Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ostriches (Struthio camelus) are the only birds known that can increase post-dead space ventilation during severe heat stress without experiencing hypocapnia and respiratory alkalosis. To determine whether this phenomenon occurs due to redistribution of pulmonary blood flow during panting, thus creating an extreme ventilation-perfusion (V/Q) imbalance, the distributions of pulmonary blood flow in ostriches at rest (15 degrees C) and in severe panting (45 degrees C) were determined using radioactively labeled microspheres. Blood flow distribution at rest was greatest in the neopulmo [18% greater than mean pulmonary blood flow (MPBF)] and the cranial (23% greater than MPBF) and distal (12% greater than MPBF) regions of the paleopulmo. During panting blood flow was not shunted around the lung, and flow to the neopulmo decreased to MPBF, became more homogeneous along the craniocaudal axis, and remained nonhomogeneous along the mediolateral axis. The results suggest that the observed decrease in gas exchange during panting is probably due primarily to shunting of the increased ventilation around the parabronchial exchange region rather than to alterations in the patterns of V/Q within the lung.
J Appl Physiol Respir Environ Exerc Physiol 1982 Dec
PMID:Pulmonary blood flow distribution in panting ostriches. 715 38

Six children who remained in deep coma after immersion accidents in fresh water received therapy to maintain normal intracranial pressure (ICP). This involved controlled ventilation to ensure hypocapnia and hyperoxaemia, maintenance of low normothermia, fluid restriction, dexamethasone (1-1.5 mg/kg initially, 1-1.5 mg/kg/day as maintenance) and barbiturates (phenobarbitone and thiopentone). The latter were given in a wide range of dosage. Increased ICP was common to all patients, but could always be kept at acceptable levels. All patients suffered from pulmonary oedema; three developed broncho-pneumonia and two developed adult respiratory distress syndrome. All children survived with good recovery, two needed active rehabilitation for several months.
Anaesthesia 1982 Dec
PMID:Intensive care after fresh water immersion accidents in children. 718 Oct 62

We determined the effects of sleep state on the ventilatory response following transient airway occlusion and on the response to vagal blockade in the unanesthetized sleeping dog. Three tracheotomized dogs underwent repeated occlusions (159 trials) during rapid eye movement (REM) and nonrapid eye movement (NREM) sleep. In all sleep states we found significant but variable transient hyperventilation following release of occlusion. In NREM sleep, a significant central apnea [expiratory time (TE) prolonged 2-10 times control] followed the hyperpneic response, so long as the increase in tidal volume (VT) during the hyperpnea exceeded three times control VT, that is, a volume-dependent apneic threshold. In REM sleep with maintained levels of eye movement density, hyperventilation commonly followed release of obstruction but only very rarely did VT exceed the volume threshold, and central apnea was rare. Cervical vagal blockade was used to show that significant inhibitory pulmonary stretch receptor reflexes were present in both NREM and REM sleep, although the strength of the reflex was diminished in REM. We postulate that the phasic events of REM sleep inhibit the increase in VT in response to the chemical stimuli accumulated during airway occlusion and also interfere with the prolongation of TE in response to lung stretch and/or transient hypocapnia. The result is that central apnea occurs only very rarely in REM sleep.
Sleep 1994 Dec
PMID:Effects of REM sleep on the ventilatory response to airway occlusion in the dog. 770 Nov 78

We have previously shown that hypocapnia triggers Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). Nasal continuous positive airway pressure (NCPAP) may attenuate CSR-CSA in patients with CHF and CSR-CSA. Accordingly, we hypothesized that attenuation of CSR-CSA by NCPAP would be related to an increase in PCO2. Therefore, we examined the effect of NCPAP on the frequency of apneas and hypopneas, transcutaneous PCO2 (PtcCO2), and minute volume of ventilation (VI) in 12 consecutive patients with CHF and CSR-CSA during stage 2 sleep. A control group of six patients, who did not receive NCPAP, was also studied. In the control group, there were no changes from baseline to 1 mo in the frequency of central apneas and hypopneas, mean PtcCO2, mean VI, or mean SaO2 during stage 2 sleep. In contrast, from baseline to 1 mo the NCPAP group experienced a decrease in the frequency of apneas and hypopneas (58.7 +/- 5.2 to 23.2 +/- 6.0/h of sleep, p < 0.001), an increase in mean PtcCO2 (34.6 +/- 1.4 to 40.8 +/- 1.1 mm Hg, p < 0.001), a reduction in mean VI (8.1 +/- 1.0 to 5.2 +/- 0.5 L/min, p < 0.01) and an increase in mean SaO2 (91.6 +/- 1.1 to 95.0 +/- 0.5%, p < 0.025) during stage 2 sleep while on 10.2 +/- 0.5 cm H2O nasal CPAP. We conclude that likely mechanisms through which NCPAP reduces CSR-CSA are by increasing SaO2 and raising PaCO2 during sleep toward or above the apneic threshold.
Am J Respir Crit Care Med 1994 Dec
PMID:Effect of continuous positive airway pressure on central sleep apnea and nocturnal PCO2 in heart failure. 795 21

