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)

Breathing 100% O2 at 1 atmosphere absolute (ATA) is known to be associated with a decrease in cerebral blood flow (CBF). It is also accompanied by a fall in arterial Pco2 leading to uncertainty as to whether the cerebral vasoconstriction is totally or only in part caused by arterial hypocapnia. We tested the hypothesis that the increase in arterial Po2 while O2 was breathed at 1.0 ATA decreases CBF independently of a concurrent fall in arterial Pco2. CBF was measured in seven healthy men aged 21-62 yr by using noninvasive continuous arterial spin-labeled-perfusion MRI. The tracer in this technique, magnetically labeled protons in blood, has a half-life of seconds, allowing repetitive measurements over short time frames without contamination. CBF and arterial blood gases were measured while breathing air, 100% O2, and 4 and 6% CO2 in air and O2 backgrounds. Arterial Po2 increased from 91.7 +/- 6.8 Torr in air to 576.7 +/- 18.9 Torr in O2. Arterial Pco2 fell from 43.3 +/- 1.8 Torr in air to 40.2 +/- 3.3 Torr in O2. CBF-arterial Pco2 response curves for the air and hyperoxic runs were nearly parallel and separated by a distance representing a 28.7-32.6% decrement in CBF. Regression analysis confirmed the independent cerebral vasoconstrictive effect of increased arterial Po2. The present results also demonstrate that the magnitude of this effect at 1.0 ATA is greater than previously measured.
J Appl Physiol (1985) 2003 Dec
PMID:Independent cerebral vasoconstrictive effects of hyperoxia and accompanying arterial hypocapnia at 1 ATA. 1293 24

The present study tests the hypothesis that a PaCO(2) of 27 mmHg for 1 hr results in increased neuronal nuclear Ca(++)/calmodulin-dependent protein kinase IV (CaM kinase IV) activity, pro-apoptotic protein expression and DNA fragmentation in the cerebral cortex of newborn piglets. Hypocapnic (HC) and normocapnic newborn piglets were studied. Tissue levels of ATP and phosphocreatine (PCr) were lower in the HC group. CaM kinase IV activity and Bax protein density were higher in the HC group. Bcl-2 protein density was the same in both groups, resulting in an increased ratio of Bax/Bcl-2 in the HC group. Density of nuclear DNA fragments was greater in the HC group and varied inversely with ATP and PCr levels. We conclude that hypocapnia (PaCO(2) 27 mmHg) results in increased expression of pro-apoptotic proteins and fragmentation of nuclear DNA in newborn piglets.
Neurosci Lett 2003 Dec 11
PMID:The effect of hypocapnia (PaCO2 27 mmHg) on CaM kinase IV activity, Bax/Bcl-2 protein expression and DNA fragmentation in the cerebral cortex of newborn piglets. 1462 22

