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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We tested the hypothesis that differential sympathetic innervation explains the attenuated cerebral blood flow (CBF) response to hypercapnia (hyper) in fore-brain (fb) compared with brain stem in 1- to 2-wk-old piglets. In pentobarbital sodium-anesthetized piglets, CBF (microspheres) was measured during hypocapnia, normocapnia (normo), and hypercapnia [arterial CO2 partial pressure (PaCO2) of 25, 40, and 65 mmHg, respectively] in random sequence. After pretreatment values were obtained, piglets were randomized to undergo sham treatment (n = 5), high cervical spinal cord transection (n = 6), or pharmacological alpha-adrenergic blockade (prazosin 1 mg/kg + yohimbine 1 mg/kg, n = 6). After each experimental treatment, CO2 reactivity was again measured. Before experimental manipulation, hypercapnic reactivity [(CBFhyper - CBFnormo)/(PaCO2hyper - PaCO2normo)] in brain stem was approximately three times greater than in forebrain (e.g., sham; 3.6 +/- 0.8 vs. 1.2 +/- 0.3 ml.min-1.100 g-1.mmHg-1). Hypercapnic reactivity in forebrain was not increased by cord transection (1.4 +/- 0.3 vs. 1.1 +/- 0.2 ml.min-1.100 g-1.mmHg-1) or alpha-blockade (1.6 +/- 0.6 vs. 1.2 +/- 0.4 ml.min-1.100 g-1.mmHg-1). Likewise, hypercapnic cerebral vascular resistance (CVR) was unchanged by experimental treatment (e.g., CVRfb; cord transection 1.1 +/- 0.1 vs. 1.0 +/- 0.1; alpha-blockade 1.1 +/- 0.2 vs. 1.0 +/- 0.1 mmHg.ml-1.min-1.100 g-1). Hypocapnic vasoconstriction, however, was attenuated by both cord transection and alpha-blockade in forebrain and brain stem. We conclude that physiological stimulation of the noradrenergic component of the sympathetic nervous system does not explain regional differences in CBF reactivity during hypercapnia in 1- to 2-wk-old piglets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypercapnic blood flow reactivity not increased by alpha-blockade or cordotomy in piglets. 135 31

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

The cerebrovascular response to CO2 has been reported to be preserved during propofol anesthesia, but no comparison with awake control values has been made, and the additional influence of N2O has not been investigated. Using the noninvasive technique of transcranial Doppler ultrasonography, this study investigated the cerebrovascular response to varying levels of PaCO2 while awake and during anesthesia with propofol and propofol/N2O. Seven adults without systemic diseases undergoing nonneurologic surgery were studied. A pulsed-wave Doppler monitor was used to measure the mean middle cerebral artery flow velocity (Vmca) during varying levels of PaCO2 (25-55 mmHg) under the following conditions: 1) awake; 2) propofol 2.5 mg.kg-1 bolus followed by continuous infusion of 150 micrograms.kg-1.min-1; and 3) propofol as in the condition above plus 70% N2O. During the awake study condition, hypocapnia was induced by voluntary hyperventilation, and hypercapnia was induced with rebreathing of 7% CO2 in a closed circuit. During the anesthetized study conditions, hypocapnia and hypercapnia were induced by adjustment of minute ventilation. A minimum of five to six simultaneous Vmca and PaCO2 measurements were obtained under each of the study conditions. Systemic blood pressure was monitored via a radial arterial catheter, and phenylephrine was administered if mean arterial blood pressure decreased below 60 mmHg (phenylephrine was used in three of five patients in the propofol-N2O group). Linear regression and analysis of covariance were used for statistical analysis of Vmca-PaCO2 relationships.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of propofol with and without nitrous oxide on cerebral blood flow velocity and CO2 reactivity in humans. 144 39

