OBJECTIVETo study the effect of Simulated Microgravity and its Associated Mechanism on Pulmonary Circulation in Rats).

METHODSRat tail-suspension model was used to simulate the physiological effects of microgravity and changes in pulmonary blood vessel morphology, pulmonary arterial and venous blood pressure, pulmonary vascular resistance, pulmonary vasomotoricity, as well as the regulation of pulmonary circulation by cytokines produced and released by the lung of rats were measured.

RESULTSThe walls of pulmonary blood vessels of rats were thickened, and the pulmonary artery was reconstructed with increased pulmonary vascular resistance. The pulmonary blood vessels of rats became more prone to dilation as contractions increased. Rat epithelial Adrenomedulin gene transcription and protein expression were upregulated. The level of basic fibroblast growth Factor of rat was also elevated.

CONCLUSIONFindings from the present study on rats revealed that the microgravity can affect pulmonary blood vessel structure, pulmonary arterial pressure, and pulmonary blood vessel self-regulation and cytokine production.

Animals ; Hemodynamics ; Male ; Pulmonary Artery ; physiology ; Pulmonary Circulation ; physiology ; Rats ; Rats, Wistar ; Weightlessness

Echocardiography, Transesophageal ; Humans ; Monitoring, Physiologic ; standards ; Pulmonary Circulation ; physiology ; Pulmonary Wedge Pressure ; Stroke Volume

Based on the principles of the sheet-flow model, oxygen transport in pulmonary capillaries was considered as a process in which oxygen first enters plasma through the respiratory membranes, and then combines with the Hbc. A novel mathematical model about oxygen transport in pulmonary capillaries was established according to the relationship of the oxygen concentration inside the red blood cells with the concentration of haemoglobin and the blood saturation, and according to the basic formula for the correlation between blood saturation and oxygen partial pressure. Furthermore, we adopted the Lax-Wendroff Finite Difference Method and obtained certain valuable results under different physiological states. It was well concluded that the established model could be used to provide useful data for medical researchers as well as doctors.
Biological Transport ; physiology ; Capillaries ; physiology ; Humans ; Models, Biological ; Oxygen ; blood ; Partial Pressure ; Pulmonary Alveoli ; blood supply ; Pulmonary Circulation ; physiology ; Pulmonary Gas Exchange

Lung electrical impedance signal carries the information of hemodynamics such as pulmonary blood supply intensity, vessel elasticity, blood flow resistance and so on. It can be used to diagnose and distinguish various kinds of heart diseases and to judge cardiac functions. The character points of lung impedance are the main basis to analyze the information of hemodynamics. This article is based on wavelet transformation to extract the character points of lung impedance. First we used the scale waveform of character points of lung impedance to make the template. Then we got wavelet ratio wave form from lung impedance by wavelet transformation. Finally we used the wavelet ratio wave form to do matching operation with the template in order to locate character points. The result of experiment demonstrates that it is an efficient and feasible method to locate character points by wavelet transformation because of its strong real time and high detection efficiency.
Electric Impedance ; Hemodynamics ; physiology ; Humans ; Lung ; blood supply ; physiology ; Pulmonary Circulation ; physiology ; Signal Processing, Computer-Assisted ; Wavelet Analysis

BACKGROUNDThe breathhold contrast-enhanced three-dimensional magnetic resonance angiography (MRA) using T1-weighted gradient-echo imaging sequence is the standard technique for MRA of the thorax. However, this technique is not desirable for certain patients with respiratory insufficiency, serious renal impairment, or allergy to contrast agents. The objective of this study was to optimize and evaluate a non-contrast-enhanced free-breathing pulmonary MRA protocol at 3 Tesla.

METHODSThe time-of-flight protocol was based on a two-dimensional T1-weighted turbo field echo sequence with slice-selective inversion recovery and magnetization transfer preparation together with respiratory navigator gating, cardiac gating, and parallel imaging. Optimal values for time of inversion delay, flip angle and slice thickness were experimentally determined and used for all subjects.

RESULTSExcellent pulmonary MRA images, in which the 7th order branches of pulmonary arteries could be reliably identified, were obtained in the 12 free-breathing healthy volunteers. TI of approximately 300 ms provides the best suppression of background thoracic and cardiac muscles and effective inflow enhancement. With increasing flip angle, the pulmonary vessels gradually brightened and exhibited optimal contrast at 20 degrees-30 degrees. The 2 mm slice thickness and 0.5 mm slice overlap is suitable for visualization of the peripheral pulmonary vessel.

