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)

To determine whether afferents in the middle cardiac nerves (MCN) contribute to extrapulmonary PaCO2 sensitivity, we did the following: we anesthetized six cockerels with sodium pentobarbital (25-35 mg/kg), and cannulated the cutaneous ulnar vein, and the carotid and brachial arteries. The thorax was opened and each lung unidirectionally ventilated from separate gas delivery systems. A ligature, which temporarily occluded blood flow, was placed around the right pulmonary artery. Both cardiac sympathetic nerves were cut, as well as the left vagus just above the level of the recurrent branch. We exposed the non-perfused right lung to 105 Torr PCO, to silence intrapulmonary chemoreceptors (IPC). We measured blood pressure, heart rate and ventilatory movements while the denervated left lung was used to fix PaCO2 at seven levels ranging from 7-140 Torr. As arterial PCO2 increased, ventilatory amplitude increased from 0.3 mm to 3.6 mm, while frequency decreased from 140 to 24 per min. After cutting the MCN, ventilatory movements were less responsive to PaCO2 changes. Ventilatory amplitude was 3.0 mm at the lowest PaCO2 and increased to 4.0 at the highest PaCO2. We conclude that: 1) when IPC discharge is low, afferents in the MCN inhibit ventilatory movements during hypocapnia, and 2) these afferents may contribute to systemic CO2 sensitivity.
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PMID:Middle cardiac nerve section alters ventilatory response to PaCO2 in the cockerel. 212 69

On 18 dogs the effects of hypoxia (12, 10, 7.5% O2) and hypoxia and hypercapnia (10% O2 + 5, 7.5, 11% CO2) on breathing, pulmonary vascular resistance, cardiac output and on the arterial and venous oxygen pressure were investigated. The relationship between arterial oxygen pressure to Pap as to vascular resistance is not in the mean linear. There are good, bad and nearly nonresponders in respect to the vascular resistance on the dogs. Therefore, calculation and evaluation of mean values are less helpful. A similar variation on men could help to understand also better the large scatter which is always shown on correlations between PO2a : Pap or PO2a : vascular resistance. Also the different pattern of the V/Q relationship may be influenced by the amount of the vascular response to local alveolar hypoxia. An increase of PCO/a potentiates the local vasoconstrictor effect of hypoxia. Mainly this was seen in the range between hypocapnia and moderate rates of hypercapnia. Hypoxia shows an increase of breathing frequency, hypercapnia shows and increase in tidal volume. Also under hypercapnia there are nonresponders and better responders in response to the vascular resistance in the lung circulation. Mechanical airway obstruction is followed by an increase of tidal volume; obstruction caused by acetylcholine is followed by a decrease of tidal volume and an increase of breathing frequency. Changes in the arterial blood gases are caused by changes in the ventilation perfusion relationship only under acetylcholine obstruction. Influences on the lung circulation by the airway obstruction under these experimental conditions as direct effects are small or not existent.
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PMID:[Experimental studies on cardiopulmonary relation under hypoxia, hypercapnia and airway obstruction in dog (author's transl)]. 722 Nov 90

Since high PCO in the dark works like hypoxia in the carotid body chemoreceptors and since hypoxia shows a stimulus interaction with CO2, it is hypothesized that high PCO will show a similar interaction with PCO2 in the chemosensory excitation in the dark. We tested the hypothesis using cat carotid body perfused and superfused in vitro with Po2 of about 100 Torr. In one series, the chemosensory discharges were tested at three levels of PCO2 at high PCO of 500 Torr in the absence and presence of light. In the dark, normocapnia (PCO2 approximately 30 Torr) with high PCO promptly stimulated the sensory discharges to a peak, subsiding to a lower level. In hypocapnia (PCO2 approximately 18 Torr) with high PCO, all phases of activities were significantly lower than those of normocapnia, showing stimulus interaction. Hypercapnia saturated the activity with high PCO and seems to preclude a clear demonstration of stimulus interaction. In another series, an intermediate level of PCO (approximately 150 Torr), which showed a half-maximal activity in normoxia, showed a clear interaction with hypercapnia in the dark. With high PCO, bright light promptly reduced the activity to baseline at all PCO2 levels. This then increased somewhat to a steady-state. Withdrawal of the light was followed by a sharp rise in the activity to a peak which then fell to a somewhat lower level of steady-state. The peak discharge rate in the presence of light did not differ significantly from those of PCO2 alone.
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PMID:Stimulus interaction between CO and CO2 in the cat carotid body chemoreception. 868 Aug 75

