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

Seven human spinal cord-lesioned subjects (SPL) underwent electrically induced muscle contractions (EMC) of the quadriceps and hamstring muscles for 10 min: 5 min control, 2 min with venous return from the legs occluded, and 3 min postocclusion. Group mean changes in CO2 output compared with rest were +107 +/- 30.6, +21 +/- 25.7, and +192 +/- 37.0 (SE) ml/min during preocclusion, occlusion, and postocclusion EMC, respectively. Mean arterial CO2 partial pressure (PaCO2) obtained from catheterized radial arteries at 15- to 30-s intervals showed a significant (P less than 0.05) hypocapnia (36.2 Torr) during occlusion and a significant (P less than 0.05) hypercapnia (38.1 Torr) postocclusion relative to a group mean preocclusion EMC PaCO2 of 37.5 Torr. Relative to preocclusion EMC, expired ventilation (VE) decreased during occlusion and increased after release of occlusion. However, changes in VE always occurred after changes in end-tidal PCO2 (mean 41 s after occlusion and 10 s after release of occlusion). In the two subjects investigated during hyperoxia, the VE and PaCO2 responses to occlusion and release did not differ from normoxia. We conclude that the data do not support mediation of the EMC hyperpnea in SPL by humoral mechanisms that others have proposed for mediation of the exercise hyperpnea in spinal cord-intact humans.
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PMID:Ventilatory response of spinal cord-lesioned subjects to electrically induced exercise. 238 11

We assessed respiratory muscle response patterns to chemoreceptor stimuli (hypercapnia, hypoxia, normocapnic hypoxia, almitrine, and almitrine + CO2) in six awake dogs. Mean electromyogram (EMG) activities were measured in the crural (CR) diaphragm, triangularis sterni (TS), and transversus abdominis (TA). Hypercapnia and normocapnic hypoxia caused mild to marked hyperpnea [2-5 times control inspiratory flow (VI)] and increased activity in CR diaphragm, TS, and TA. When hypocapnia was permitted to develop during hypoxia and almitrine-induced moderate hyperpnea, CR diaphragm activity increased, whereas TS and TA activities usually did not change or were reduced below control. Over time in hypercapnia, CR diaphragm, TS, and TA were augmented and maintained at these levels over many minutes; with hypoxic hyperventilation CR diaphragm, TS, and TA were first augmented but then CR diaphragm remained augmented while TS and, less consistently, TA were inhibited over time. Marked hyperpnea (4-5 times control) due to carotid body stimulation increased TA and TS EMG activity despite an accompanying hypocapnia. We conclude that in the intact awake dog 1) carotid body stimulation augments the activity of both inspiratory and expiratory muscles; 2) hypocapnia overrides the augmenting effect of carotid body stimulation on expiratory muscles during moderate hyperpnea, usually resulting in either no change or inhibition; 3) at higher levels of hyperpnea both chemoreceptor stimulation and stimulatory effects secondary to a high ventilatory output favor expiratory muscle activation; these effects override any inhibitory effects of a coincident hypocapnia; and 4) expiratory muscles of the rib cage/abdomen may be augmented/inhibited independently of one another.
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PMID:Differential responses of expiratory muscles to chemical stimuli in awake dogs. 249 85

To examine whether CPB influences pulmonary vascular sensitivity to CO2, we compared the effect of slight induced hypocarbia and hypercarbia on pulmonary circulation before and after CPB in ten mechanically ventilated patients undergoing CABG. Hypocarbia was produced by increasing tidal volume slightly and hypercarbia was then induced by adding CO2 to the inspired gas mixture. In another ten patients, hypercarbia was produced after CPB by decreasing ventilator rate and the cardiopulmonary responses to hypercarbia, produced by the two methods of CO2 elevation, were compared. Slight respiratory acidosis induced by CO2 inhalation did not change PVR before CPB but effected a 50 percent increase after CPB. Hypercarbia induced by alveolar hypoventilation after CPB increased PVR by 40 percent. During the increased CO2 production after hypothermic CPB, pulmonary vasoconstriction would be expected to occur and impair right ventricular performance. Therefore, tight control of PaCO2 with appropriate adjustment of ventilatory support is mandatory.
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PMID:Pulmonary vascular resistance before and after cardiopulmonary bypass. The effect of PaCO2. 249 21

