Disease relevance of Hypercapnia

• Accordingly, ventilatory responses to hypoxia and to hypercapnia were measured before and after administration of 7.5 mg of morphine sulfate subcutaneously in six normal subjects [1].
• METHODS: We randomly assigned 220 infants with a birth weight of 501 to 1000 g who were treated with mechanical ventilation within 12 hours after birth to receive dexamethasone or placebo with either routine ventilatory support or permissive hypercapnia [2].
• Letter: The use of oral diazepam in patients with obstructive lung disease and hypercapnia [3].
• These results therefore indicate that histidine residues contribute to the sensitivity of the ROMK1 channel to hypercapnia and intracellular acidosis [4].
• For example, in patients with hypercapnia and normoxemia, the mean (+/- SD) systolic blood pressure was 183+/-31 mm Hg and the mean norepinephrine level was 494+/-107 pg/mL, as compared with 150+/- 6 mm Hg and 243+/-58 pg/mL in those with normocapnia and hypoxemia (both P<0.05) [5].

Psychiatry related information on Hypercapnia

• Independent predictors of hypercapnia were fentanyl and midazolam doses, oxygen requirement, and dementia [6].
• In hypercapnia, however, the normal declines in GG activity from non-REM to REM sleep, and wakefulness to REM sleep, were reduced with mianserin (p < 0.005) [7].
• Attempts to measure HCVR during adenosine infusion were unsuccessful because of frequent arousals and continued periodic breathing despite hyperoxic hypercapnia [8].
• Sleep-related hypoxemia and hypercapnia are well recognized in COPD and are most pronounced in rapid eye movement sleep [9].
• Treatment with nocturnal O2 during a 2-yr period was associated with stable cardiovascular function but severe morning headaches and lethargy, presumably related to nightly bouts of hypercapnia and acidosis during sleep [10].

High impact information on Hypercapnia

• PC were stimulated by hypoxia (10% O2/90% N2) (n = 6) and central chemoreceptors by hypercapnia (7% CO2/93% O2) (n = 6) [11].
• Hypercapnia during baroreflex activation with PE increased SNA from 32 +/- 25 U/min during PE alone to 61 +/- 26 U/min during hypercapnia and PE (P less than 0.05) [11].
• Acute hypercapnia (arterial PCO2, 120 mmHg; blood pH, 7.02) was induced by ventilation with a 10% CO2-90% O2 gas mixture [12].
• Effect of acute hypercapnia on renal and proximal tubular total carbon dioxide reabsorption in the acetazolamide-treated rat [12].
• This study was designed to establish the relationship between urinary pCO2 and systemic blood pCO2 during acute hypercapnia and to investigate the significance of this relationship to collecting duct hydrogen ion (H+) secretion when the urine is acid and when it is highly alkaline [13].

Chemical compound and disease context of Hypercapnia

• Blood flow was measured with microspheres during maximal vasodilatation in the coronary bed (adenosine) and cerebral bed (hypercapnia) [14].
• After biperiden treatment, however, hypercapnia elicited a response profile similar to that elicited by air, whereby subjective anxiety remained similar to preinhalation levels [15].
• N omega-Methyl-L-arginine (1 mM) attenuated the cerebrovasodilation elicited by hypercapnia by 44 +/- 4% (n = 8; P less than 0.001), an effect completely reversed by coapplication of L-arginine (10 mM; P greater than 0.05; n = 13) [16].
• Those pathways are involved in the vasodilations elicited by a wide variety of stimuli, which include hypoxia and hypercapnia and agonist/receptor interactions (e.g. muscarinic, beta-adrenergic, and prostacyclin receptors) [17].
• An earlier study has demonstrated that indomethacin, a prostaglandin synthesis inhibitor, blocks the cerebrovascular response to hypercapnia [18].