The quantitative autoradiographic [14C]iodoantipyrine technique was applied to measure the effects of an acute hypoxic exposure on rates of local cerebral blood flow (LCBF) in the 10 (P10)-, 14 (P14)- and 21 (P21)-day-old rat. The animals were exposed to hypoxic (7% O2/93% N2) or control gas mixtures (21% O2/79% N2) for 40 min before the initiation of the 1-min LCBF measurement. At P10, hypoxia induced a 142-415% increase in LCBF over control levels, which affected the 45 structures studied. The highest increases in LCBF were noticed in posterior midbrain and brainstem regions. These increases are in good accordance with hypoxia-induced increases in LCBF recorded during acute hypoxia exposure in both newborn and adult animals. At P14 and P21, rates of LCBF decreased with hypoxia. These decreases were significant in 23 and 21 brain regions, respectively, belonging to all systems studied. These changes in LCBF are in quite good correlation with our previous data on the effects of acute hypoxia exposure on cerebral glucose utilization but the decrease in LCBF is of higher amplitude than the one in cerebral glucose utilization translating into a relative hypoperfusion at a constant metabolic level at P14 and P21. However, arterial blood pressure was reduced by 16 mmHg and arterial pCO2 was significantly decreased at the two latter ages in hypoxic animals compared to controls. These two systemic factors, and mainly hypocapnia, are rather responsible for the cerebral hypoperfusion recorded at P14 and P21 in hypoxic rats whereas the circulatory response seems to be predominantly hypoxic at P10.
Brain Res Dev Brain Res 1993 Dec 17
PMID:Regional cerebral blood flow response to acute hypoxia changes with postnatal age in the rat. 814 86

The minute ventilation required to maintain either hypocapnia (FE'CO2 = 4.0 kPa, group A, n = 36) or normocapnia (FE'CO2 = 5.0 kPa, group B, n = 38) in 74 adult patients was determined for the Bain system with controlled ventilation at 10 breath.min-1 and fresh gas flow equal to minute ventilation. Males required a greater minute ventilation and fresh gas flow than females (p < 0.01) in each group (group A, males approximately 90 ml.min-1.kg-1, females approximately 80 ml.min-1.kg-1; group B, males approximately 75 ml.min-1.kg-1; females approximately 65 ml.min-1.kg-1). Where capnography is not available, it may be safer to ventilate patients' lungs using the minute volume and fresh gas flow requirements established in group A patients. The administration of 5% carbon dioxide in oxygen for 2 min safely re-established normocapnia and spontaneous respiration in hypocapnic patients when ventilated with the same minute volume, fresh gas flow and respiratory rate required during surgery. Only one patient required greater than 400 ml.min-1 of carbon dioxide to produce a 5% concentration. Maximum flow from the carbon dioxide flowmeter may be restricted to 400 ml.min-1 rather than the 500 ml.min-1 currently recommended.
Anaesthesia 1993 Dec
PMID:Controlled ventilation with the Bain co-axial system. A rationalisation of gender-related minute volume requirements and carbon dioxide replacement therapy. 828 29

The purpose of this study is to investigate the effects of hyperventilation on the wide dynamic range (WDR) cell of the dorsal horn of the feline lumbar spinal cord. Cats received midcollicular decerebration and lumbar laminectomy. The spinal cord was transected at T12-L1. WDR cells were sampled with microelectrode at the depth of 2,000 microns from the cord dorsum. Following the control period with PaCO2 of 35-45 mmHg, respiratory rate and tidal volume were adjusted to make a level of hypocapnia as low as 20-25 mmHg. The recovery of cell activity was followed when normocapnia was restored. Hypocapnia with PaCO2 of 25-30 mmHg and 20-25 mmHg suppressed the activity of WDR cell significantly. At PaCO2 of 25-30 mmHg, the spontaneous activity was suppressed for about 20% and evoked activity for 27%. At PaCO2 of 20-25 mmHg, the spontaneous activity was suppressed for about 50% and evoked activity for 33%. The results suggest that the hyperventilation has suppressive effects on single-unit activity of WDR cell.
Masui 1993 Dec
PMID:[The effects of hyperventilation upon the spinal pain modulating system]. 830 24

