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)

Patterns of anterior border zone (ABZ) and middle cerebral artery (MCA) cerebral blood flow (CBF) asymmetry were readily seen during both normocapnic room air (RA) and induced hypercapnic (CO2) inhalation using fluoro-methane and a multislice, high-resolution positron scanner. Wilcoxon two-sample rank testing showed symptomatic-over-nonsymptomatic CBF ratios for unilateral greater than 75% carotid stenosis patients (n = 8) to be 1.05 +/- 0.07 (p less than 0.008 as compared with control of 0.97 +/- 0.02) ABZ RA, 0.98 +/- 0.11 ABZ Co2, 0.98 +/- 0.04 MCA RA, and 0.98 +/- 0.06 MCA CO2. Unilateral carotid occlusion patients (n = 8) had ratios of 0.90 +/- 0.16 ABZ RA, 0.81 +/- 0.19 (p less than 0.002) ABZ CO2, 0.90 +/- 0.12 and 0.89 +/- 0.13 for MCA RA and CO2, respectively (both p less than 0.008 as compared with control 0.99). These preliminary results suggest an upgrade of autoregulation (ie, very high ratio) in the ABZ of high-grade stenosis patients during normocapnia. CBF was preferentially higher on the symptomatic side and then either did not increase or paradoxically fell in response to hypercapnia. In comparison, carotid occlusion patients had low ABZ and MCA ratios during normocapnia, also unable to increase with hypercapnia. The fall in ratios from normocapnia to hypercapnia indicates that these areas, already subject to maximal vasodilation, fail to increase CBF or actually become hypoperfused following induced hypercapnia. These results aid in understanding the concept of "hemodynamic significance."
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PMID:Blood flow asymmetry in carotid occlusive disease. 153 70

In early phases of respiratory disease, patients are more likely to experience intermittent hypercapnia than a continuous increase in PCO2. The effect of intermittent arterial PCO2 elevation on subsequent breathing patterns is unclear. To examine this issue, a series of six ventilatory challenges (CH1-CH6), consisting of 2 min of breathing 5% CO2 in O2, followed by 5 min in room air (RA) were performed in 10 naive healthy subjects (age 12-39 yr). Minute ventilation (VE) increased from 11.9 +/- 1.0 (SE) l/min in RA to 27.6 +/- 3.0 l/min in 5% CO2 (P < 0.0005) in each of the six hypercapnic challenges. Respiratory rate increased from 21.3 +/- 2.6 breaths/min on RA to 29.6 +/- 3.9 breaths/min during CH1 (P < 0.05). However, respiratory rate consistently decreased with successive CO2 challenges (CH6: 21.5 +/- 2.6 breaths/min; P < 0.02). Thus, maintenance of VE was achieved by gradual increases in tidal volume with each of the first four consecutive CO2 challenges (CH1: 1.05 +/- 0.09 liters; CH4: 1.44 +/- 0.13 liters; P < 0.002). Similarly, the ratio of tidal volume to inspiratory time increased from CH1 (1.16 +/- 0.16 l/s) to CH6 (1.57 +/- 0.21 l/s; P < 0.001). These changes in ventilatory strategy were not observed when RA recovery periods were extended to 15 min in five subjects. We conclude that during repeated short hypercapnic challenges similar levels of VE are achieved. However, increased mean inspiratory flows are generated to maintain VE. We speculate that intermittent hypercapnia either modifies central controller gain or induces a long-term modulatory effect to account for the progressive changes in ventilatory components.
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PMID:Ventilatory responses to repeated short hypercapnic challenges. 761 45