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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently we have found that hypercapnia induces nuclear protein (FOS) expression in the brainstem chemosensitive neurons, including catecholamine-containing cells. In the present studies we examined the role of protein kinase C (PKC) pathway in CO2-induced c-fos expression. Because of the complexity of the CNS system, experiments were performed in pheochromocytoma cells (PC12 cells). These cells originate from neuronal crest and express catecholaminergic traits. We depleted PKC from PC12 cells by prolonged (48 h) exposure to high concentration of phorbol 12-myristate, 13-acetate (PMA, 100 nM), and then determined the expression of: (1) c-fos mRNA by Northern blot (2) PKC isoforms, tyrosine phosphorylated and unphosphorylated MAP (mitogen activated protein) kinases by Western blot. Depletion of PKC abolished the effect of CO2 on c-fos mRNA expression, inhibited MAP kinases tyrosine phosphorylation and suppressed the expression of PKC(alpha) and PKC(zeta). These results suggest that MAP kinases, PKC(alpha) and/or PKC(beta) might be involved in CO2-induced c-fos mRNA expression.
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PMID:A possible role for protein kinase C in CO2/H+-induced c-fos mRNA expression in PC12 cells. 957 65

The effects of hypoxemia and hypercapnia in acute cardiovascular response to periodic non-obstructive apneas were explored in seven preinstrumented, sedated paralyzed and ventilated pigs under three conditions: room air breathing (RA), O2 supplementation (O2), and supplementation with O2 and CO2 (CO2). EEG monitoring showed no arousal under any conditions. RA apneas increased mean arterial pressure (MAP, from baseline 95.9 +/- 4.5 to late apnea 124.4 +/- 7.8 Torr, P < 0.01), left ventricular end-diastolic pressure, end-diastolic and end-systolic myocardial fiber lengths and systemic vascular resistance, but decreased cardiac output (CO, 3.09 +/- 0.34-2.37 +/- 0.26 L/min, P < 0.01), heart rate (HR, 115.1 +/- 7.5-102.0 +/- 7.8 bpm, P < 0.01), and stroke volume (SV, 29.6 +/- 0.7 21.1 +/- 1.8 ml, P < 0.01). 02 apneas produced similar decreases in HR (114.0 +/- 11.8-105.4 +/- 8.7 bpm, P < 0.05) as with RA apneas, but smaller increases in MAP (94.5 +/- 1.8-103.4 +/- 2.8 Torr, P < 0.01) and in the variables of pre- and after-load. CO and SV remained unchanged with O2 apneas. CO2 was associated with higher MAP, CO, and HR at baseline relative to RA, but similar cardiovascular response during apneas in direction and magnitude to those of O2 apneas. We conclude that in this model hypoxemia is a major but not the sole determinant of the pressor response during apneas. Hypercapnia cannot explain the pressor response seen when hypoxemia is abolished. The HR fall during apneas is independent of hypoxemia, hypercapnia and the pressor response.
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PMID:Role of hypoxemia and hypercapnia in acute cardiovascular response to periodic apneas in sedated pigs. 962 31

Six horses were randomly assigned to receive either frusemide (F) (0.5 mg/kg i.v.) or an equivalent volume of saline (S) i.v., 4 h prior to treadmill exercise. Horses were instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP), and diastolic (DAP) carotid arterial pressures, pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), blood gases, and cardiac output (CO). Plasma (PV) and blood volumes (BV) were measured using 2 injections of Evan's Blue dye. Baseline parameters were recorded while the horse stood quietly. Horses were then administered F or S. Four hours later, they were warmed up for 3 min at 4 m/s and then exercised to the point of fatigue at 115% VO2max. Horses were anaesthetised immediately following exercise by administration of detomidine (0.04 mg/kg bwt i.v.) followed 5 min later by tiletamine-zolazepam (1.25 mg/kg bwt i.v.). After transporting the horse to a recovery stall, anaesthesia was maintained with isoflurane in 100% O2. Data were analysed using a 2-way ANOVA with repeated measures with post hoc differences identified using the Student-Newman-Keul's procedure. Exercise was associated with increases in HR, SAP, MAP, DAP, PAP, CVP, TEMP, PCV, and BV, and decreases in PV, pH, arterial bicarbonate and base excess. Anaesthesia was associated with marked hypercapnia, a decrease in HR following detomidine administration, and persistent pulmonary hypertension despite carotid arterial pressure which returned to baseline. No effects attributable to F were identified at any time during the study.
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PMID:Effects of pre-exercise frusemide administration and post exercise anaesthesia on cardiopulmonary and acid-base parameters and blood and plasma volumes in horses exercised supramaximally to fatigue. 1065 46

