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 aim of this study was to assess Near-infrared spectroscopy (NIRS) as a tool for testing CO2 reactivity in patients with carotid occlusive disease. One hundred sixty patients were examined (age range 44 to 85 years). Monitored parameters included transcranial Doppler flow velocity (FV), changes in concentration of oxy-(HbO2) and deoxy (Hb) haemoglobin, cutaneous Laser Doppler blood flow (LDF), endtidal CO2, ABP, and SaO2. Hypercapnia was induced using a 5% CO2 air mixture for inhalation. To estimate the skin flow contribution to NIRS during reactivity testing, the superficial temporal artery was compressed, and the NIRS changes in response to the fall in LDF recorded. FV and HbO2 derived reactivity values were related to the severity of the stenosis (p = 0.0001 and 0.021 respectively). The correlation between the two modalities was significant (r = 0.47, p < 0.000001). The average estimated skin contribution to NIRS changes was 16.5%. Reproducibility of HbO2-reactivity was similar but worse than FV reactivity (19.1% and 13.8% variation respectively). The clinical correlations improved when our method of correction for skin influence was used. NIRS shows potential as an alternative technique for testing CO2 reactivity in patients with carotid disease provided the conditions are carefully controlled and the contribution from extracranial tissue is taken into account.
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PMID:Assessment of cerebrovascular reactivity in patients with carotid artery disease using near-infrared spectroscopy. 977 2

Some metabolic and endocrine effects of hypoxaemia were studied during halothane anaesthesia in six ponies. Each was anaesthetised twice; on one occasion a 20-minute period of hypoxaemia (arterial oxygen tension between 4.4 and 5.8 [mean 5.3] kPa) was imposed during 120 minutes of anaesthesia. On the second occasion arterial oxygen tension was maintained above 17 kPa throughout. Routine cardiovascular monitoring was performed and blood samples were taken to measure haematocrit, cortisol, insulin, glucose and lactate. Anaesthesia was associated with hypotension in both groups (mean ABP < 70 mmHg) but pulse rate changed little from control. Hypercapnia (PaCO2 > 7.0 kPa) developed in the normoxic group and acidosis was more severe than in the hypoxic group. Haematocrit changed little but was higher in the hypoxic group after the hypoxic period (0.39[0.06] vs 0.32[0.06] litre litre(-1)). Plasma cortisol increased significantly during anaesthesia in both groups (maximum values: hypoxic group 418[96], normoxic group 492[102] nmol litre(-1)) and there was no significant difference between them. Glucose concentration increased in the hypoxic group and was significantly higher than in the normoxic group during the hypoxic period (8.8[1.5] vs 6.4[1.5] mmol litre(-1)). Insulin decreased in both groups but this was significant only in the normoxic group (from 34[19] to a nadir of 12[9] iu ml(-1)) and the groups were not significantly different. Lacticacidaemia developed in both groups but was more severe in the hypoxic group (maximum values 2.3[0.6] and 1.3[0.5] mmol litre(-1)). It was concluded that 20 minutes of hypoxia during halothane anaesthesia in ponies did not markedly alter the stress response already induced by anaesthesia.
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PMID:Effects of hypoxia on endocrine and metabolic responses to anaesthesia in ponies. 1008 10

The time constant of cerebral arterial bed (in brief time constant) is a product of brain arterial compliance (C(a)) and resistance (CVR). We tested the hypothesis that in normal subjects, changes in end-tidal CO(2) (EtCO(2)) affect the value of the time constant. C(a) and CVR were estimated using mathematical transformations of arterial pressure (ABP) and transcranial Doppler (TCD) cerebral blood flow velocity waveforms. Responses of the time constant to controlled changes in EtCO(2) were compared in 34 young volunteers. Hypercapnia shortened the time constant (0.22 s [0.17, 0.26] vs. 0.16 s [0.13, 0.20]; p = 0.000001), while hypocapnia lengthened the time constant (0.22 s [0.17, 0.26] vs. 0.23 s [0.19, 0.32]; p < 0.0032). The time constant was negatively correlated with changes in EtCO(2) (R(partial) = -0.68, p < 0.000001). This was associated with a decrease in CVR when EtCO(2) increased (R(partial) = -0.80, p < 0.000001) and C(a) remained independent of changes in EtCO(2). C(a) was negatively correlated with mean ABP (R(partial) = -0.68, p < 0.000001). In summary, the time constant shortens with increasing EtCO(2). Its potential role in cerebrovascular investigations needs further studies.
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PMID:Time constant of the cerebral arterial bed in normal subjects. 2267 54

Objectives: The critical closing pressure (CrCP) defines arterial blood pressure below which cerebral arteries collapse. It represents a clinically relevant parameter for the estimation of cerebrovascular tone. Although there are few methods to assess CrCP, there is no consensus which of them estimates this parameter most accurately. The aim of present retrospective, experimental study was to compare three methods of CrCP estimation: conventional Aaslid's formula and methods based on the cerebrovascular impedance: the established continuous flow forward (CFF) and a new pulsatile flow forward (PFF) model.Methods: The effects of the following physiological manoeuvres on the CrCP were studied in New Zealand white rabbits: lumbar infusion of Hartmann's solution to induce mild intracranial hypertension, sympathetic blockade to induce arterial hypotension, and modulation of respiratory tidal volume to induce hypocapnia or hypercapnia.Results: During intracranial hypertension, all CrCP estimates were significantly higher than at baseline, decreased with decreasing ABP and increased with gradual hypocapnia. During hypercapnia, all CrCP estimates were significantly decreased but only in the case of CrCPA the negative, non-physiological values were observed (16% of the cases). The Bland-Altman analysis revealed that a good agreement between each impedance method and Aaslid's method deteriorated significantly in the low range of the average numerical value of the estimates.Discussion: Our results confirm the limited usage of Aaslid's formula for the calculation of CrCP. Although both impedance methods seem to be equivalent, the fact that PFF model better describes cerebrovascular hemodynamic allows the recommendation of this model for the calculation of CrCP.
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PMID:Critical closing pressure during experimental intracranial hypertension: comparison of three calculation methods. 3216 31