Variation of PCO2 with concomitant changes in extracellular pH (pHo) may modulate cerebrovascular resistance, but the direct actions of carbon dioxide and pHo on human cerebral arteries are unknown. In this study, we have evaluated the effects of different carbon dioxide tensions (2.7, 4.2 and 7.2 kPa) with either fixed (pHo = 7.44) or concomitant changes in pHo, on contractions induced by depolarization (potassium) or receptor stimulation (prostaglandin F2 alpha) in isolated human pial arteries. Isolated changes in PCO2 had no significant effect on either potency (unchanged EC50 value) or the maximum response (Emax) in potassium-contracted arteries. Hypercapnia with uncompensated pHo significantly decreased both EC50 and Emax values, whereas uncompensated hypocapnia significantly increased the EC50 value without any effect on Emax. Concentration-response curves induced by prostaglandin (PG) F2 alpha were shifted significantly to the right (increased EC50 = decreased potency) during both hypo- and hypercapnia, independent of changes in pHo. The maximal responses were enhanced significantly during hypocapnia (Emax = 110 (SEM 2)%), but this enhancement was converted into a slight attenuation when pHo was compensated (Emax = 92 (4)%). Hypercapnia, with or without compensation of pHo, decreased the Emax values to 69 (16)% and 73 (9)%, respectively. We conclude that hypocapnia increases contractility in human pial arteries--an effect which is reversed by compensation of pHo. In contrast, the hypercapnic decrease of PGF2 alpha-induced contractions appears to be independent of pHo. The results confirm a relationship between contractility and pHo, but do not exclude a direct action of carbon dioxide in receptor-stimulated arteries.
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PMID:Modulation by carbon dioxide and pH of the contractile responses to potassium and prostaglandin F2 alpha in isolated human pial arteries. 146 6

In the present study, changes in frequency and amplitude of the rhythmic variations (vasomotion) in blood flow in the intact cerebral circulation of the rat were investigated using laser-Doppler flowmetry (LDF) during stepwise decrease in mean arterial blood pressure (MABP) and hyper- and hypocapnia. Experiments were performed on 12 adult Sprague-Dawley rats of either sex, anesthetized with alpha-chloralose. The rat's head was fixed on a stereotaxic frame and a small hole was made in the parietal bone but the dura and a thin inner bone layer were kept intact. The microvascular blood flow of the parietal cortex on the right or on both sides was continuously recorded by the laser-Doppler flowmeter (Periflux PF2B, Perimed, Stockholm, Sweden). The cerebral circulation of the rat exhibited vasomotion in control conditions with a frequency of 8-10 cycles per minute (cpm) and an amplitude of 5-10% of the cerebral blood flow (CBF). No significant changes in CBF could be detected when the MABP was above 60 mmHg, but it decreased significantly when MABP was reduced below 50 mmHg. However, during stepwise pressure reduction the vasomotion frequency decreased progressively while its amplitude showed a reversed U-shaped curve with a peak at 60-80 mmHg. During hypercapnia, the rhythmical oscillations showed a decrease in both frequency and amplitude, whereas during hypocapnia their frequency did not change but their amplitude increased. These results support the hypothesis that the vasomotion frequency might be dependent of the wall tension and cellular pH while its amplitude could be related to decreased tissue oxygenation.
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PMID:Vasomotion in the rat cerebral microcirculation recorded by laser-Doppler flowmetry. 149 61

Carbon dioxide (CO2) has been well documented to act as a potent vasodilator of coronary vessels under normal conditions. But there is little data available on the effect of CO2 on the collateral perfusion of patients with coronary insufficiency. We studied the effects of CO2 on the myocardial tissue PO2 in anesthetized dogs with critical coronary stenosis. Twelve mongrel dogs were anesthetized with pentobarbital and ventilated with 100% O2 to maintain normocapnia. Electromagnetic blood flow (BF) probe was applied on the left anterior descending artery (LAD). Regional myocardial PO2 was measured at two different sites using two pairs of monopolar polarographic needle electrodes; one inserted in the epicardial (EPI) layer, and the other in the endocardial (ENDO) layer. These were placed in the regions supplied by LAD and circumflex. Following the baseline recording, critical stenosis of LAD was produced by adjusting a copper-wire clamp occluder until LADBF was reduced by 50%. After a stable normocapnic ventilation, hypocapnia was produced by hyperventilation. To induce hypercapnia, exogenous CO2 was added to the inspired gas stepwise until end-tidal CO2 fraction reached 10%. Hypocapnia resulted in a significant reduction in myocardial PO2 in both EPI and ENDO non-stenotic areas, while hypercapnia increased these PO2 values dose-dependently. After coronary stenosis, hypocapnia resulted in a small but significant reduction of PO2 in endocardial ischemic area. Hypercapnia did not induce any sign of reduced regional myocardial PO2 or evidence of regional or intramural "steal" phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of carbon dioxide (hypocapnia and hypercapnia) on regional myocardial tissue oxygen tension in dogs with coronary stenosis]. 155 62