This investigation was designed to determine if suppression of testosterone alters the ventilatory response to carbon dioxide in the presence of high and low levels of oxygen. Eleven healthy male subjects completed a series of rebreathing trials during wakefulness, before and after treatment with a long-acting gonadotropin-releasing hormone agonist. Five subjects also completed studies during non-rapid eye movement (NREM) sleep. During wakefulness, subjects initially hyperventilated to reduce the partial pressure of carbon dioxide (P(ET,CO2)) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr) or high oxygen (140 Torr) gas mixture. During each trial P(ET,CO2) increased while oxygen was maintained at a constant level. The threshold of the ventilatory response to carbon dioxide was considered to be the point at which minute ventilation began to rise in a linear fashion as P(ET,CO2) increased. The slope of the ventilatory response above the threshold was used as a measure of sensitivity to carbon dioxide. During NREM sleep, hypocapnia was induced via nasal mechanical ventilation. Several trials were completed until the cessation of mechanical ventilation resulted in a central apnoea which demarcated the threshold of the ventilatory response to carbon dioxide. In response to treatment with leuprolide acetate, the threshold measured in wakefulness decreased during carbon dioxide rebreathing in the presence of low (41.05 +/- 0.77 versus 39.40 +/- 0.83 Torr; P = 0.01) and high (46.32 +/- 0.56 versus 44.78 +/- 0.83 Torr; P = 0.01) oxygen levels. An increase in sensitivity (4.82 +/- 0.61 versus 7.17 +/- 1.20 l min(-1) Torr(-1); P = 0.02) was also observed during rebreathing in the presence of high but not low oxygen levels. The increase in sensitivity was accompanied by an increase in carbon dioxide production. The findings observed during NREM sleep were similar to those observed during wakefulness, since the P(ET,CO2) that demarcated the threshold was decreased after leuprolide treatment (42.1 +/- 0.6 versus 39.6 +/- 0.6 Torr; P = 0.002). Additionally, the decrease in P(ET,CO2) required to induce an apnoea was greater after treatment with leuprolide (2.56 +/- 0.25 versus 4.06 +/- 0.29 Torr; P = 0.004). We conclude that suppression of testosterone decreases the threshold of the ventilatory response to carbon dioxide during both wakefulness and sleep.
J Physiol 2004 Dec 01
PMID:Treatment with leuprolide acetate decreases the threshold of the ventilatory response to carbon dioxide in healthy males. 1548 11

The blood oxygenation level-dependent (BOLD) responses to visual stimuli, using both a 1-s long single trial stimulus and a 20-s long block stimulus, were measured in a 4-T magnetic field both before and immediately after a 200-mg caffeine dose. In addition, resting levels of cerebral blood flow (CBF) were measured using arterial spin labeling. For the single trial stimulus, the caffeine dose significantly (p<0.05) reduced the time to peak (TTP), the time after the peak at which the response returned to 50% of the peak amplitude (TA50), and the amplitude of the poststimulus undershoot in all subjects (N=5). Other parameters, such as the full-width half-maximum (FWHM) and the peak amplitude, also showed significant changes in the majority of subjects. For the block stimulus, the TTP, TA50, and the time for the response to reach 50% of the peak amplitude (T50) were significantly reduced. In some subjects, oscillations were observed in the poststimulus portion of the response with median peak periods of 9.1 and 9.5 s for the single trial and block responses, respectively. Resting CBF was reduced by an average of 24%. The reproducibility of the results was verified in one subject who was scanned on 3 different days. The dynamic changes are similar to those previously reported for baseline CBF reductions induced by hypocapnia and hyperoxia.
Neuroimage 2004 Dec
PMID:Caffeine alters the temporal dynamics of the visual BOLD response. 1558 4

Nimodipine is a calcium entry blocker that shows promise in the therapy for cerebral ischemia. This study was undertaken to examine the interaction of nimodipine with the use of hypocapnia to control cerebral blood volume by reduction in cerebral blood flow (CBF), as might be applicable to patients undergoing anesthesia for neurosurgical procedures. Male adult Sprague-Dawley rats were anesthetized with pentobarbital 50 mg/kg i.p. and were mechanically ventilated at either normocapnia (Paco2 35-40 mm Hg) or hypocapnia (Paco2 23-25 mm Hg). Animals were randomized into four experimental groups in a 2 x 2 factorial design, employing Paco2 level and drug group as between-group factors: vehicle plus normocapnia (group 1, n = 6), nimodipine plus normocapnia (group 2, n = 7), vehicle plus hypocapnia (group 3, n = 6), and nimodipine plus hypocapnia (group 4, n = 6). Nimodipine (1 mug/kg/min) or vehicle was administered i.v. for a period of 45 min. CBF was then measured using [C]iodoantipyrine autoradiography. Hypocapnia decreased global CBF (p <0.0001) and nimodipine increased CBF (p <0.05). Although nimodipine increased global CBF (p <0.05) during normocapnia (89 +/- 8 versus 61 +/- 4 ml/100 g/min), during hypocapnia there was no significant difference between nimodipine and vehicle (45 +/- 3 versus 40 +/- 2 ml/100 g/min). Hypocapnia decreased local CBF in all structures examined, whereas nimodipine increased local CBF in some, but not all structures. In this model, prior institution of hypocapnia prevented nimodipine-induced global CBF increases.
J Neurosurg Anesthesiol 1990 Dec
PMID:Nimodipine does not increase cerebral blood flow during hypocapnia in the rat. 1581 65

