Disease relevance of Pulmonary Ventilation

• 1. In cats anaesthetized with a mixture of chloralose and urethane, stimulation of pulmonary C fibres by right atrial injections of phenylbiguanide caused, after a latency of about 3 s, a reduction in pulmonary ventilation or apnoea, bradycardia and systemic hypotension, confirming previous work [1].
• A few of these birds developed a tachypneic response to hypoxia with no apparent change in the effective pulmonary ventilation, which was partly overcome during the O2-test [2].
• Changes from normocapnia to hypocapnia (and vice versa) were induced in dogs lightly anesthetized with nitrous oxide and halothane and subjected to passive pulmonary ventilation [3].
• In the control and sensitized groups quinacrine had no effect on pulmonary ventilation and lung mechanics, and in the challenged group it reduced the intensity of anaphylactic bronchospasm [4].
• Furthermore, a close relationship was found in this study between dopamine concentration measured at exhaustion ([DA]0) and maximal pulmonary ventilation per kilogram of body weight (V.Emax/W) (r = -0.668, p < 0.05) or maximum oxygen uptake per kilogram of body weight (VO2MAX/W) (r = 0.720, p < 0.05) [5].

High impact information on Pulmonary Ventilation

• Diacetylmorphine (heroin) was administered into several cerebroventricular regions of chloralose-anesthetized cats, while monitoring pulmonary ventilation with a Fleisch pneumotachograph [6].
• In contrast, plasma catecholamines, leg glucose uptake and leg lactate release, arterial carbon dioxide tension and pulmonary ventilation were not affected [7].
• 1. In cats anaesthetized with a mixture of chloralose and urethane, stimulation of cardiac receptors by left atrial injections of veratridine had little or no effect on pulmonary ventilation but caused bradycardia, systemic hypotension and hindlimb vasodilation with a latency of 3.3 s [8].
• Quantitative evaluation of regional pulmonary ventilation using PET and nitrogen-13 gas [9].
• Due to the solubility of xenon-133 in blood and tissues, errors are introduced in the determination of regional pulmonary ventilation [10].

Chemical compound and disease context of Pulmonary Ventilation

• These results indicate that the ventilatory response to hypercapnia is markedly improved by the two caudal blocks, but resting ventilation is slightly impaired by caudal block with lidocaine, and from the aspect of pulmonary ventilation bupivacaine is better than lidocaine for caudal anaesthesia [11].
• At HA, resting pulmonary ventilation was increased, resulting in marked hypocapnia with appropriate base deficit in blood plasma; CSF became more alkaline; CO2-response curves were shifted to lower PCO2 levels, and their slopes were steeper than at SL [12].

Biological context of Pulmonary Ventilation

• We studied the role of neural transmission from hypermetabolic peripheral tissues in the regulation of cardiac output and pulmonary ventilation in chloralose-anesthetized dogs [13].
• Heart rate, FeO2, and FeCO2 were stable during the period from 20 to 80 min, VO2 was constant from 30 to 80 min, while work output, pulmonary ventilation, blood lactate, and VCO2 decreased significantly over the 90-min performance [14].
• Oxygen consumption (VO2) and pulmonary ventilation (VE) were measured in conscious rats at Ta = 27 degrees C (warm) and 11 degrees C (cold), breathing air or two levels of asphyxic gases, moderate (10% O2-4% CO2), or severe (10% O2-8% CO2), for approximately 30 min each [15].
• Steady-state pulmonary ventilation (Vg) and breathing pattern (VT, fR), oxygen consumption (MO2), O2 concentrations (C) and pressures (P) in the arterial (a) and mixed venous blood (v), hematocrit (Ht) and acid-base status in arterial blood, and heart frequency (fH) were measured [16].
• Compared with pretraining, this SCI group exhibited significantly (p less than or equal to .05) higher posttraining peak PO (+45%), oxygen uptake ([O2], + 23%), pulmonary ventilation (+27%), heart rate (+11%), cardiac output ([Qt], + 13%) and significantly lower total peripheral resistance ([TPR], - 14%) during FES-LCE posttests [17].

Anatomical context of Pulmonary Ventilation

• When pulmonary ventilation or central respiratory drive (in terms of phrenic nerve activity) was related to brainstem ECF-pH, no unique function resulted for respiratory (CO2-induced) and metabolic (lactic acid induced) acid-base changes, thus contradicting the "reaction theory" for central respiratory chemosensitivity [18].

Associations of Pulmonary Ventilation with chemical compounds

• Peak pulmonary ventilation, metabolic rate, and arterial PO2 were significantly higher in the tetracycline-treated group [19].
• We asked whether repeated hypoxic exposures during the early neonatal periods could affect the ventilatory control, such as the lung volume-dependent ventilatory inhibition (HBR), pulmonary ventilation (VE), and CO2 production (VCO2) [20].
• A new strategy for a quantitative measurement of regional pulmonary ventilation using hyperpolarized helium-3 (3He) MRI has been developed [21].
• Taken with existing evidence that hyperoxia stops pulmonary ventilation even under conditions in which PaCO2 is elevated this suggests that hypoxic and hypercapnic stimuli summate to drive lung ventilation in the toad [22].
• First, halothane anesthesia does not modify pulmonary ventilation, but a tachypnea much more intense in intact than in decerebrated cats is observed [23].

Gene context of Pulmonary Ventilation

• A simplified method of CPAP delivery to the nonventilated lung during unilateral pulmonary ventilation [24].
• Heretofore, the technical difficulties encountered in the measurement of blood nitrogen tension (PN2) by gas chromatographic techniques effectively prevented the utilization of PN2 as a clinical tool to characterize mismatching of pulmonary ventilation and perfusion [25].
• Because not all children could walk at all speeds on the treadmill, an ANOVA was performed on data for children who walked at 3 km.h(-1) and CWS (N = 8 for HR; N = 9 for pulmonary ventilation and metabolic variables) and a t-test on data at 90% of FWS (N = 9 for HR; N = 8 for pulmonary ventilation and metabolic variables) [26].
• Intratracheal pulmonary ventilation and congenital diaphragmatic hernia: a report of two cases [27].
• The hypothesis that histamine H2 receptor blockade adversely affects neuromuscular function was tested, in vivo, in rats anaesthetised with urethane during mechanical pulmonary ventilation [28].

Analytical, diagnostic and therapeutic context of Pulmonary Ventilation

• The influence of caudal analgesia on pulmonary ventilation and gas exchange was studied in 26 children during halothane anaesthesia with spontaneous breathing [29].
• BACKGROUND: Intratracheal pulmonary ventilation (ITPV) is a form of tracheal gas insufflation through a reverse thrust catheter that facilitates expiration and enhances CO2 removal [30].
• Technical and analytical advances in pulmonary ventilation SPECT with xenon-133 gas and Tc-99m-Technegas [31].
• 1. The effects of intravenous injections of adenosine agonists and antagonists on pulmonary ventilation were investigated in conscious male Sprague-Dawley rats [32].
• Using an animal model of acute respiratory failure (ARF), we evaluated two treatments: conventional mechanical pulmonary ventilation (MV) and continuous positive airway pressure (CPAP) with extracorporeal removal of CO2 by an artificial membrane lung [33].

References