Biological context of Hypercapnia

• Ventilatory and heart-rate responses to hypercapnia were evaluated by a CO2 rebreathing technique in 56 patients with acute ischemic stroke and 14 normal controls [19].
• The present study was designed to determine whether relaxations induced by hypercapnia depend upon nitric oxide (NO) derived from the endothelium, and whether NO-mediated relaxant response to electrical and chemical stimulation of vasodilator nerves is modulated by hypercapnia [20].
• Patients were 57 +/- 8 yr of age with severe COPD, hyperinflation, and air trapping (FEV1, 0.73 +/- 0.2 L; TLC, 7.3 +/- 1.6 L; residual volume [RV], 4.8 +/- 1.4 L), and moderate resting hypercapnia (PaCO2, 44 +/- 7 mm Hg; range, 32 to 56 mm Hg) [21].
• Hyperglycemia and hypercapnia suppress BDNF gene expression in vulnerable regions after transient forebrain ischemia in the rat [22].
• 4. Hypercapnia produced by inhalation of either 5% or 10% CO2 for 30 min stimulated maximal release of adrenal glucocorticoids and caused a substantial rise in plasma glucagon concentration [23].

Anatomical context of Hypercapnia

• The separate effects of hypoxia and hypercapnia on the force-velocity relation of rabbit myocardium were compared in 10 papillary or trabecular muscles superfused using control (95% O2-5% CO2), hypoxic (18% O2), and hypercapnic (20% CO2) physiological salt solutions [24].
• Relative flow velocity changes within the middle cerebral artery were measured by means of transcranial Doppler during hyper- and hypocapnia (VMRTOT), during hypercapnia alone (VMRCO2), and after injection of 1 g acetazolamide (VMRACE) [25].
• The effect of local administration of vasodilative concentrations of the adenosine receptor agonist 2-chloroadenosine (2-CADO) on the hyperemic responses of the pial and parenchymal microcirculations to graded hypercapnia was determined [26].
• Thus, lesion of the locus ceruleus and the resultant depletion of endogenous cortical and hippocampal norepinephrine, does not influence the cerebrovascular response to hypercapnia [27].
• We investigated the effect changes in end-expiratory lung volume (EEVL) had on the response to progressive hypercapnia (CO2-response curve) in eight open-chest, anesthetized dogs, in order to clarify the role that vagal lung mechanoreceptors have in altered respiratory drive during permissive hypercapnia [28].

Gene context of Hypercapnia

• NS398 did not affect arterial pressure, resting CBF or the CBF reactivity to hypercapnia in anesthetized iNOS null mice (P > .05) [29].
• Baseline breathing variables and ventilatory responses to hypercapnia were normal in the ECE-1+/- newborn mice [30].
• In air and in response to hypercapnia, VE, VT, and f were similar in Cftr-/- mice and in controls [31].
• Attenuation of the reflex PNA response to hypercapnia was also observed in the medulla-spinal cord preparation from ET-1-/- mice [32].
• However, reflex increases of ventilation to hypoxia and hypercapnia were significantly attenuated in ET-1+/-, ET-1-/- and ETA-/- mice [32].

Analytical, diagnostic and therapeutic context of Hypercapnia

• In the presence of L-arginine (10 mmol/L topical suffusion, 300 mg/kg intravenous infusion), the dilation of pial arterioles (n = 6) to hypercapnia was partially restored to 30 +/- 6% at 2 hours after injury [33].
• Relaxations, caused by transmural electrical stimulation and nicotine, of canine cerebral arterial strips contracted with prostaglandin F2 alpha, were potentiated only slightly by hypercapnia, but the potentiation of the response to exogenous NO (acidified NaNO2) was clearly greater [20].
• METHODS: Four groups of eight anesthetized dogs underwent 12 minutes of complete ischemia followed by 4 hours of reperfusion with either 1) normocapnia, 2) normocapnia and acetazolamide (25 mg/kg at reperfusion plus 12.5 mg/kg per hour, 3) hypocapnia, or 4) hypercapnia [34].
• However, the inferior region failed to increase in perfusion during hypercapnia and experienced significant mean blood flow reduction; flow reduction in the pixels at the 25th, 50th, 75th, and 90th percentile of flow; and an increased percentage of pixels without measurable flow, during hyperoxia (each P < 0.05) [35].
• Unlike during hypercapnia, microdialysis of 30 mM DPAT into the MRR did not change the ventilatory response to 10% O2 [36].

References