CONCLUSIONSThe MRA protocol at 3 Tesla may have clinical significance for pulmonary vascular imaging in patients who are not available for contrast-enhanced 3D MRA and CT angiography examination or are unable to sustain a long breath-hold.

Adult ; Aged ; Contrast Media ; Female ; Humans ; Magnetic Resonance Angiography ; methods ; Male ; Middle Aged ; Pulmonary Artery ; anatomy & histology ; Pulmonary Circulation ; physiology ; Pulmonary Veins ; anatomy & histology ; Young Adult

Although hypoxic pulmonary vasoconstriction (HPV) has been recognized by many researchers, the precise mechanism remains unknown. As isolated pulmonary arteries will constrict in vitro in the response to hypoxia, the oxygen sensor/transduction mechanism must reside in the pulmonary arterial smooth muscle or in the endothelium, or in both. Unfortunately, much of the current evidence is conflicting, especially as to the dependency of HPV on the endothelium and the role of a K+ channel. Therefore, this experiment was attempted to clarify the dependency of HPV on the endothelium and the role of a K+ channel on HPV in rat pulmonary artery. The effects of hypoxia were investigated in isolated main pulmonary arteries precontracted with norepinephrine. Vascular rings were suspended for isometric tension recording in an organ chamber filled with a Krebs-Henseleit solution. Hypoxia was induced by gassing the chamber with 95% N2 + 5% CO2 and this was maintained for 20 min. Hypoxia elicited a vasoconstriction in arteries with endothelium. Mechanical disruption of the endothelium abolished HPV. There was no difference between the amplitude of the HPV induced by two consecutive hypoxic challenges and the effect of normoxic and hyperoxic control Krebs-Henseleit solution on a subsequent response to hypoxia. Inhibition of NO synthesis by treatment with N(omega)-nitro-L-arginine reduced HPV, but inhibition of a cyclooxygenase pathway by treatment with indomethacin had no effect on HPV. Blockades of a tetraetylammonium chloride-sensitive K+ channel abolished HPV. Verapamil, a Ca2+ entry blocker reduced HPV. In conclusion, these results suggest that HPV was dependent on the endothelium and that HPV can be considered to be induced by inhibition of the mechanisms of NO-dependent vasodilation such as the opening of a K+ channels.
Animal ; Anoxia/physiopathology* ; Blood Vessels/physiopathology ; Calcium Channel Blockers/pharmacology ; Cyclooxygenase Inhibitors/pharmacology ; Enzyme Inhibitors/pharmacology ; Indomethacin/pharmacology ; Nitroarginine/pharmacology ; Pulmonary Circulation/physiology* ; Pulmonary Circulation/drug effects ; Rats ; Tetraethylammonium/pharmacology ; Vasoconstriction/physiology* ; Vasoconstriction/drug effects ; Verapamil/pharmacology

OBJECTIVETo investigate the changes in respiratory and circulatory functions in chronic obstructive pulmonary disease (COPD) patients during sequential invasive-noninvasive mechanical ventilation therapy, and evaluate the effects of this new technique.

METHODSTwelve COPD patients with type II respiratory failure due to severe pulmonary infection were ventilated through an endotracheal tube. When the pulmonary infection control window (PIC-Window) occurred, the patients were extubated and were ventilated with a facial mask using pressure support ventilation combined with positive end-expiratory pressure. The parameters of hemodynamics, oxygen dynamics, and esophageal pressure were measured at the PIC-Window during invasive mechanical ventilation, one hour after oxygen therapy via a naso-tube, and three hours after non-invasive mechanical ventilation.

RESULTSThe variation in esophageal pressure was 20.0 +/- 6 cmH(2)O during naso-tube oxygen therapy, and this variation was higher than that during non-invasive mechanical ventilation (10 +/- 6 cmH(2)O, P < 0.01). The changes in respiratory and circulatory parameters were not significantly different between invasive mechanical ventilation and noninvasive mechanical ventilation (P > 0.05).

CONCLUSIONSThe respiratory and circulatory functions of COPD patients remained stable during sequential invasive-noninvasive mechanical ventilation therapy using PIC-Window as a switch point for early extubation. The COPD patients can tolerated the transition from invasive mechanical ventilation to noninvasive mechanical ventilation.