Rings of canine bronchi were studied in vitro to determine the effects of halothane on the responses of airway smooth muscle to hypercapnia and hypocapnia. Bronchi were first contracted to 50% of maximal active force with acetylcholine (ACh), 5-hydroxytryptamine (5HT), potassium chloride (KCl), or the muscarinic agonist McN-A-343 (McN). The CO2 concentration of the bathing solution was then changed from 6% to either 1% (hypocapnia) or 10% (hypercapnia). In the absence of halothane, changes in CO2 concentration had no significant effect on muscles contracted with ACh. With all other contractile agonists, increasing the CO2 concentration caused bronchial relaxation, while decreasing the CO2 concentration caused contraction. In the presence of 2 MAC halothane, hypocapnia relaxed bronchi contracted with the muscarinic agonists ACh or McN; the responses to hypocapnia of bronchi contracted with KCl and 5HT were not significantly changed by halothane. Halothane had no effect on the responses of the bronchi to hypercapnia. We conclude that airway smooth muscle contracted with cholinergic agonist relaxes in response to hypocapnia when exposed to 2 MAC halothane; this mechanism may contribute to the depression of hypocapnic bronchoconstriction caused by halothane in vivo.
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PMID:Halothane alters the response of isolated airway smooth muscle to carbon dioxide. 156 97

Alterations in arterial oxygen and carbon dioxide influence cerebrovascular resistance and therefore cerebral blood flow (CBF), but the magnitude of these CBF responses have not been well defined in normal humans. Duplex scanning (B-mode imaging and pulsed Doppler shift analysis) was used to measure internal carotid blood flow (ICBF) as an indicator of CBF in 20 normal subjects during alterations of arterial O2 and CO2. End-tidal PCO2 (PETCO2) was measured by mass spectrometry, arterial oxygen saturation by pulse oximetry, and unilateral (right) ICBF by duplex scanning. A variety of gas mixtures were administered to achieve hypoxemia (FIO2 = 0.075-0.10) and hypercapnia (FICO2 = 0.05) or the subject was asked to hyperventilate to PETCO2 = 16-24 mm Hg. The ICBF was determined five times in each of six conditions: (1) normoxia/normocapnia; (2) normoxia/hypercapnia; (3) normoxia/hypocapnia; (4) hypoxia/normocapnia; (5) hypoxia/hypercapnia; and (6) hypoxia/hypocapnia. During normoxia and normocapnia, the mean ICBF was 330 +/- 19 (SEM) mL/min. Specific CO2 reactivity was 7.4 +/- 0.7 mL/min/mmHg, which is equivalent to 2.3% +/- 0.1% of normocapnic blood flow per mm Hg change in CO2. During normocapnia, ICBF increased by 2.9 +/- 0.9 mL/min for each percentage decrease in oxygen saturation. Using an ANOVA with repeated measures to fit the responses, the following statistically significant relationship was found: ICBF (mL/min) = 333 + 6.3.(PETCO2 - 40) + 2.7 DSO2 +/- 81 where DSO2 is arterial desaturation (100 - arterial saturation). An additional "between subject" variation had a mean of 0 and a standard deviation of 82 mL/min. There was no statistically significant evidence of an interaction between O2 and CO2 response. Our data suggest that hypoxia and carbon dioxide changes will alter CBF simultaneously and additively. Duplex scanning of the internal carotid artery, which can be performed at the bedside, is sufficiently sensitive to detect changes in ICBF and internal carotid artery oxygen delivery.
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PMID:Human cerebrovascular response to oxygen and carbon dioxide as determined by internal carotid artery duplex scanning. 158 51