Currently, no ideal method exists for monitoring the injured brain. Recently, a single, compact, fiberoptic sensor has become available for measuring oxygen, CO2, pH and temperature in blood. We have adapted this instrument for continuous use in brain tissue to measure oxygen tension, carbon dioxide tension (pCO2), pH, and temperature. To evaluate this new technique, we produced hypercapnia, hypocapnia, intracranial pressure increase, and hypoxemia in seven normal cats. In an additional six animals, sensors were placed within a zone of focal brain ischemia induced by occluding the left middle cerebral artery. The sensor readings were compared with cerebral blood flow measurements, intracranial pressure, and brain histological findings. An in vitro experiment was also performed using human blood to test the accuracy of the sensor over a wide range of pCO2 and oxygen tension values. After careful precalibration and rigid cranium fixation, stable measurements could be obtained throughout the 6- to 8-hour experiments. In normal animals, brain oxygen was 42 +/- 9 mm Hg, brain CO2 was 59 +/- 14 mm Hg, brain pH was 7.0 +/- 0.2, and brain temperature was 36.7 +/- 0.7 degrees C. Hypocapnia and hypoxemia produced a significant decline in tissue oxygen (< or = 30 +/- 3 mm Hg; P < 0.001), whereas hypercapnia caused by hypoventilation and intracranial pressure increase produced a significant increase in tissue CO2 (> or = 74 +/- 4 mm Hg; P < 0.001). Focal ischemia produced a rapid 42% decline in brain oxygen (25 +/- 7 mm Hg) and a 25% increase in tissue pCO2 (71 +/- 23 mm Hg). Brain oxygen further decreased to 19 +/- 6 mm Hg toward the end of the experiment, 4 hours later. After middle cerebral artery occlusion, the regional cerebral blood flow decreased to 10 +/- 5 ml per 100 g per minute, within the 1st hour, from a baseline value of 65 +/- 15 ml per 100 g per minute. It then gradually increased to 15 +/- 5 ml per 100 g per minute by the end of the 4-hour experiment. Brain pH was closely and inversely related to brain CO2. The brain temperature in the focally ischemic tissue decreased from 36.7 +/- 0.7 to 35.5 +/- 1.6 degrees C by the end of the experiment. The in vitro experiment demonstrated good linear correlation between the sensor readings and the blood gas analysis. Continuous monitoring of oxygen, CO2, pH, and temperature in damaged or at-risk brain tissue using a single sensor is now feasible and will, thus, allow improved continuous monitoring of neurosurgical patients who are at risk of significant secondary brain damage.
Neurosurgery 1995 Dec
PMID:Brain oxygen, CO2, pH, and temperature monitoring: evaluation in the feline brain. 858 58

The response of respiratory motor output to CO2 in the hypocapnic range (< 36 Torr PCO2) in the absence of hypoxemia is not well characterized in awake normal humans. We induced hypocapnia with hyperoxia in 16 normal volunteers by placing them on a volume-cycled ventilator in the assist mode. Subjects were not aware of the purpose of the study. All subjects continued rhythmic breathing despite high tidal volumes and severe hypocapnia (approximately 25 Torr alveolar PCO2). Inspired CO2 fraction was increased in steps, and changes in respiratory motor output were quantitated from changes in airway pressure at constant volume and flow, changes in respiratory rate, and change in rate of decline in airway pressure before triggering (dP/dt). There was a significant increase in respiratory muscle pressure, but not in respiratory rate, from 26 to 36 Torr PCO2. The slope of the response increased gradually from 26 to 41 Torr PCO2. Respiratory rate significantly increased only above 36 Torr. We conclude that the response to PCO2 in the hypocapnic range is basically nonlinear with no clear CO2 threshold and the CO2 responsiveness extends well below eupneic CO2 levels.
J Appl Physiol (1985) 1995 Dec
PMID:Respiratory response to CO2 in the hypocapnic range in awake humans. 884 74

We describe a method to assess the effects of PCO2, around and below eucapnia, on the neuromuscular ventilatory response to a standard peripheral chemoreceptor stimulus. Subjects were "passively" hyperventilated (without respiratory muscle activity), at a constant level of ventilation. Stimuli (3-7 breaths N2) were delivered over a range of steady-state PETCO2 (25-43 mmHg). Stimuli during hypocapnia were coupled with a transient increase in FICO2 so that the stimulus to the peripheral chemoreceptors was always "hypoxia at eucapnia". Responses to the stimuli (quantified from the reduction in peak inflation pressure and the magnitude of the evoked diaphragm electromyographic activity) decreased in a graded manner as steady-state PETCO2 fell, disappearing at 7.5 mmHg below eucapnia. Carotid body chemoreceptor recordings from two anaesthetised cats, indicated that the peak firing rate during such stimuli was independent of steady-state PETCO2. The results suggest that the central sensitivity to a peripheral chemoreceptor input may be modulated by changes in steady-state PCO2 around eucapnia and during mild hypocapnia.
Respir Physiol 1995 Dec
PMID:Modulation by "central" PCO2 of the response to carotid body stimulation in man. 890 7


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>