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)

Respiratory values were determined in guinea pigs studied under normal laboratory conditions in Denver. The effects of anesthesia and acute hypercapnia were also assessed. In normal laboratory conditions, VO2 and VE were proportional to body weight (BW). Specific VO2 and VE for small guinea pigs (mean BW: 269 g) were 1.14 +/- 0.04 (SEM) and 57.5 +/- 3.9 ml/g X h, respectively, compared to 0.82 +/- 0.03 (P less than 0.001) and 29.9 +/- 0.8 ml/g X h (P less than 0.001), respectively, for large animals (mean BW: 817 g). Tidal volume (VT) was related to BW by the following equation: VT (ml) = 3.97 X 10(-3) BW (g) + 2.05 (r = 0.82; P less than 0.001). During anesthesia VO2 decreased 25-63% and VE was reduced by 45% in those animals having the largest change in VO2. In hypercapnia, VE was more than twice that in normocapnia primarily due to a 75-95% elevation in VT.
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PMID:Ventilation and oxygen consumption in the guinea pig. 405 92

The response of ventilation and of heart rate to hypoxia and hypercapnia was determined in eight young normal men age 22-30 yr and eight elderly men age 64-73. The elderly men were selected and carefully screened to eliminate the possibility of cardiopulmonary disease. All the subjects were born at low altitude and had no significant prior exposure to hypoxia. The ventilatory response to hypoxia was measured as the exponential slope constant. k, of regression lines relating the logarithm of incremental ventilation to PAo(2) during isocapnic progressive hypoxia. The heart rate response to hypoxia was measured as the percentage change in heart rate between PAo(2) = 100 and PAo(2) = 40 mm Hg. The ventilatory response to hypercapnia was measured as the slope of regression lines relating ventilation to PAco(2) during rebreathing with PAo(2) > 200 mm Hg. The heart rate response to hypercapnia was measured as the percentage change in heart rate between control values at the start of the rebreathing test and PACO(2) = 55 mm Hg. The ventilatory and heart rate responses to both hypoxia and hypercapnia were significantly decreased in the elderly men as compared to the young men. Hypoxic ventilatory drive was decreased by 51+/-6% (mean +/-SEM: P < 0.001) and hypercapnic drive by 41+/-7% (P < 0.025). The percentage change in heart rate produced by hypoxia was 34+/-5% (mean +/-SEM) in the young normals and 12+/-2% in the old normals (P < 0.005). Similar figures for heart rate in response to hypercapnia were 15+/-3% and -1+/-1% for the young and old normal groups (P < 0.001). We conclude that ventilatory and heart rate responses to hypoxia and hypercapnia diminish with age. These alterations in both ventilatory and circulatory controls could make older individuals more vulnerable to hypoxic disease states.
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PMID:Attenuation of the ventilatory and heart rate responses to hypoxia and hypercapnia with aging in normal men. 471 63

Patients with pulmonary dysfunction and CO2 retention have renal hemodynamic abnormalities accompanied by increased plasma renin activity. To determine if hypercapnia impairs renal function, particularly through the renin-angiotensin system, the effects of acute hypercapnic acidosis (HC), using 8.5% CO2, were measured in five unanesthetized dogs during (a) the intact state; (b) renin-angiotensin antagonism using either 1-sarcosine, 8-glycine angiotensin II ( [Sar1, Gly8] AII) or SQ 14,225; and (c) exogenous angiotensin II infusion. As partial arterial carbon dioxide pressure (PaCO2) increased (p less than 0.05) from control (C) of 35 +/- 1 (SEM) to 48 +/- 1 mm Hg during HC, arterial pH fell (p less than 0.05) from 7.36 +/- 0.01 to 7.24 +/- 0.005. Renal function was uncompromised with HC, and glomerular filtration rate (GFR) and urinary sodium excretion increased (p less than 0.05) despite a fourfold rise in plasma renin activity from C of 0.6 +/- 0.3 to 2.2 +/- 0.8 ng AI ml-1 h-1 during HC. Administration of [Sar1, Gly8] AII during HC did not consistently alter systemic or renal hemodynamic responses, and effects of SQ 14,225 during HC were also observed during normocapnia. Although systemic vascular responses to exogenous AII infusion were similar, the renal vasoconstrictor response was antagonized during HC with unchanged GFR and renal blood flow. These findings indicate that despite activation of the renin-angiotensin system, acute hypercapnic acidosis is unassociated with impairment of renal function in unanesthetized dogs. This may be related to diminished renal vascular AII responsiveness during hypercapnia.
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PMID:Renal and cardiovascular responses to acute hypercapnic acidosis in conscious dogs: role of renin--angiotensin. 618 44