Progesterone is known to cause hyperventilation and hypercapnia in the luteal phase of a normal menstrual cycle. Viewing this fact lung functions were measured in 71 girls with a mean age of 14.5 years during their follicular and luteal phase of menstrual cycle. Subjects were grouped into I, II and III depending on the age range. Respiratory functions comprising of FVC, FIVC, TLC, RV/TLC, FEV1, FEV1/FVC, FRC, PEFR, FEF 25%, FEF 50%, FEF 75%, PIFR, RAW and KST respectively were performed using Spiro 232 of PK Morgan under standardized laboratory settings. The anthropometric parameters such as height, weight and arm span were also recorded. The majority of pulmonary functions reflect better values in luteal phase as compared with follicular phase however, a statistically significant higher results of FVC, FIVC, FEV1, and TLC were noticed in group I and group III. These observations suggest a possible role in increased level of progesterone in luteal phase on respiratory system.
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PMID:Status of pulmonary function tests in adolescent females of Delhi. 1121 99

Methods of laser Doppler perfusion monitoring (LDPM) and imaging (LDPI) have been validated and found useful for measurements of brain blood flow in several studies. The present work was undertaken to examine the cortical blood flow autoregulatory phenomenon as it has lately been questioned and claimed to be method-dependent and related to sample volume. Spatial variations in cerebral cortical blood flow (CBF(cortex)) in the pressure range 20-140 mmHg (static cerebral autoregulation; caval block/angiotensin infusion) were studied in six mechanically ventilated (hypocapnic, normocapnic and hypercapnic) pigs anaesthetized with propofol and fentanyl. Although the cortical blood flow values sampled were highly heterogeneously distributed, they were strongly pressure-dependent as well as CO2-dependent (P < 0.001). A cumulative cerebral blood flow (CBF)-pressure (MAP) plot comprising all values obtained indicated a pressure range between 70 and 120 mmHg where CBF remained almost constant. However, at the local level in the cortex (mm2) the same type of 'classic' autoregulatory flow : pressure graphs (FPG) were found in only a few of the cases of the cortical areas examined (n = 96). Alterations in blood P(a)CO2 saturation did not affect the pressure : flow relationship at low perfusion pressures, whereas at normal or above normal values, and as anticipated, hypercapnia considerably increased CBF (P < 0.001). 'Classic' autoregulatory FPGs were found only when all values sampled were clustered together, whereas, as a new finding, data are presented indicating that autoregulatory capacity is lacking at the local level at some cortical surface areas.
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PMID:Cortical blood flow autoregulation revisited using laser Doppler perfusion imaging. 1244 30

We tested the hypothesis that integrated sympathetic and cardiovascular reflexes are modulated by systemic CO2 differently in hypoxia than in hyperoxia (n = 7). Subjects performed a CO2 rebreathe protocol that equilibrates CO2 partial pressures between arterial and venous blood and that elevates end tidal CO2 (PET(CO2)) from approximately 40 to approximately 58 mmHg. This test was repeated under conditions where end tidal oxygen levels were clamped at 50 (hypoxia) or 200 (hyperoxia) mmHg. Heart rate (HR; EKG), stroke volume (SV; Doppler ultrasound), blood pressure (MAP; finger plethysmograph), and muscle sympathetic nerve activity (MSNA) were measured continuously during the two protocols. MAP at 40 mmHg PET(CO2) (i.e., the first minute of the rebreathe) was greater during hypoxia versus hyperoxia (P < 0.05). However, the increase in MAP during the rebreathe (P < 0.05) was similar in hypoxia (16 +/- 3 mmHg) and hyperoxia (17 +/- 2 mmHg PET(CO2)). The increase in cardiac output (Q) at 55 mmHg PET(CO2) was greater in hypoxia (2.61 +/- 0.7 L/min) versus hyperoxia (1.09 +/- 0.44 L/min) (P < 0.05). In both conditions the increase in Q was due to elevations in both HR and SV (P < 0.05). Systemic vascular conductance (SVC) increased to similar absolute levels in both conditions but rose earlier during hypoxia (> 50 mmHg PET(CO2)) than hyperoxia (> 55 mmHg). MSNA increased earlier during hypoxic hypercapnia (> 45 mmHg) compared with hyperoxic hypercapnia (> 55 mmHg). Thus, in these conscious humans, the dose-response effect of PET(CO2) on the integrated cardiovascular responses was shifted to the left during hypoxic hypercapnia. The combined data indicate that peripheral chemoreceptors exert important influence over cardiovascular reflex responses to hypercapnia.
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PMID:Peripheral chemoreceptor contributions to sympathetic and cardiovascular responses during hypercapnia. 1256 39

The cardiopulmonary effects of desflurane and sevoflurane anesthesia were compared in cats breathing spontaneously. Heart (HR) and respiratory (RR) rates; systolic (SAP), diastolic (DAP) and mean arterial (MAP) pressures; partial pressure of end tidal carbon dioxide (PETCO2), arterial blood pH (pH), arterial partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2); base deficit (BD), arterial oxygen saturation (SaO2) and bicarbonate ion concentration (HCO3) were measured. Anesthesia was induced with propofol (8+/-2.3mg/kg IV) and maintained with desflurane (GD) or sevoflurane (GS), both at 1.3 MAC. Data were analyzed by analysis of variance (ANOVA), followed by the Tukey test (P<0.05). Both anesthetics showed similar effects. HR and RR decreased when compared to the basal values, but remained constant during inhalant anesthesia and PETCO2 increased with time. Both anesthetics caused acidemia and hypercapnia, but BD stayed within normal limits. Therefore, despite reducing HR and SAP (GD) when compared to the basal values, desflurane and sevoflurane provide good stability of the cardiovascular parameters during a short period of inhalant anesthesia (T20-T60). However, both volatile anesthetics cause acute respiratory acidosis in cats breathing spontaneously.
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PMID:Cardiopulmonary and acid-base effects of desflurane and sevoflurane in spontaneously breathing cats. 1577 45

