Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of sufentanil on human cerebral blood flow (CBF) was studied in seven unpremedicated, healthy volunteers 31 +/- 3.5 yr of age (mean +/- SD) and either sex. CBF (ml.100 g-1.min-1) was measured noninvasively with the 133Xe clearance technique and a scintillation camera before and after sufentanil 0.5 micrograms/kg administered intravenously. This technique provides values for global blood flow and for gray and white matter blood flow, and from 13 preselected regions in one hemisphere. After the administration of sufentanil, the volunteers were stimulated verbally in order to prevent their loss of consciousness and hypercarbia. Heart rate (HR), arterial pressure, oxyhemoglobin saturation, and end-tidal CO2 (ETCO2 were recorded during the measurements. Neither global CBF (46.1 +/- 1.6 control and 43 +/- 1.9 after sufentanil, mean +/- SEM) nor gray (76.5 +/- 3.2 and 70.9 +/- 6.1) or white (22.7 +/- 1.5 and 24.2 +/- 1.6) matter blood flow changed significantly after sufentanil administration. As well, no significant differences in HR (72 +/- 4 control and 79 +/- 4 beats per min after sufentanil) and ETCO2 (39.8 +/- 1.4 and 41.1 +/- 1.1 mmHg) were observed. It is concluded that sufentanil has no significant effect on CBF in healthy human volunteers.
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PMID:Sufentanil does not increase cerebral blood flow in healthy human volunteers. 214 62

1. The aim of this investigation was to measure the change in intracellular pH of human brain in vivo in response to hypercapnia. 2. Five healthy male subjects inspired air for 20 min and then 5% CO2/95% O2 for 30 min, of which the first 10 min was used to achieve a steady-state end-tidal CO2 measurement. 3. 31P nuclear magnetic resonance spectroscopy was used to measure intracellular pH while breathing air and during hypercapnia. Simultaneous localization between superficial and deep brain was achieved by using the phase-modulated rotating frame imaging technique. One subject volunteered to breath air for a further phase-modulated rotating frame imaging study while recovering from hypercapnia. 4. End-tidal CO2 increased when breathing 5% CO2/95% O2 (on air, 5.57 +/- 0.21%; on 5% CO2/95% O2, 6.41 +/- 0.16%; rise = +0.84 +/- 0.09%; means +/- SEM) causing a reduction in brain intracellular pH, which was more pronounced in deep brain (5 cm = mainly white matter, from 7.02 +/- 0.006 pH units to 6.96 +/- 0.001 pH units, mean +/- SEM) than in superficial brain (2 cm = mainly grey matter, from 7.02 +/- 0.006 pH units to 7.00 +/- 0.006 pH units, mean +/- SEM). 5. The white matter responded to hypercapnia with a greater fall in intracellular pH than the grey matter. This could either be due to differences in blood flow between grey and white matter in response to hypercapnia or to differences in intracellular pH regulation/buffering between these two tissues.
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PMID:Response of the human brain to a hypercapnic acid load in vivo. 216 84

Fifty-four patients with obstructive sleep apnea (OSA) syndrome received long-term treatment with nasal continuous positive airway pressure (CPAP). The effects on daytime lung function and pulmonary hemodynamics were prospectively evaluated by repeating pulmonary function tests, including right heart catheterization after a follow-up period of at least 1 yr (554 +/- 28 days, mean +/- SEM). PaO2 increased in the patient group as a whole from 69.9 +/- 1.4 to 72.8 +/- 1.4 mm Hg (p less than 0.02). The increase in PaO2 was greater (from 60.4 +/- 1.0 to 66.4 +/- 2.1, p less than 0.01) in those patients who were hypoxemic prior to treatment. PaCO2 decreased significantly only in the subgroup of patients with significant hypercapnia prior to treatment (n = 7), from 48.5 +/- 1.3 to 44.5 +/- 1.5 mm Hg (p less than 0.01). The improvement in daytime blood gases seemed to be related to an increase in the alveolar ventilation, from 5.2 +/- 0.2 to 5.9 +/- 0.3 L/min without a change in the alveolar-arterial PO2 difference, as calculated in 25 patients. Both the red blood cell count and the hematocrit decreased significantly, from 5,347 +/- 90 to 5,024 +/- 61 10(3)/mm3 and from 49.4 +/- 0.9 to 47.1 +/- 0.6%, p less than 0.001 and p less than 0.02, respectively. No change was observed in the resting pulmonary arterial pressure. We conclude that nasal CPAP is effective in improving daytime blood gases in patients with OSA.
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PMID:Long-term effects of treatment with nasal continuous positive airway pressure on daytime lung function and pulmonary hemodynamics in patients with obstructive sleep apnea. 218 56