Increased episodes and duration of apnea during sleep associated with arterial oxygen desaturation have been reported after administration of flurazepam. We postulated that an alteration in respiratory control during sleep might be the underlying mechanism of this observation. Accordingly, we measured isocapnic hypoxic and hyperoxic hypercapnic ventilatory and arousal responses during natural (NS) and during flurazepam-induced (FS) sleep. We found no significant difference in the ventilatory response to hypoxia during FS compared with that during NS in 8 normal subjects. Similarly, although the ventilatory response to hypercapnia was performed in only 4 of the 8 subjects during FS, no significant difference from that during NS was noted in these subjects. There was, however, a significant decrease in the number of hypercapnic response tests in which arousal occurred after flurazepam administration (85% in NS versus 54% in FS; p less than 0.005). Additionally, an increase was seen in the mean PACO2 level at which arousal occurred during FS (51 +/- 1.6, means +/- SEM) as compared with that during NS (49 +/- 0.9; p less than 0.07). A similar but not significant decrease was noted in the number of hypoxic response tests in which arousal occurred (28% during NS versus 17% during FS). We conclude that while ventilatory responses to hypoxia and hypercapnia are normal during sleep after flurazepam administration, a decrease in arousal response is seen after administration of this drug in normal subjects. This alteration in arousal response may be the pathogenic mechanism of the increased duration of apnea reported in association with flurazepam.
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PMID:Flurazepam attenuates the arousal response to CO2 during sleep in normal subjects. 641 46

Sleep deprivation is common in acutely ill patients because of their underlying disease and can be compounded by aggressive medical care. While sleep deprivation has been shown to produce a number of psychological and physiologic events, the effects on respiration have been minimally evaluated. We therefore studied resting ventilation and ventilatory responses to hypoxia and hypercapnia before and after 24 h of sleeplessness in 13 healthy men. Hypoxic ventilatory responses (HVR) were measured during progressive isocapnic hypoxia, and hypercapnic ventilatory responses (HCVR) were measured using a rebreathing technique. Measures of resting ventilation, i.e., minute ventilation, tidal volume, arterial oxygen saturation, and end-tidal gas concentrations, did not change with short-term sleep deprivation. Both HVR and HCVR, however, decreased significantly after a single night without sleep. The mean hypoxic response decreased 29% from a slope of 1.20 +/- 0.22 (SEM) to 0.85 +/- 0.15 L/min/% saturation (p less than 0.02), and the slope of the HCVR decreased 24% from 2.07 +/- 0.17 to 1.57 +/- 0.15 L/min/mmHg PCO2 (p less than 0.01). These data indicate that ventilatory chemosensitivity may be substantially attenuated by even short-term sleep deprivation. This absence of sleep could therefore contribute to hypoventilation in acutely ill patients.
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PMID:Sleep deprivation and the control of ventilation. 641 47

The rate and regularity of fetal breathing movements (FBM) were determined in 14 women with uncomplicated singleton pregnancies, eight of whom were between 30 and 33 weeks gestation and six between 37 and 40 weeks gestation. Similar observations were made in 19 women with pregnancies complicated by severe intrauterine growth retardation, 11 of whom were between 30 and 33 weeks and eight between 37 and 40 weeks. In normal pregnancy recordings of breath-to-breath intervals showed that FBM became more regular with advancing gestational age, and the rate [breaths/min, mean (SEM)] slowed from 57.2 (1.3) at 30-33 weeks to 47.9 (0.8) at 37-40 weeks. FBM in the growth-retarded group were regular at each gestation studied and the rate was even slower than in the normal group at term, being 41.9 (1.2) at 30-33 weeks and 41.1 (1.0) at 37-40 weeks. Hyperoxia and hypercapnia appeared to have no consistent effect on fetal breathing rate. Fasting for greater than 12 h considerably reduced the rate of FBM in the normal fetus but only marginally so in those with growth retardation. It is concluded that the pattern of FBM provides more information about the fetus than the amount of time spent breathing, particularly when growth is retarded.
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PMID:The rate and regularity of breathing movements in the normal and growth-retarded fetus. 641 69

The authors studied the effect of lidocaine infusion on the ventilatory response to isocapnic hypoxia in nine healthy male subjects. Lidocaine infusion (serum concentration 3.6 +/- 0.1 micrograms/ml) was associated with a decrease in the shape factor, "A," of the hypoxic ventilatory response in eight of our nine subjects (P less than 0.02). Overall, "A" decreased from 419 +/- 102 1 . min-1 . mmHg before lidocaine to 335 +/- 77 1 . min-1 . mmHg during lidocaine infusion (mean +/- SEM, N = 9). The authors conclude that despite significant intersubject variability, clinically useful serum lidocaine concentrations depress hypoxic ventilatory drive. Patients with carbon dioxide retention, whose resting ventilation depends on hypoxic drive, may be at risk of ventilatory failure when lidocaine is administered for arrhythmia control or regional anesthesia.
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PMID:The effect of lidocaine infusion on the ventilatory response to hypoxia. 650 23