The relative importance of CO2 and sympathetic stimulation in the regulation of cerebral and peripheral vasculatures has not been previously studied in humans. We investigated the effect of sympathetic activation, produced by isometric handgrip (HG) exercise, on cerebral and femoral vasculatures during periods of isocapnia and hypercapnia. In 14 healthy males (28.1 +/- 3.7 (mean +/- S.D.) years), we measured flow velocity (VP; transcranial Doppler ultrasound) in the middle cerebral artery during euoxic isocapnia (ISO, +1 mmHg above rest) and two levels of euoxic hypercapnia (HC5, end-tidal P(CO(2)), P(ET,CO2), = +5 mmHg above ISO; HC10, P(ET,CO2) = +10 above ISO). Each P(ET,CO2) level was maintained for 10 min using the dynamic end-tidal forcing technique, during which increases in sympathetic activity were elicited by a 2-min HG at 30% of maximal voluntary contraction. Femoral blood flow (FBF; Doppler ultrasound), muscle sympathetic nerve activity (MSNA; microneurography) and mean arterial pressure (MAP; Portapres) were also measured. Hypercapnia increased VP and FBF by 5.0 and 0.6% mmHg-1, respectively, and MSNA by 20-220%. Isometric HG increased MSNA by 50% and MAP by 20%, with no differences between ISO, HC5 and HC10. During the ISO HG there was an increase in cerebral vascular resistance (CVR; 20 +/- 11%), while VP remained unchanged. During HC5 and HC10 HG, VP increased (13% and 14%, respectively), but CVR was unchanged. In contrast, HG-induced sympathetic stimulation increased femoral vascular resistance (FVR) during ISO, HC5 and HC10 (17-41%), while there was a general decrease in FBF below ISO. The HG-induced increases in MSNA were associated with increases in FVR in all conditions (r = 0.76-0.87), whereas increases in MSNA were associated with increases in CVR only during ISO (r = 0.91). In summary, in the absence of hypercapnia, HG exercise caused cerebral vasoconstriction, myogenically and/or neurally, which was reflected by increases in CVR and a maintained VP. In contrast, HG increased FVR during conditions of ISO, HC5 and HC10. Therefore, the cerebral circulation is more responsive to alterations in PCO2, and less responsive to sympathetic stimulation than the femoral circulation.
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PMID:Differential responses to CO2 and sympathetic stimulation in the cerebral and femoral circulations in humans. 1589 Jun 97

Pulmonary complications from both obstetrical and non-obstetrical causes contribute to a mortality rate as high as 80% in the pregnant population. The effect of numerous mechanical and biochemical physiologic alterations during pregnancy can influence the maternal and fetal outcomes in a woman with a pulmonary complication. Progesterone, the primary hormone of pregnancy, is a respiratory stimulant that enhances carbon dioxide release and alters the maternal pH in favor of releasing oxygen to the fetus. During systemic compromise, which may be experienced as an acute asthmatic attack or respiratory distress syndrome, desaturation and carbon dioxide retention ensue. Under these conditions, the fetus is at risk for perinatal hypoxemia. Although prompt recognition and treatment are important to minimize maternal, fetal, and neonatal morbidity and mortality, evidence-based literature regarding critical care techniques that promote optimal obstetrical outcomes is limited. Therefore, a collaborative approach to the care of these women is warranted. In addition to critical care, emergency medicine, and obstetrical nurses, the medical team may include an obstetrician, a perinatologist, a neonatologist, a pulmonologist, an intensivist, and an immunologist.
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PMID:The effects of rhinitis, asthma, and acute respiratory distress syndrome as acute or chronic pulmonary conditions during pregnancy. 1671 14

The physiopathology of obstructive sleep apnea syndrome is multifactorial. Gender and obesity status, as well as genetic, anatomic, and hormonal factors, together with ventilatory drive, interact in a diverse manner in the physiopathology and clinical expression of the disease. Obesity is the main risk factor, since increases in body mass index, visceral fat, and neck circumference are strong predictors of the disease. Progesterone increases the activity of the upper airway dilator muscles and therefore plays a protective role in premenopausal women. This explains the fact that the prevalence of the disease is higher in postmenopausal patients, in patients with polycystic ovary syndrome, as well as in males. Evidence supports the fact that, as individuals grow older, there is a decrease in muscle tonus, with a consequent reduction in the dimensions of the upper airway lumen. Craniofacial anomalies, such as in retrognathia or micrognathia, are accompanied by posterior positioning of the tongue and can result in narrowing of the upper airway lumen. Finally, decreased ventilatory drive has been detected in patients with obstructive sleep apnea syndrome and hypercapnia.
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PMID:Physiopathology of obstructive sleep apnea-hypopnea syndrome. 1756 74


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