The effect of dantrolene on ventilation and ventilatory muscle activity was evaluated in spontaneously breathing anaesthetized dogs. When administered as a bolus of 1.5 mg kg-1 i.v., dantrolene caused hypercapnia. Under isocapnic conditions, with end-tidal PCO2 maintained at 8.1 (SEM 0.3) kPa by adjusting inspired carbon dioxide, dantrolene decreased tidal volume from 475 (66) to 254 (46) ml and breathing rate from 21 (4) to 15 (3) b.p.m. (P less than 0.01 for both). Occlusion pressure was reduced, but the rate of rise of the diaphragm and intercostal EMG were unchanged and peak activity increased only as a result of prolongation of inspiration. Respiratory variables returned gradually to baseline values 1 h after dantrolene administration. Phrenic nerve stimulation revealed a marked reduction in the ability of the diaphragm to generate pressure, particularly at low frequencies of stimulation. Only partial recovery was observed after 1 h. It is concluded that dantrolene causes hypoventilation in the anaesthetized dog when given in large doses i.v.
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PMID:Effect of dantrolene on ventilation and respiratory muscle activity in anaesthetized dogs. 231 23

In the present study the functional and morphologic effects of two pulmoplegic solutions are evaluated. Single left-lung allotransplantation with ligation of the right pulmonary artery was performed in 15 piglets (13-20 kg). The lungs were preserved after donor prostaglandin E-1 treatment with single pulmonary artery flush with either modified Euro-Collins solution (mECS) (9 pigs) or oxygenated fluorocarbon emulsion (FC-43) (6 pigs) and transplanted after 6-hr storage in cold Physiosol solution. Tidal volumes of 15 ml/kg x fr (18) with 40% inspired oxygen were used for ventilation during reperfusion. Function of the transplanted lung was monitored for 4 hr postoperatively by determining pa CO2 and pa O2 levels from arterial samples and by noninvasive monitoring of end-tidal CO2 values and arterial oxygen saturations. Sequential morphologic changes in pulmonary artery flow surface and lung tissue were studied after 6-hr storage and 4-hr reperfusion, using light, scanning, and transmission electron microscopy (LM, SEM, TEM). There was no mortality. After transplantation the mECS group experienced significant hypoxia and hypercarbia and had low end-tidal CO2 values as signs of defective oxygenation and gas exchange, whereas the FC-43 group was normoxic and normoventilated without disturbed elimination of carbon dioxide. After storage and reperfusion, LM showed signs of increased vascular permeability and reperfusion damage--more evident in the mECS group compared with the FC-43 group--while the lymphoid cell population was more intensely activated in the latter group. Electron microscopy after storage showed good overall preservation of structures in both groups. After reperfusion preservation of pulmonary artery flow surface and lung tissue was estimated to be moderate in the mECS group, whereas it was good-to-moderate in the FC-43 group by SEM (NS). TEM of lung tissue, however, showed significantly better-preserved alveolar epithelial lining in the FC-43 group compared with the mECS group. In conclusion, oxygenated fluorocarbon (FC-43) pulmoplegia gave better functional and morphologic preservation of lung grafts compared with modified Euro-Collins solution.
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PMID:Single lung allotransplantation in pigs. A morphologic study of tissue preservation with modified Euro-Collins and fluorocarbon solutions. 236 Feb 50

The minimal anesthetic concentration (MAC) for isoflurane was determined during spontaneous ventilation in nine male Peking ducks (7 to 12 weeks of age; 3.0 +/- 0.4 kg). While each bird was awake, arterial blood was collected for analysis of pH, PaCO2, and PaO2. After anesthesia was induced with isoflurane in oxygen, MAC was determined for isoflurane in each bird during spontaneous ventilation in a manner similar to MAC determinations in mammals. Pulmonary dose-response data were collected at 1 MAC and 1.5 MAC. Anesthetic index (Al; an index of anesthetic-induced apnea) was calculated from ducks that became apneic. The MAC for isoflurane was 1.30 +/- 0.23% (mean +/- SD). There was a dose-dependent decrease in ventilation as evidenced by a statistically significant increase in PaCO2. Apnea or unacceptable hypercarbia (PaCO2 greater than 110 mm Hg), or both, were common occurrences at end-tidal isoflurane concentrations greater than 1.5 MAC. Anesthetic index calculated from four ducks was 1.65 +/- 0.13 (mean +/- SEM). There was no significant difference between the means of either heart rate or mean arterial blood pressure in birds at 1.0 and 1.5 MAC.
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PMID:Minimal anesthetic concentration and cardiopulmonary dose response of isoflurane in ducks. 238

The build-up and clearance of halothane in rat brain have been measured non-invasively by 19F NMR spectroscopy using a surface coil placed on the intact scalp. When the halothane supply (3% in O2/N2O, 33/66%) was turned off, the 19F signal decreased exponentially to approximately 50% of the initial value, with a time constant, in normal rats, of 8.6 +/- 0.7 min (mean +/- SEM, n = 16), followed by a decay slower by at least one order of magnitude. The time constant of the rapid decay (tau), which was found to be specific for brain, was reduced in hypoxic/hypercapnic (5% O2/5% CO2) rats to 2.9 +/- 0.2 min (p = 0.001, n = 4), in rats infused with physostigmine (20 micrograms/kg/min i.v.) to 5.7 +/- 0.3 min (p = 0.005, n = 6) and increased in rats injected with pentothal (40 mg/kg i.p.) to 10.7 +/- 1.6 min (p = 0.2, n = 5). Based on the theory of exchange of inert gas at the lungs and tissues developed by Kety, the rapid exponential decay of the 19F signal was used to calculate relative cerebral blood flow (CBF). Assuming the cortical CBF in a normal rat to be about 130 mL min-1 100 g-1, the following CBF values (means +/- SEM) were obtained: controls 130 +/- 10, hypoxia/hypercapnia 390 +/- 59, hypercapnia 220 +/- 25, physostigmine 195 +/- 26, pentothal 105 +/- 23 mL min-1 100 g-1. These values are in good agreement with published values obtained with established methods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Non-invasive determination of cerebral blood flow changes by 19F NMR spectroscopy. 251 56