We investigated the interaction between hypoxia and hypercapnia on ventilation and on cerebro-cardio-vascular control. A group of 12 healthy subjects performed rebreathing tests to determine the ventilatory response to hypoxia, at different levels of carbon dioxide (CO(2)), and to normoxic hypercapnia. Oxygen saturation (SaO(2)), end-tidal CO(2) (et-CO(2)), minute ventilation, blood pressure, R-R interval and mid-cerebral artery flow velocity (MCFV) were continuously recorded. The hypoxic ventilatory response significantly increased under hypercapnia and decreased under hypocapnia (slopes L/min/% Sa O(2): -0.33 +/- 0.05, -0.74 +/- 0.02 and -1.59 +/- 0.3, p < 0.0001, in hypocapnia, normocapnia and hypercapnia, respectively). At similar degrees of ventilation, MCFV increased more markedly during normocapnic hypoxia than normoxic hypercapnia; the slopes linking MCFV to hypoxia remained unchanged at increasing levels of et-CO(2), whereas the regression lines were shifted upward. The R-R interval decreased more markedly during normocapnic hypoxia than normoxic hypercapnia and the arterial baroreflex sensitivity was decreased only by hypoxia. Cardiovascular responses to hypoxia were not affected by different levels of et-CO(2). We conclude that concomitant hypoxia and hypercapnia, while increasing ventilation synergistically, exert an additive effect on cerebral blood flow. Increased sympathetic activity (and reduced baroreflex sensitivity) is one of the mechanisms by which hypoxia stimulates cardiac sympathetic activity.
Clin Auton Res 2005 Dec
PMID:Interaction between central-peripheral chemoreflexes and cerebro-cardiovascular control. 1636 39

This study examined the effects of menstrual cycle phase on ventilatory control. Fourteen eumenorrheic women were studied in the early follicular (FP; 1-6 days) and mid-luteal (LP; 20-24 days) phase of the menstrual cycle. Blood for the determination of arterial PCO(2) (PaCO(2)) , plasma strong ion difference ([SID]), progesterone ([P(4)]), and 17beta-estradiol ([E(2)]) concentrations were obtained at rest. Subjects performed a CO(2) rebreathing procedure that included prior hyperventilation and maintenance of iso-oxia to evaluate central and peripheral chemoreflex, and nonchemoreflex drives to breathe. Resting PaCO(2) and [SID] were lower; minute ventilation (V (E)), [P(4)] and [E(2)] were higher in the LP versus FP. Within the LP, significant correlations were observed for PaCO(2) with [P(4)], [E(2)] and [SID]. Menstrual cycle phase had no effect on the threshold or sensitivity of the central and/or peripheral ventilatory chemoreflex response to CO(2). Both (V (E)) and the ventilatory response to hypocapnia (representing nonchemoreflex drives to breathe) were approximately 1L/min greater in the LP versus FP accounting for the reduction in PaCO(2) . These data support the hypothesis that phasic menstrual cycle changes in PaCO(2) may be due, at least in part, to the stimulatory effects of [P(4)], [E(2)] and [SID] on ventilatory drive.
Respir Physiol Neurobiol 2006 Dec
PMID:Phasic menstrual cycle effects on the control of breathing in healthy women. 1654 84

