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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperammonemia increases brain glutamine levels, causes astrocytic swelling, and depresses cerebral blood flow (CBF) responsivity to CO2. Methionine sulfoximine (MSO) inhibition of glutamine synthetase activity, known to be enriched in astrocytes, prevents ammonia-induced increases in brain glutamine and water content. We tested the hypothesis that inhibition of glutamine accumulation restores CBF responsivity to CO2 during acute hyperammonemia. Pentobarbital-anesthetized rats treated with either vehicle or MSO (150 mg/kg i.p.) received a 6-hour intravenous infusion of either sodium or ammonium acetate. With subsequent induction of hypercapnia, CBF increased from 113 +/- 14 (mean +/- SEM) to 194 +/- 9 ml/min per 100 g in control rats but was unchanged from 107 +/- 13 to 79 +/- 10 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats restored the CBF response to hypercapnia (from 73 +/- 8 to 141 +/- 14 ml/min per 100 g). With induction of hypocapnia, CBF decreased from 114 +/- 11 to 88 +/- 11 ml/min per 100 g in control rats but increased from 112 +/- 13 to 142 +/- 19 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats did not fully restore the response to hypocapnia but prevented the paradoxical increase in CBF (from 80 +/- 8 to 80 +/- 8 ml/min per 100 g). In control rats, MSO did not affect CO2 responsivity. Treatment with MSO prevented ammonia-induced increases in intracranial pressure. Hyposmotic-induced increases in brain water content and intracranial pressure attenuated the CBF response to hypercapnia but, unlike hyperammonemia, did not attenuate the response to hypocapnia. In contrast to hypercapnia, vasodilation in response to arterial hypotension was intact in hyperammonemic rats. We conclude that the grossly abnormal CBF responsivity to CO2 alterations during hyperammonemia is linked to glutamine accumulation rather than ammonia per se. Cerebral edema secondary to glutamine accumulation may contribute in part to abnormal CBF responses, although other aspects of astrocyte dysfunction are likely to be important.
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PMID:Restoration of cerebrovascular CO2 responsivity by glutamine synthesis inhibition in hyperammonemic rats. 139 82

This study examines the effects of hypoxia/hypercapnia and hypoxia/hypercapnia with hypotension (hypotensive-hypoxia/hypercapnia) on blood-to-brain transfer constants (K1) for sodium and mannitol and brain water and electrolyte contents in newborn piglets. Hypoxia/hypercapnia was induced for 60 min with the piglets breathing a gas mixture of 15% carbon dioxide, 10-12% oxygen, and 73-75% nitrogen adjusted to achieve an arterial pH less than 7.15, pO2 less than 40, and pCo2 greater than 60 mmHg and hypotension for 20 min by rapid phlebotomy to achieve a mean arterial blood pressure less than 40 mmHg. Piglets were studied during 1 h of, and 24 h after resuscitation from hypoxia/hypercapnia (arterial pH 6.9 +/- 0.18, pO2 36 +/- 6 mmHg, pCO2 68 +/- 8 mmHg, mean +/- S.D.) and 10 min, and 24 h after resuscitation from hypotensive-hypoxia/hypercapnia (mean arterial blood pressure 28 +/- 10 mmHg, mean +/- S.D.). Values for K1 for sodium and mannitol, measured using the integral technique were 15.9 and 5.2 ml.g-1.min-1 x 10(4) respectively, in 2-4-day-old controls, suggesting that the barrier is fully developed in newborn piglets. Values were not different during or after hypoxia/hypercapnia or 24 h after hypotensive-hypoxia/hypercapnia. Ten to forty min after hypotensive-hypoxia/hypercapnia, there was a proportional decrease in the K1 for sodium and mannitol of about 40%. These results suggest that the newborn piglet is similar to the adult with respect to impermeability of the blood-brain barrier to ions and small molecules and resistance of this barrier to systemic hypoxia/hypercapnia and hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood-brain barrier integrity and brain water and electrolytes during hypoxia/hypercapnia and hypotension in newborn piglets. 142 34

Peripheral chemoreceptors generally play a limited role in the initial development of diving bradycardia in mammals. However, T.F. Huang and Y.I. Peng (Jpn. J. Physiol. 26: 395-401, 1976) reported that peripheral chemoreceptors are very important for manifestation of the diving response in conscious rats. The objectives of this study were to reinvestigate those findings and determine whether the cardiovascular responses to simulated diving in the rat were potentiated during preexisting hypoxia or hypercapnia. Responses to simulated diving were elicited by nasal water flow with concurrent apnea in paralyzed, artificially ventilated Sprague-Dawley rats anesthetized with Innovar. The experiments show that nasal stimulation in the rat results in rapid bradycardia and hypotension and that these responses are not due to laryngeal stimulation. The data also suggest that chemoreceptors do not play a role in the initiation of the responses to simulated diving in rats and that preexisting chemoreceptor drive does not alter the cardiovascular responses. Additionally, we found that concomitant expiratory apnea is necessary to sustain the profound initial cardiovascular changes induced by nasal water flow.
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PMID:Cardiovascular responses to nasal water flow in rats are unaffected by chemoreceptor drive. 144 22