Two female patients revived from fulminant attacks of asthma are described. Ventilatory responses to asphyxia in these patients were 0.70 +/- 0.10 l min-1 % SaO2-1 and 0.64 +/- 0.21 l min-1 % SaO2-1 (mean +/- SEM), respectively. These values were significantly less than the responses of seven normal female subjects (1.54 +/- 0.11 l min-1 % SaO2-1 mean +/- SEM; p less than 0.01). Ventilatory responses to hypercapnia of the two patients were in the low normal range. Dopamine-receptor blockade with prochlorperazine significantly increased the ventilatory response to asphyxia in normal subjects (p less than 0.05 or less for each subject) but did not alter the depressed responses in the asthmatic patients. In one patient, naloxone in a dose of 400 micrograms reversed the decreased ventilatory responsiveness; the response to asphyxia was increased from 0.72 l min-1 % SaO-1 to 1.80 l min-1 % SaO2-1 (p less than 0.01) and the response to hypercapnia was increased from 0.90 l min-1 mmHg-1 to 4.80 l min-1 mmHg-1 (p less than 0.01). Naloxone had no effect in the second asthmatic patient nor in five normal subjects. Defective chemoreceptor responses to chemical stimuli may play a role in sudden death from asthma; endogenous opioids may mediate this disorder of ventilatory control.
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PMID:Ventilatory control in two asthmatics resuscitated from respiratory arrest. 659 13

The effect of metabolic and respiratory acidosis on bilirubin and albumin entry into the brain was studied in 24 awake and unanesthetized rats. Hyperbilirubinemia was established by infusion of unconjugated bilirubin at a rate of 30 mg/kg/h for three hours. After two hours, metabolic acidosis was produced in eight rats by infusion of 0.5 N hydrochloric acid at a rate of 0.02 mL/g/h. This reduced the pH level to 7.03 +/- 0.01 (mean +/- SEM) with a normal value for PCO2. Respiratory acidosis was produced in another group of eight animals who breathed 20% CO2 in a balanced gas mixture for the last hour of the study period. This resulted in a reduction of pH to 7.04 +/- 0.01 with PCO2 of 100.4 +/- 2.3 mm Hg. A third group of eight rats served as controls and were given equal volumes of saline infusion. No increase in brain bilirubin or brain albumin was found in the group with metabolic acidosis, but in the group with respiratory acidosis both bilirubin and albumin concentrations in the brain increased significantly. No significant differences were found between the groups in serum total or apparent unbound bilirubin, albumin, or osmolality. The results indicate that a brief period of acidosis per se does not increase bilirubin entry into the brain, but hypercarbia does so by opening of the blood-brain barrier.
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PMID:Effect of acidosis on bilirubin deposition in rat brain. 670 23

We studied the effects of sleep fragmentation on arousal and ventilatory responses to hyperoxic hypercapnia, isocapnic hypoxia, and chemical stimulation of the larynx during sleep in 5 dogs. Sleep fragmentation was induced by repeatedly arousing the dogs with acoustic stimuli throughout 2 to 3 consecutive nights. Responses to respiratory stimuli were then studied during a subsequent daytime sleep. Arterial O2 saturation was measured with an ear oximeter, and sleep stage was determined by electroencephalographic and behavioral criteria. Hypercapnic and hypoxic ventilatory responses were unimpaired by sleep fragmentation. In contrast, alveolar PCO2 levels at arousal increased after sleep fragmentation, from a mean +/- SEM of 52.2 +/- 1.4 mm Hg to 55.6 +/- 1.5 mm Hg (p < 0.05) during slow-wave sleep, and from 57.9 +/- 1.5 mm Hg to 61.3 +/- 2.2 mm Hg (p < 0.05) during rapid-eye movement sleep. Similarly, arterial O2 saturation at arousal decreased after sleep fragmentation from 80.1 +/- 1.0% to 70.2 +/- 2.7% (p < 0.05) during slow-wave sleep, and from 66.3 +/- 3.6% to < 55% (p < 0.05) during rapid-eye-movement sleep. Arousal responses to laryngeal stimulation were also impaired after sleep fragmentation. We conclude that arousal responses to respiratory stimuli are decreased by sleep fragmentation.
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PMID:Effect of sleep fragmentation on ventilatory and arousal responses of sleeping dogs to respiratory stimuli. 677 83


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