The effects of hypocapnia [arterial PCO(2) (Pa(CO(2))) 15 Torr] on splanchnic hemodynamics and gut mucosal-arterial P(CO(2)) were studied in seven anesthetized ventilated dogs. Ileal mucosal and serosal blood flow were estimated by using laser Doppler flowmetry, mucosal PCO(2) was measured continuously by using capnometric recirculating gas tonometry, and serosal surface PO(2) was assessed by using a polarographic electrode. Hypocapnia was induced by removal of dead space and was maintained for 45 min, followed by 45 min of eucapnia. Mean Pa(CO(2)) at baseline was 38.1 +/- 1.1 (SE) Torr and decreased to 13.8 +/- 1.3 Torr after removal of dead space. Cardiac output and portal blood flow decreased significantly with hypocapnia. Similarly, mucosal and serosal blood flow decreased by 15 +/- 4 and by 34 +/- 7%, respectively. Also, an increase in the mucosal-arterial PCO(2) gradient of 10.7 Torr and a reduction in serosal PO(2) of 30 Torr were observed with hypocapnia (P < 0.01 for both). Hypocapnia caused ileal mucosal and serosal hypoperfusion, with redistribution of flow favoring the mucosa, accompanied by increased PCO(2) gradient and diminished serosal PO(2).
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PMID:Splanchnic hemodynamics and gut mucosal-arterial PCO(2) gradient during systemic hypocapnia. 1048 83

In previous analyses of the occurrence of central (CSA) and obstructive sleep apnea (OSA) in patients with congestive heart failure (CHF), only men were studied and risk factors for these disorders were not well characterized. We therefore analyzed risk factors for CSA and OSA in 450 consecutive patients with CHF (382 male, 68 female) referred to our sleep laboratory. Risk factors for CSA were male gender (odds ratio [OR] 3.50; 95% confidence interval [CI], 1.39 to 8.84), atrial fibrillation (OR 4.13; 95% CI 1.53 to 11. 14), age > 60 yr (OR 2.37; 95% CI 1.35 to 4.15), and hypocapnia (PCO(2 )< 38 mm Hg during wakefulness) (OR 4.33; 95% CI 2.50 to 7. 52). Risk factors for OSA differed by gender: in men, only body mass index (BMI) was significantly associated with OSA (OR for a BMI > 35 kg/m(2), 6.10; 95% CI 2.86 to 13.00); whereas, in women, age was the only important risk factor (OR for age > 60 yr, 6.04; 95% CI 1.75 to 20.0). We conclude that historical information, supplemented by a few simple laboratory tests may enable physicians to risk stratify CHF patients for the presence of CSA or OSA, and the need for diagnostic polysomnography for such patients. Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD. Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure.
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PMID:Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure. 1050 91

We have determined whether changes in PCO(2) above and below eucapnia modulate the precision of the voluntary control of breathing. Twelve trained subjects performed a compensatory tracking task in which they had to maintain the position of a cursor (perturbed by a variable triangular forcing function) on a fixed target by breathing in and out of a spirometer (ventilatory tracking; at 10 l/min). Before each task, subjects hyperventilated for 5 min, and the end-tidal PCO(2) (PET(CO(2))) was controlled; tracking was then performed separately at hypocapnia, eucapnia, and hypercapnia (PET(CO(2)) approximately 25, 37, and 43 Torr, respectively). Ventilatory tracking error was unchanged during hypocapnia (P > 0.05) but was significantly worse during hypercapnia (P < 0.003), compared with eucapnia; arm tracking error, performed as a control, was not significantly affected by PET(CO(2)) (P > 0. 05). In conclusion, ventilatory tracking performance is unaffected by the eucapnic PCO(2). From this, we suggest that resting breathing in awake humans may be independent of chemical drives and of the prevailing PCO(2).
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PMID:Modulation of the corticospinal control of ventilation by changes in reflex respiratory drive. 1056 38

We hypothesized that a decreased susceptibility to the development of hypocapnic central apnea during non-rapid eye movement (NREM) sleep in women compared with men could be an explanation for the gender difference in the sleep apnea/hypopnea syndrome. We studied eight men (age 25-35 yr) and eight women in the midluteal phase of the menstrual cycle (age 21-43 yr); we repeated studies in six women during the midfollicular phase. Hypocapnia was induced via nasal mechanical ventilation for 3 min, with respiratory frequency matched to eupneic frequency. Tidal volume (VT) was increased between 110 and 200% of eupneic control. Cessation of mechanical ventilation resulted in hypocapnic central apnea or hypopnea, depending on the magnitude of hypocapnia. Nadir minute ventilation in the recovery period was plotted against the change in end-tidal PCO(2) (PET(CO(2))) per trial; minute ventilation was given a value of 0 during central apnea. The apneic threshold was defined as the x-intercept of the linear regression line. In women, induction of a central apnea required an increase in VT to 155 +/- 29% (mean +/- SD) and a reduction of PET(CO(2)) by -4.72 +/- 0.57 Torr. In men, induction of a central apnea required an increase in VT to 142 +/- 13% and a reduction of PET(CO(2)) by -3.54 +/- 0.31 Torr (P = 0.002). There was no difference in the apneic threshold between the follicular and the luteal phase in women. Premenopausal women are less susceptible to hypocapnic disfacilitation during NREM sleep than men. This effect was not explained by progesterone. Preservation of ventilatory motor output during hypocapnia may explain the gender difference in sleep apnea.
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PMID:Effect of gender on the development of hypocapnic apnea/hypopnea during NREM sleep. 1090 52