We evaluated the cognitive effects of hypoxemia independent of hypocapnia in 20 right-handed male subjects using a battery of brief neuropsychological tests. Results of a profile analysis indicated that performance during hypoxia was reliably different for Digit Symbol and Finger Tapping tests. Trend analysis demonstrated a significant linear pattern for Finger Tapping results, such that lower levels of oxygen were associated with slower rates of tapping. No significant trends were observed for Digit Symbol results. The observation of hypoxic effects on Digit Symbol and Finger Tapping tests is consistent with previous findings of neuropsychological changes secondary to hypoxia. The negative results observed for the remaining tests are inconsistent with past literature. It is likely that methodological differences contributed to these discrepancies, including previous reliance on inspired air to index hypoxemia rather than monitoring arterial oxygen saturation directly and failure to control for differences in CO2 levels during induced hypoxia. These variables should be controlled in future research.
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PMID:Isocapnic hypoxemia and neuropsychological functioning. 249 22

Magnetic resonance imaging was used to measure the effect of inhalation of 7% CO2 and hyperventilation with 60% O2 on human cranial cerebrospinal fluid volume. During CO2 inhalation there was a reduction in the cranial CSF volume ranging from 0.7-23.7 ml (mean 9.36 ml). The degree of reduction in cranial CSF volume was independent of the individual subject's increase in end-expiratory pCO2 or mean arterial blood pressure, in response to hypercapnia. During hyperventilation with high concentration oxygen the cranial CSF volume increased in all subjects (range 0.7-26.7 ml, mean 12.7 ml). The mean changes in cranial CSF volume, induced by hypercapnia and hypocapnia, were very similar to the expected reciprocal changes in cerebral blood volume.
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PMID:Changes in cranial CSF volume during hypercapnia and hypocapnia. 249 39

The ventilatory response following 15 seconds of inspiratory airway occlusion at functional residual capacity (FRC) was studied in nine normal supine awake subjects. Expired minute ventilation (VE), CO2 output (VCO2), tidal volume (VT), and end-tidal PCO2 (PETCO2) were measured on a breath-by-breath basis. Alveolar PCO2 rose 5.6 mm Hg during the apnea (P less than 0.001). Ventilation rose 10.8 L/min on the first breath following apnea and remained elevated above control measurements for five breaths (P less than 0.05). The persistent hyperpnea was due to an increase in tidal volume and was associated with alveolar hypocapnia for 6 breaths or 30 sec (P less than 0.05) and an increase in CO2 output for 4 breaths (P less than 0.05). Changes in end-tidal PCO2 correlated with excess CO2 output relative to control measurements immediately prior to airway occlusion (P less than 0.03). After 15 sec airway occlusion at FRC, there is alveolar hypercapnia with a 2.6-fold first breath rise in ventilation. Persistent alveolar hyperventilation lasting 30 sec following airway occlusion may be due to delays in central chemoreceptor response or an afterdischarge phenomenon. This overshoot hypercapnia following airway occlusion may have some relevance to the development of central apneas following obstructive apnea episodes.
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PMID:Awake inspiratory airway occlusion in normal humans is followed by hyperpnea and hypocapnia. 249 5

Cerebral blood flow (CBF) responsiveness to alterations in arterial CO2 tensions (PaCO2) during 1.4% and 2.8% isoflurane anesthesia was assessed. Dogs were initially anesthetized with thiopental (12 mg/kg, iv bolus), their tracheae intubated, after which anesthesia was maintained with 1.4% isoflurane. In eight animals three levels of PaCO2 (25, 40, and 60 mmHg) were studied during 1.4% and 2.8% isoflurane. Mean arterial blood pressure, sagittal sinus pressure, and cerebrospinal fluid pressure were measured and CBF was determined using radiolabeled microspheres. Cerebral perfusion pressure (CPP) was maintained constant at approximately 80 mmHg by inflation of a balloon in the midthoracic aorta. CBF during normocapnia was 70 +/- 14 and 118 +/- 18 ml.min-1.100 g-1 with 1.4% and 2.8% isoflurane, respectively. As PaCO2 was decreased and increased, CBF decreased and increased to 42 +/- 7% and 185 +/- 16% of control, respectively, during 1.4% isoflurane. During 2.8% isoflurane, hypocapnia decreased CBF to 39 +/- 6% of control, but CBF did not increase with hypercapnia. In a second group of animals (n = 8), the effects of changes in CPP during hypercapnia with 1.4% and 2.8% isoflurane were assessed. Increasing CPP approximately 25 mmHg with both 1.4% and 2.8% isoflurane increased CBF but did not change CVR from control. With 1.4% isoflurane, the cerebral vasculature constricts with hypocapnia and dilates with hypercapnia, whereas with 2.8% isoflurane, vasoconstriction to hypocapnia is retained but vasodilation to hypercapnia is absent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebrovascular responsiveness to carbon dioxide in dogs with 1.4% and 2.8% isoflurane. 249 63