1. In four awake dogs we measured EMG activity of three inspiratory and four expiratory muscles during sustained central chemoreceptor stimulation (CO2 inhalation), and peripheral chemoreceptor stimulation (intravenous infusion of almitrine bismesylate (almitrine)). By using this selective pharmacological stimulation of the peripheral chemoreceptors and reversibly cold-blocking pulmonary stretch receptors, we were able to determine the effects of each type of stimulation on respiratory muscle recruitment in the absence of such complicating influences as pulmonary stretch receptor feedback, cerebral hypoxia or hypocapnia, and differences in breathing pattern. 2. During 10 min of steady-state hyperpnoea (minute ventilation VI, approximately twice eupnoea) caused by either hypercapnia or isocapnic stimulation of the carotid bodies with almitrine, all three inspiratory and all four expiratory muscles demonstrated significant and sustained elevations in EMG activity. 3. With both types of chemoreceptor stimulation, as tidal volume, VT, increased, so did the mean electrical activities of the crural diaphragm (r = 0.88), costal diaphragm (r = 0.93), parasternals (r = 0.82), triangularis sterni (r = 0.74), transversus abdominis (r = 0.77), external obliques (r = 0.68) and internal intercostals (r = 0.75). 4. In each dog, the response of ventilation and of the diaphragmatic EMG to a given level of central or peripheral chemoreceptor stimulation is highly reproducible from one test day to the next. On the other hand, accessory inspiratory and expiratory abdominal and rib cage muscles in two of the four dogs showed highly significant changes from day to day in the amount of their EMG activity at any given VT. 5. During steady-state ventilatory stimulation, 2 min intervals were chosen during which the two types of chemoreceptor stimulation had caused hyperpnoeas with similar values for VT, total time per breath (TTOT) and inspiratory time divided by the total time (TI/TTOT). Comparison of EMG activities during these matched hyperpnoeas revealed that there were no differences in the activities of any of the muscles between the two forms of stimulation. We conclude that peripheral chemoreceptor stimulation causes significant and sustained recruitment of expiratory muscles even in the absence of pulmonary feedback and that both expiratory and inspiratory muscles are recruited to the same extent during peripheral chemoreceptor stimulation as they are during an identical hyperpnoea caused by central chemoreceptor stimulation.
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PMID:Respiratory muscle recruitment during selective central and peripheral chemoreceptor stimulation in awake dogs. 159 81

Ventilatory acclimatization (VA) to hypoxia alters cerebrovascular responses to arterial blood gas perturbations. For example, after VA, cerebral blood flow (CBF) is elevated, at a given arterial CO2 tension (PaCO2), compared to CBF before VA. This experiment examined the effects of VA to 72 h of normobaric hypoxia [arterial O2 tension (PaO2) approx. 40 mmHg, O2 saturation in arterial blood approx. 50%] on total and regional cerebrovascular resistance (CVR and rCVR) and cerebral O2 extraction fraction (OEF) in 32 conscious sheep. Four different O2-CO2 gas combinations were sequentially administered to each sheep before and after VA. CVR and rCVR were calculated from CBF (radiolabeled microspheres) and arterial and cerebral downstream pressures; OEF was calculated from arterial and cerebral venous O2 contents. After VA, during hyperoxia, CVR and rCVR tended to be lower during both hypocapnia and hypercapnia. During hypoxia, although CVR and rCVR were slightly less during hypocapnia, CVR and rCVR during hypercapnia were surprisingly increased. The post-VA increases in mean CVR and mean rCVR during hypoxic gas combinations differed from the post-VA decreases during hyperoxic gas combinations (0.04 less than or equal to P less than or equal to 0.11). In contrast, although VA decreased OEF during three of four gas combinations (P less than or equal to 0.003), there was a greater mean post-VA decrease in OEF during hypercapnic gas combinations than during hypocapnic gas combinations (P = 0.025); decreases in OEF were correlated with decreases in cerebral O2 consumption. The post-VA CVR responses may reflect altered neurocirculatory control by the arterial chemoreflex; the OEF responses suggest relative cerebral hyperperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acclimatization to hypoxia alters cerebral convective and diffusive O2 delivery. 161 32


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