To evaluate the effect of respiratory syncytial virus (RSV) infection on reflex apnea elicited by application of water on the laryngeal mucosa, 11 healthy, term lambs were chronically instrumented at 2 wk of age. Six lambs were inoculated with bovine RSV, and five lambs were mock-infected. The lambs were studied awake and unsedated before and 4, 8, 14, and 21 d after infection. RSV infection was associated with slight rhinorrhea and with moderately increased tracheal mucous discharge. There was an average increase of 0.5 degrees C in body temperature. Arterial pH, PO2, and PCO2 remained within the normal range. The ventilatory response to laryngeal chemostimulation measured as the percentage of decrease in ventilation from control was significantly (p less than 0.05) larger among the infected animals when compared with controls on d 4 and 8. There were no differences in indices of respiratory drive (airway occlusion pressure and mean inspiratory flow), ventilatory response to hypoxia (0.10 fraction of inspired O2), or hypercarbia (0.03 fraction of inspired O2). We speculate that RSV infection alters the sensitivity of the laryngeal chemoreceptors so that a prolonged or even fatal apnea may result from stimulation of these receptors. These results may be relevant to the pathogenesis of sudden infant death syndrome associated with RSV infection.
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PMID:Respiratory syncytial virus infection reinforces reflex apnea in young lambs. 157 Feb 5

Pressure ventilation of the newborn can adversely affect the cardiovascular system. Increasing airway pressure increases cerebral venous pressure, thus stressing brain vasculature. To test the hypothesis that cerebral venous distension caused by mechanical ventilation alters cerebral microvascular responses, we studied cerebrovascular responses before, during, and after positive pressure ventilation. Anesthetized newborn pigs were ventilated with a standard time-cycled, pressure-limited infant respirator. Pial arterioles were measured in response to hypercapnia, topical isoproterenol, and topical norepinephrine during control [mean airway pressure (Paw) = 0.9 +/- 0.05 kPa (4.8 +/- 0.3 cm H2O)] conditions, during 40-60 min of increased Paw [2.5 +/- 0.2 kPa (13.9 +/- 1.3 cm H2O)], and when the Paw was lowered again. Pial arteriolar dilation in response to hypercapnia was not changed by increasing Paw. Similarly, responses to isoproterenol and norepinephrine were unaltered during raised Paw. However, a significant decrease in responses to topical isoproterenol and norepinephrine was observed after increased Paw. These experiments show that specific prostanoid-independent cerebrovascular responses are altered subsequent to pressure ventilation, whereas prostanoid-dependent dilation to hypercapnia was not affected. These changes suggest that the newborn cerebral vasculature is affected by positive pressure ventilation, further raising the possibility that ventilation-induced alterations in microvascular responses could make the brain more vulnerable to added stresses after pressure ventilation.
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PMID:Alterations in cerebrovascular reactivity after positive pressure ventilation. 163 36

A technique has been developed for proton magnetic resonance imaging (MRI) of perfusion, using water as a freely diffusable tracer, and its application to the measurement of cerebral blood flow (CBF) in the rat is demonstrated. The method involves labeling the inflowing water proton spins in the arterial blood by inverting them continuously at the neck region and observing the effects of inversion on the intensity of brain MRI. Solution to the Bloch equations, modified to include the effects of flow, allows regional perfusion rates to be measured from an image with spin inversion, a control image, and a T1 image. Continuous spin inversion labeling the arterial blood water was accomplished, using principles of adiabatic fast passage by applying continuous-wave radiofrequency power in the presence of a magnetic field gradient in the direction of arterial flow. In the detection slice used to measure perfusion, whole brain CBF averaged 1.39 +/- 0.19 ml.g-1.min-1 (mean +/- SEM, n = 5). The technique's sensitivity to changes in CBF was measured by using graded hypercarbia, a condition that is known to increase brain perfusion. CBF vs. pCO2 data yield a best-fit straight line described by CBF (ml.g-1.min-1) = 0.052pCO2 (mm Hg) - 0.173, in excellent agreement with values in the literature. Finally, perfusion images of a freeze-injured rat brain have been obtained, demonstrating the technique's ability to detect regional abnormalities in perfusion.
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PMID:Magnetic resonance imaging of perfusion using spin inversion of arterial water. 172 91

We evaluated the physiologic effects of pressure support ventilation by nasal route (NPSV) in eight patients with severe stable COPD and chronic hypercapnia who were randomly submitted to 2-h sessions of NPSV both with a portable ventilator (Respironics BIPAP device) and with a standard ventilator (Bird 6400ST device) at an inspiratory airway pressure of 22 cm H2O. Two sessions with each ventilator were performed using an FIO2 of 0.21 in each patient on two consecutive days. One patient did not tolerate either form of ventilation. Comparison of spontaneous with BIPAP ventilation showed a significant improvement in pH, PaCO2, and PaO2. Ventilatory pattern assessed by a respiratory inductive plethysmograph showed a significant increase in minute ventilation (VE), VT, and Ttot. Integrated surface diaphragmatic EMG activity measured only during BIPAP device ventilation decreased from that measured during spontaneous breathing. Similar changes in blood gases and ventilatory pattern were observed during ventilation by the Bird 6400ST except for VT/Ti ratio, which significantly increased. Comparison of baseline with measurements performed 12 h after the whole cycle of treatment showed a significant increase in pH and VE and a decrease in PaCO2. We conclude that short-term NPSV may be useful in improving respiratory pattern and blood gases in stable COPD patients with chronic hypercapnia.
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PMID:Physiologic evaluation of pressure support ventilation by nasal mask in patients with stable COPD. 173 60

