Respiration physiology
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Respiration physiology · Jan 2002
Brain electrical activity during combined hypoxemia and hypoperfusion in anesthetized rats.
In order to investigate the effects of moderate hypoxemia on brain electrical activity and the consequences of an altered cerebro-vascular response to hypoxemia, we recorded changes in electrical activity of the brain in anesthetized rats following unilateral carotid artery ligation (UCAL). In these animals, on the clamped side, cerebral blood flow, whilst normal during normoxia, shows less augmentation during hypoxemia. Six anesthetized (Halothane) Sprague-Dawley rats with UCAL were studied during 20 min periods of baseline (FI(O(2))=30%), hypoxemia (FI(O(2))=9.5%) and recovery (FI(O(2))=30%): mean arterial pressure of oxygen (PA(O(2))) achieved was 177.0, 37.6 and 160.1 mmHg, respectively. ⋯ M.) during baseline, which was not reversed during recovery (3.27+/-0.11 Hz) (ANOVA, P<0.01). The total power of the signal (Pw) was unaffected on the intact hemisphere but diminished on the clamped side during hypoxemia. Our results show that a significant slowing of ECoG is observed during hypoxemia of moderate intensity (40 mmHg) even when cerebro-vascular response to hypoxemia is preserved and that total power of the ECoG signal is severely diminished when the cerebro-vascular response to hypoxemia is impaired.
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The present study was aimed at assessing laryngeal dynamics and their consequences during anoxic gasping in ketamine-sedated lambs. We first verified that the glottis was closed between gasps during anoxic gasping in seven chronically instrumented lambs, aged 11-15 days. Recording of glottal constrictor muscle electrical activity, subglottal pressure and lung volume, together with endoscopic observation, confirmed the presence of active glottal closure with maintenance of a high lung volume between gasps. ⋯ No significant difference was found in time to eupnea resumption, hemodynamic parameters or arterial blood gases. We conclude that a high lung volume is actively maintained by glottal closure between anoxic gasps in sedated lambs. Further studies are however needed to define the importance of laryngeal dynamics during gasping.
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Acute lung inflammation is an important component of a number of pulmonary diseases, including acute respiratory distress syndrome (ARDS). Much has been learned about the manner in which various insults to lung, such as infection or trauma, bring about recruitment of neutrophils into alveoli and small airways, resulting in parenchymal damage and organ dysfunction. In this brief review, we discuss the endogenous mechanisms in which the lung regulates the acute inflammatory response in rats to intrapulmonary deposition of IgG immune complexes. Emphasis is given to the participation of the transcription factor, NF-kappaB, in the development of lung injury and the endogenous mediators which attempt to control the extent of lung inflammation by modulating the activation of NF-kappaB.
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Respiration physiology · Oct 2001
ReviewGenetic and environmental modulation of chronic obstructive pulmonary disease.
Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of morbidity and mortality throughout a large part of the western world. Although personal tobacco use has been implicated in a large number of these cases, it is also true that only a fraction of smokers ever develop respiratory problems. Therefore, the question of host susceptibility and other environmental factors should be considered. This paper will briefly review evidence for host susceptibility to COPD, review evidence for additional environmental risk factors for the development of COPD, and give an example of environmental interactions with a known genetic risk factor that further increase the risk of COPD.
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Respiration physiology · Sep 2001
Development of in vivo ventilatory and single chemosensitive neuron responses to hypercapnia in rats.
We used pressure plethysmography to study breathing patterns of neonatal and adult rats acutely exposed to elevated levels of CO2. Ventilation (VE) increased progressively with increasing inspired CO2. The rise in VE was associated with an increase in tidal volume, but not respiratory rate. ⋯ At all ages studied, LC neurons increased their firing rate by approximately 44% in response to hypercapnic acidosis (10% CO2, pH 7.0). Thus the in vivo ventilatory response to hypercapnia was not correlated with the V(m) response of individual LC neurons to hypercapnic acidosis in neonatal rats. These data suggest that CO2 sensitivity of ventilation in rats may exist in two forms, a high-sensitivity neonatal (or fetal) form and a lower-sensitivity adult form, with a critical window of very low sensitivity during the period of transition between the two (approximately P8).