We hypothesized that chronic intermittent hypoxia (CIH) would induce a predisposition to apnea in response to induced hypocapnia. To test this, we used pressure support ventilation to quantify the difference in end-tidal partial pressure of CO(2) (Pet(CO(2))) between eupnea and the apneic threshold ("CO(2) reserve") as an index of the propensity for apnea and unstable breathing during sleep, both before and following up to 3-wk exposure to chronic intermittent hypoxia in dogs. CIH consisted of 25 s of Pet(O(2)) = 35-40 Torr followed by 35 s of normoxia, and this pattern was repeated 60 times/h, 7-8 h/day for 3 wk. The CO(2) reserve was determined during non-rapid eye movement sleep in normoxia 14-16 h after the most recent hypoxic exposure. Contrary to our hypothesis, the slope of the ventilatory response to CO(2) below eupnea progressively decreased during CIH (control, 1.36 +/- 0.18; week 2, 0.94 +/- 0.12; week 3, 0.73 +/- 0.05 l.min(-1).Torr(-1), P < 0.05). This resulted in a significant increase in the CO(2) reserve relative to control (P < 0.05) following both 2 and 3 wk of CIH (control, 2.6 +/- 0.6; week 2, 3.7 +/- 0.8; week 3, 4.5 +/- 0.9 Torr). CIH also 1) caused no change in eupneic, air breathing Pa(CO(2)); 2) increased the slope of the ventilatory response to hypercapnia after 2 wk but not after 3 wk compared with control; and 3) had no effect on the ventilatory response to hypoxia. We conclude that 3-wk CIH reduced the sensitivity of the ventilatory response to transient hypocapnia and thereby increased the CO(2) reserve, i.e., the propensity for apnea was reduced.
J Appl Physiol (1985) 2007 Dec
PMID:Chronic intermittent hypoxia increases the CO2 reserve in sleeping dogs. 1793 1

Inadequate dipping in nighttime blood pressure (BP) is associated with cerebrovascular disease. The authors aimed to determine whether inadequate nocturnal dipping was associated with abnormalities in cerebrovascular hemodynamics in individuals without stroke. Participants in this study underwent 24-hour ambulatory BP monitoring followed by morning transcranial Doppler measurements of blood flow velocities (BFVs) in the middle cerebral artery during supine rest, head-up tilt, hypocapnia, and hypercapnia. Nighttime BP decline by <10% was considered nondipping. Of the 102 nonstroke participants (mean age, 53.6 years), 35 (34%) were dippers. Although nondippers had similar BFV and cerebrovascular resistance (CVR) while supine, they had a lower BFV (P=.04) and greater CVR (P=.02) during head-up tilt compared with dippers. Moreover, greater nighttime dipping in both systolic BP (P=.006) and diastolic BP (P=.03) were associated with higher daytime BFV and lower CVR (P=.01 for systolic BP; P=.02 for diastolic BP). Inadequate nocturnal BP dipping is associated with lower daytime cerebral blood flow, especially during head-up tilt.
J Clin Hypertens (Greenwich) 2007 Dec
PMID:The relationship between nighttime dipping in blood pressure and cerebral hemodynamics in nonstroke patients. 1804 99

Human pregnancy is characterized by significant increases in ventilatory drive both at rest and during exercise. The increased ventilation and attendant hypocapnia of pregnancy has been attributed primarily to the stimulatory effects of female sex hormones (progesterone and estrogen) on central and peripheral chemoreflex drives to breathe. However, recent research from our laboratory suggests that hormone-mediated increases in neural (or non-chemoreflex) drives to breathe may contribute importantly to the hyperventilation of pregnancy. This review challenges traditional views of ventilatory control, and outlines an alternative hypothesis of the control of breathing during human pregnancy that is currently being tested in our laboratory. Conventional wisdom suggests that pregnancy-induced increases in central respiratory motor output command in combination with progressive thoraco-abdominal distortion may compromise the normal mechanical response of the respiratory system to exercise, increase the perception of exertional breathlessness, and curtail aerobic exercise performance in otherwise healthy pregnant women. The majority of available evidence suggests, however, that neither pregnancy nor advancing gestation are associated with reduced aerobic working capacity or increased breathlessness at any given work rate or ventilation during exhaustive weight-supported exercise.
Appl Physiol Nutr Metab 2007 Dec
PMID:Chemical and mechanical adaptations of the respiratory system at rest and during exercise in human pregnancy. 1805 2


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