Hypoxia in fetal sheep depresses respiratory activity. To determine if this effect is counterbalanced by hypercarbia we studied the effects of two levels of asphyxia produced by occlusions of the maternal uterine artery. Moderate asphyxia (PaO2 16.8 +/- 1.6 (SEM) PaCO2 48.9 +/- 1.0 torr) produced no changes in the percent time fetal breathing movements occupied each hour which ranged from 25.6 +/- 7.0 to 32.4 +/- 6.2%. However, a more marked asphyxia (PaO2 12.0 +/- 0.3, PaO2 57.0 +/- 1.6) resulted in a decrease in fetal respiratory activity to 8.7 +/- 3.7% during the first hour. This depression was sustained over the next 2 h but by the 5th hour breathing had returned to 26.2 +/- 7.3%. We concluded that hypercarbia can offset the respiratory inhibition of acute moderate hypoxia, but not that of a more marked lowering of PaO2 in fetal sheep. Severe asphyxia causes an initial inhibition of respiration which is followed by a return to normal respiratory activity.
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PMID:Effect of asphyxia on respiratory activity in fetal sheep. 262 16

We examined mitochondrial oxidative function 5 minutes and 2 hours after a gradual asphyxial insult in newborn lambs. We subjected 16 ventilated newborn lambs to 75-90 minutes of hypoxia and hypercarbia that resulted in bradycardia and systemic hypotension over the final 15 minutes of the insult. At the end of asphyxia, the lambs were resuscitated and returned to control ventilator settings. Samples of brain were removed 5 minutes (n = 8) and 2 hours (n = 8) after asphyxia. Each group of eight lambs was subdivided into those less than 3 or greater than 3 days old to evaluate the effect of age on postasphyxia mitochondrial function. After classification into nonsynaptic and synaptic mitochondria, mitochondrial respiration (oxygen consumption) was measured using five different substrates. Data from asphyxiated lambs were compared with that from a control group of ventilated nonasphyxiated lambs (n = 8). In the lambs less than 3 days old, there was significant depression of mean +/- SEM nonsynaptic mitochondrial state 3 (adenosine diphosphate-dependent) respiration to 29.5 +/- 5.2% of control with four of the five substrates and of state 4 respiration to 33.7 +/- 0.9% of control with three of the five substrates 5 minutes after asphyxia. By 2 hours after asphyxia, mean +/- SEM nonsynaptic mitochondria state 3 respiration increased to 70.4 +/- 6.4% of control while state 4 respiration increased to 58.2 +/- 4.5% of control. In contrast, lambs greater than 3 days old exhibited no inhibition of nonsynaptic mitochondrial function after asphyxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitochondrial function after asphyxia in newborn lambs. 271 9

The blood flow to the diaphragm, external and internal intercostal muscles, abdominal oblique muscles, and other rib-cage and abdominal muscles was measured, using radio-labelled microspheres, in 6 newborn lambs quietly breathing in air and during 3 different levels of CO2 induced hypercapnic hyperpnoea (inspired gas containing 4%, 5.5%, or 7% CO2). We also calculated the oxygen uptake of the diaphragm (VO2di). While the lambs were breathing air diaphragmatic blood flow (Qdi, 38.2 +/- 4.0 SEM ml.min-1.100 g-1) was similar to external intercostal muscle blood flow (Qei, 37.1 +/- 8.1 ml.min-1.100 g-1), and both were greater than internal intercostal muscle blood flow (Qii, 24.8 +/- 6.1 ml.min-1.100 g-1; P less than 0.05). During hyperpnoea Qdi, Qei, and Qii were augmented with Qdi equal to 200.1 +/- 12.2 ml.min-1.100 g-1 in 7% CO2 and Qei equal to 88.4 +/- 14.1 ml.min-1.100 g-1 in 7% CO2 (Qdi was greater than Qei, P less than 0.01). Qii was 40.7 +/- 5.6 ml.min-1.100 g-1 in 7% CO2 being less than Qdi (P less than 0.01) and Qei (P less than 0.05). The abdominal oblique muscles also had augmented flow in response to hyperpnoea. The level of hypercapnia that resulted in an augmentation of Qdi (5.5% inspired CO2) was lower than that which augmented Qei and Qii (7% inspired CO2). VO2di was linearly related to Qdi (r = 0.98). Our results suggest that in the newborn lamb the diaphragm is the dominant respiratory muscle in response to hypercapnia.
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PMID:Blood flow to the respiratory muscles during hypercapnic hyperpnoea in the newborn lamb. 272 19


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