Arterial hypocapnia has been associated with orthostatic intolerance. Therefore, we tested the hypothesis that hypocapnia may be detrimental to increases in muscle sympathetic nerve activity (MSNA) and total peripheral resistance (TPR) during head-up tilt (HUT). Ventilation was increased approximately 1.5 times above baseline for each of three conditions, whereas end-tidal PCO(2) (PET(CO(2))) was clamped at normocapnic (Normo), hypercapnic (Hyper; +5 mmHg relative to Normo), and hypocapnic (Hypo; -5 mmHg relative to Normo) conditions. MSNA (microneurography), heart rate, blood pressure (BP, Finapres), and cardiac output (Q, Doppler) were measured continuously during supine rest and 45 degrees HUT. The increase in heart rate when changing from supine to HUT (P < 0.001) was not different across PET(CO(2)) conditions. MSNA burst frequency increased similarly with HUT in all conditions (P < 0.05). However, total MSNA and the increase in total amplitude relative to baseline (%DeltaMSNA) increased more when changing to HUT during Hypo compared with Hyper (P < 0.05). Both BP and Q were higher during Hyper than both Normo and Hypo (main effect; P < 0.05). Therefore, the MSNA response to HUT varied inversely with levels of PET(CO(2)). The combined data suggest that augmented cardiac output with hypercapnia sustained blood pressure during HUT leading to a diminished sympathetic response.
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PMID:PET(CO(2)) inversely affects MSNA response to orthostatic stress. 1151 69

The hypothesis that intracellular calcium ([Ca(2+)](i)) release in glomus cells via ryanodine receptor (RyR) activation by caffeine may be independent of natural stimuli and chemosensory discharge was tested in the rat carotid body (CB). CB type I cells were isolated, plated and preloaded with calcium-sensitive fluorescent probe, Indo-1AM. With the increase of caffeine dose (0-50 mM) cytosolic calcium ([Ca(2+)](c)) increased from 85+/-15 nM to 1933+/-190 nM (n=6) at normoxia (PO(2)=125-130 Torr, PCO(2)=25-30 Torr, pH 7.30-7.35). Hypoxia (PO(2)=10-15 Torr) increased and hypocapnia (PCO(2)=7-9 Torr) decreased the cytoplasmic calcium [Ca(2+)](c) levels, independent of caffeine. Caffeine-related [Ca(2+)](c) increase was the same in the presence and the absence of extracellular calcium ([Ca(2+)](o)), indicating the source of Ca(2+) ions is the cellular store. Permeabilization of the cell membrane with saponin (25 microg/ml) retained the caffeine response. Additional treatment of the cells with 50 microM ryanodine (an inhibitor of the caffeine-activated RyR site) abolished caffeine-stimulated response. In vitro CB chemosensory (carotid sinus nerve, CSN) responses to hypoxia (PO(2)=35-40 Torr) were not altered by caffeine. These results suggest that [Ca(2+)](i) stores in CB cells, mobilized by RyR activation, do not participate in the CSN responses to natural stimuli.
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PMID:Ryanodine receptor-mediated [Ca(2+)](i) release in glomus cells is independent of natural stimuli and does not participate in the chemosensory responses of the rat carotid body. 1159 88

Ventilatory management patterns in very low birth weight newborns, particularly iatrogenic hypocapnia, have occasionally been implicated in perinatal brain damage. However, such relationships have not been explored in large representative populations. To examine the risk of disabling cerebral palsy in mechanically ventilated very low birth weight infants in relation to hypocapnia and other ventilation-related variables, we conducted a population-based prospective cohort study of 1105 newborns with birth weights of 500-2000 g born in New Jersey from mid-1984 through 1987, among whom 777 of 902 survivors (86%) had at least one neurodevelopmental assessment at age 2 y or older. Six hundred fifty-seven of 777 assessed survivors (85%), of whom 400 had been mechanically ventilated, had blood gases obtained during the neonatal period. Hypocapnia was defined as the highest quintile of cumulative exposure to arterial PCO(2) levels <35 mm Hg during the neonatal period. Disabling cerebral palsy was diagnosed in six of 257 unventilated newborns (2.3%), 30 of 320 ventilated newborns without hypocapnia (9.4%), and 22 of 80 ventilated newborns with hypocapnia (27.5%). Two additional ventilatory risk factors for disabling cerebral palsy were found-hyperoxia and prolonged duration of ventilation. In a multivariate analysis, each of the three ventilatory variables independently contributed a 2- to 3-fold increase in risk of disabling cerebral palsy. These risks were additive. Although duration of mechanical ventilation in very low birth weight newborns likely represents severity of illness, both hypocapnia and hyperoxia are largely controlled by ventilatory practice. Avoidance of arterial PCO(2) levels <35 mm Hg and arterial PO(2) levels >60 mm Hg in mechanically ventilated very low birth weight infants would seem prudent.
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PMID:Hypocapnia and other ventilation-related risk factors for cerebral palsy in low birth weight infants. 1172 29


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