It was demonstrated by experiment that exposure of non-anesthetized rabbits to rocking in the head-down position at -30 degrees led to acidosis, hypoxemia and hypercapnia, changes in impedance components that were suggestive of water imbalance in the cerebral tissue, paralytic dilation of microcirculation vessels, subarachnoidal hemorrhages, hyaline thrombi, stasis and sludge-syndrome, small perivascular extravasates in different brain compartments, marked perivascular and pericellular edema. Pretreatment with dimephosphone prevented or attenuated significantly acidosis, water imbalance, and pathomorphological disorders in the vascular system, nervous and glial elements of the brain of the rabbits examined.
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PMID:[Morphofunctional changes in the vascular system of the rabbit brain in rocking during anti-orthostatic position and administration of dimephosphon]. 177 Jul 62

In mechanically ventilated patients, disconnection from the ventilator and endotracheal suctioning can induce major arterial oxygen desaturation resulting from apnea, changes in inspired oxygen fraction, and decrease in lung volume. The aim of this study was to test the efficacy of a simple method of delivering oxygen and maintaining lung volume during this process. Our study was conducted in two parts. In the first part, constant-flow insufflation of oxygen (CFI) was used in seven patients ventilated for acute respiratory failure (PaO2/FlO2 = 347 +/- 33 mm Hg) as a means of maintaining arterial oxygenation during apnea and disconnection from the ventilator. CFI was administered via a modified endotracheal tube in which small capillaries allowed delivery of a high-velocity jet flow near the tracheal end of the tube during disconnection from the ventilator. In comparison to apnea alone, CFI prevented a fall in arterial oxygen tension (16 +/- 7 mm Hg during CFI versus 117 +/- 27 during apnea, after 90 s of disconnection in the two situations, p less than 0.001), whereas it did not reduce the development of hypercapnia. The efficacy of CFI resulted both from the injection of oxygen into the trachea and from the maintenance of positive alveolar pressure induced by air entrainment (mean 10.4 +/- 1.1 cm H2O), preventing a fall in lung volume usually occurring after disconnection (+338 +/- 88 ml during CFI versus -344 +/- 64 ml during apnea, p less than 0.01). In the second part of the study CFI was used to prevent arterial oxygen desaturation induced by endotracheal suctioning.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Constant-flow insufflation prevents arterial oxygen desaturation during endotracheal suctioning. 185 66

This study assessed the effects of experimentally elevated plasma catecholamine levels on gill ventilation in rainbow trout (Oncorhyncus mykiss) exposed to various external ventilatory stimulants. Trout were exposed to hypoxia (water PO2 (PwO2) = 90 Torr) or hypercapnia (water PCO2 (PwCO2) = 4.5 Torr) for 30 min. These conditions caused gill ventilation volume (Vw) to increase by 2.3- and 1.5-fold, respectively, but did not stimulate release of catecholamines into the blood. While the stimulus (hypoxia or hypercapnia) was maintained, fish were given a bolus injection (0.3 ml), followed by intra-arterial infusion (0.6 ml.h-1), of a catecholamine mixture (2 x 10(-5) mol.l-1 adrenaline + 5 x 10(-6) mol.l-1 noradrenaline) to mimic the physiological concentrations and ratios of these catecholamines observed under more severe hypoxic or hypercapnic conditions. In hypoxic fish, this treatment caused a significant, but transient (5 min) depression of ventilation while during hypercapnia, the administration of exogenous catecholamines caused a more prolonged hypoventilatory response. These hypoventilatory responses occurred despite a catecholamine-induced blood acidosis (a potential ventilatory stimulant). To assess the importance of initial Vw and/or blood respiratory status on catecholamine-mediated hypoventilation, these experiments were repeated under hyperoxic (PwO2 = 640 Torr) hyperoxic hypercapnic (PwO2 = 510 Torr, PwCO2 = 4.8 Torr) or normoxic (PwO2 = 151 Torr) conditions in which Vw was either depressed (3.9-fold during hyperoxia) or unaffected. Intra-arterial infusion of catecholamines did not affect Vw under either of these experimental conditions. These results demonstrate that during a respiratory challenge, such as hypoxia or hypercapnia, physiologically relevant levels of circulating catecholamines can depress Vw and therefore do not support a stimulatory role for circulating catecholamines in the control of ventilation in fish.
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PMID:The effects of catecholamines on ventilation in rainbow trout during hypoxia or hypercapnia. 190 29


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