CO2 reactivity of the brain vessels was investigated in 33 patients (Grade I-III after Hunt and Hess) with cerebral vasospasm after an aneurysmal subarachnoid haemorrhage (SAH) and after early operation within 72 hours. In all cases, transcranial Doppler sonography was used to measure flow velocities in the middle cerebral artery (MCA) and internal carotid artery (ICA) and vasomotor reactivity to CO2 changes. Vasospastic conditions lead to higher flow velocities through the narrow segment, lower peripheral stream resistance due to the post-stenotic pressure drop and lower vasodilating capacities of arterioles under hypercapnia. In severe vasospastic conditions, the peripheral stream bed is already maximally dilated and the hypercapnic response is weak. On the other hand, the peripheral vascular bed reacts normally to hypocapnia in all vasospastic situations. Our results point out two dangerous conditions of vasospastic disease: 1) exhaustion of peripheral vasodilating capacities, and 2) hyperventilatory therapy. Both of these situations can result in a reduction of CBF to brain tissue, mainly for two reasons: 1) In the former, a further increase in vasospasm cannot be compensated for anymore when the peripheral arterioles are maximally dilated, and 2) in the latter, hypocapnia produces a strong peripheral vasoconstrictor response with further reduction of CBF.
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PMID:CO2 reactivity of cerebral vasospasm after aneurysmal subarachnoid haemorrhage. 250 Aug 37

Low arterial CO2 tension (PaCO2) experienced by birds during high-altitude flight may result in cerebral vasoconstriction with reduced cerebral O2 delivery. To test this, brain redox balance and blood volume were studied during severe hypocapnia (PaCO2 11-20 mmHg) in ducks. Cerebrocortical redox balance, measured as relative [NADH], and blood volume were measured simultaneously with a fiber-optic fluorometer-reflectometer. Cerebrocortical blood volume (an index of blood flow) fell nearly linearly with PaCO2 during severe hypocapnia, even during severe hypoxemia. Cerebrocortical redox balance was shifted toward reduction of NADH ([NADH] increased) by both hypoxemia and hypocapnia. If hypocapnia causes similar changes in brain blood flow during high-altitude flight, tissue hypoxia will be exacerbated. Tolerance of brain tissue hypoxia during flight may be an important adaptation in high-flying birds.
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PMID:Effects of hypoxia and hypocapnia on brain redox balance in ducks. 250 33

1. In spontaneously breathing, anaesthetized rats, a study was made of the effects upon the graded cardiovascular responses to systemic hypoxia (inspiratory fractional O2 concentration, Fi, O2: 0.15, 0.12, 0.08, 0.06) of maintaining arterial CO2 pressure (Pa,CO2) at the air-breathing level by adding CO2 to the inspirate (eucapnic hypoxia), rather than allowing Pa,CO2 to fall (hypocapnia hypoxia). 2. At each Fi,O2, maintenance of eucapnia significantly reduced the increase in respiratory frequency, but significantly accentuated the increase in tidal and minute volume: as a result the fall in Pa,O2 at each Fi,O2 was significantly reduced. 3. Concomitantly, maintenance of eucapnia reduced the increase in heart rate (HR) and fall in arterial pressure (ABP), the effects being significant at Fi,O2 0.08 and/or 0.06. There was also a tendency for the increases in renal and femoral vascular conductances (RVC, FVC) to be reduced; at Fi,O2 0.06 mean increases from control were 2 +/- 10 vs. 16 +/- 7% (eucapnia vs. hypocapnia) for RVC, and 62 +/- 11 vs. 106 +/- 27% for FVC. 4. As maintenance of eucapnia reduced the fall in Pa,O2 at each Fi,O2, the above results were also considered as a function of Pa,O2. Then, maintenance of eucapnia had similar significant effects on the changes in respiration and HR as described above and reduced the mean increase in RVC (16 +/- 11 vs. 23 +/- 10%, at Pa,O2 31 mmHg, which was attained at Fi,O2 0.06 with eucapnia and 0.08 with hypocapnia). However, maintenance of eucapnia had no effect on the falls in ABP and accentuated the mean increase in FVC (74.9 +/- 13 vs. 57 +/- 10% at Pa,O2 31 mmHg). 5. These findings indicate that, in the rat, the hypocapnia that accompanies the hyperventilatory response to systemic hypoxia facilitates the tachycardia and may accentuate the renal vasodilation, but attenuate the hypoxia-induced vasodilatation in skeletal muscle. Possible mechanisms are discussed.
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PMID:Influences on the cardiovascular response to graded levels of systemic hypoxia of the accompanying hypocapnia in the rat. 250 77


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