished after endotoxaemia (AUC 6.1 ± 4.0%, P = 0.052, Mann,Whitney U -test). Our results indicate that the responsiveness of the bronchial circulation to inhalation of increasing doses of inhaled NO during endotoxin shock clearly differ from the responsiveness of the pulmonary circulation. The reduced responsiveness of the bronchial circulation is probably related to decreased driving pressure for the bronchial blood flow. The absence of the short rebound effect on pulmonary arterial pressure (PAP) after induction of shock could be related to maximum constriction of the pulmonary vessels at 4 h. [source] | |||||||||||||||||||||||||