Aged ; Blood Circulation ; physiology ; Female ; Humans ; Male ; Pulmonary Disease, Chronic Obstructive ; physiopathology ; therapy ; Respiration, Artificial ; methods ; Respiratory Physiological Phenomena

OBJECTIVETo investigate the mechanism of pulmonary circulation obstacle in chemicals-induced acute lung injury and its clinical significance.

METHODPulmonary arterial intubation, circulating endothelial cells (CEC) isolation and hemorheology detection technique were used to observe the changes of CEC numbers and hemorheology in rat pulmonary vascular system during oleic acid-induced acute lung injury (ALI).

RESULTSThe numbers of CEC were obviously increased even in the early phase of ALI [from (2.06 +/- 0.48)/0.9 micro l to (5.50 +/- 0.54)/0.9 micro l]; there was no obvious change in whole blood viscosity under high shear rate (200 s(-1), 30 s(-1)) but the whole blood viscosity and hematocrit were remarkably increased in pulmonary artery blood at low shear rate (5 s(-1), 1 s(-1)) (P < 0.05). Erythrocytes had increasing tendency, whereas platelets were also decreased but there was no statistical significance.

CONCLUSIONThe deterioration of pulmonary circulation may be the key point in the pathogenesis of ALI; the injury and dysfunction of pulmonary capillary endothelial cells (PCEC) may be the common starting phase in the pathological processes of ALI; the detection of CEC may offer a new valuable and sensitive index for diagnosis of ALI.

Animals ; Blood Viscosity ; Endothelial Cells ; physiology ; Male ; Pulmonary Circulation ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; blood ; diagnosis

Patients with severe Ebstein's anomaly showing in the neonatal period, represent progressive cardiac enlargement with pulmonary hypoplasia and functional pulmonary atresia with patent ductus arteriosus-dependent pulmonary circulation. Biventricular repair in these patients had been mostly unsuccessful except for Starnes' procedure that converts the anatomy to single ventricle physiology for Fontan procedure. A 4-days old male was admitted with the diagnosis of severe Ebstein's anomaly with anatomic pulmonary atresia and severe cardiac enlargement. He successfully underwent biventricular repair with vertical plication method of atrialized right ventricle, tricupid annuloplasty, transannular right ventricular outflow tract reconstruction, atrial septal defect patch closure with fenestration, and right atrial reduction angioplasty. Postoperatively, cardiothoracic ratio was significantly reduced and mild tricuspid regurgitation was remnant in echocardiography. The patient is currently 10 months old and is fully active without restrictions.
Angioplasty ; Critical Illness* ; Diagnosis ; Ebstein Anomaly* ; Echocardiography ; Fontan Procedure ; Heart Septal Defects, Atrial ; Heart Ventricles ; Humans ; Infant ; Infant, Newborn* ; Male ; Physiology ; Pulmonary Atresia ; Pulmonary Circulation ; Tricuspid Valve Insufficiency

Right-sided heart failure is a major problem among patients with congenital heart diseases, due to the prevalence of congenital heart defects and the association of pulmonary hypertension. More attention is focused on the structure of the right heart particularly in association with congenital heart defects and chronic lung disease. The right ventricle (RV) may support the pulmonary circulation, and sometimes the systemic circulation (systemic RV) in congenital heart defects. Despite major progress being made, assessing the RV remains challenging, often requiring a multi-imaging approach and expertise (echocardiography, magnetic resonance imaging, nuclear and cineangiography). Evidence is accumulating that RV dysfunction develops in many of these patients and leads to considerable morbidity and mortality. While there is extensive literature on the pathophysiology and treatment of left heart failure, the data for right-sided heart failure is scarce. Therefore RV function in certain groups of congenital heart disease patients needs close surveillance and timely and appropriate intervention to optimise outcomes. An understanding of RV physiology and hemodynamics will lead to a better understanding of current and future treatment strategies for right heart failure. This will review right-sided heart failure with the implications of volume and pressure loading of the RV in congenital heart diseases.
Heart Defects, Congenital ; Heart Diseases* ; Heart Failure* ; Heart Ventricles ; Heart* ; Hemodynamics ; Humans ; Hypertension, Pulmonary ; Lung Diseases ; Magnetic Resonance Imaging ; Mortality ; Physiology ; Prevalence ; Pulmonary Circulation