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Ventilatory and heart rate responses to hypercapnia and hypoxia were measured in the following three groups: group I, controls (n equals 15); group II, parents of threatened sudden infant death syndrome (SIDS) infants (n equals 10); and group III, parents of SIDS infants (n equals 17). We found significantly reduced heart rate responses to carbon dioxide and hypoxia in group II (1.4 plus or minus 1.9 percent and 16.0 plus or minus 4.0 percent; mean plus or minus SEM) compared with controls (7.1 plus or minus 1.4 percent and 26 plus or minus 2.4 percent; P less than .025). Ventilatory responses to hypoxia in groups II and III were not significantly different from controls. Two group II mothers had a greatly reduce ventilatory response to carbon dioxide. Four other parents in group II had abnormally low heart rate responses to hypoxia or carbon dioxide. We concluded that parents of threatened SIDS infants had reduced heart rate responses to carbon dioxide and hypoxia and may have reduced ventilatory responses to carbon dioxide.
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PMID:Attenuated responses to CO2 and hypoxia in parents of threatened sudden infant death syndrome infants. 678 12

Ventilatory, airway occlusion pressure, arterial blood pressure and heart rate responses to isocapnic progressive hypoxia and to hypercapnia in high oxygen, both induced by a rebreathing method, were measured in 20 hypertensive male subjects aged 20 to 21 years with a diastolic blood pressure of 13.1 KPa +/- 0.34 SD (98 mmHg +/- 2.6 SD) and in 20 age-matched normotensive male subjects. Ventilatory, airway occlusion pressure and blood pressure response to hypoxia was significantly greater in the hypertensive subjects. Hypoxic ventilatory drive measured as the parameter A denoting the shape of the V1-O2 curve was 28.8 +/- 2.7 SEM (range 7.0 to 44.2) in the normotensive group and 116.1 +/- 10.5 SEM (range: 71.6 to 234.77) in the hypertensive group, the difference being highly significant (P less than 0.001). The magnitude of respiratory sinus arrhythmia (RSA) recorded during progressive hypoxia and plotted against either PA. O2 or VI values was significantly greater in the hypertensive group. The difference in ventilatory and circulatory responses to hyperoxic hypercapnia between the two groups of subjects was not significant. There was a significant correlation between the responses to hypoxia and hypercapnia in the normotensive subjects (r = 0.56, t = 2.861, P less than 0.01) but no correlation in the hypertensive subjects (r = 0.07). It is concluded that dissociation of the responsiveness of the peripheral and central chemosensitivity, the former being significantly increased and predominant, occurs in early, mild hypertension.
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PMID:Increased sensitivity of the arterial chemoreceptor drive in young men with mild hypertension. 680 56

Nasal obstruction is associated with abnormal breathing during sleep. To investigate this we measured ventilation and isocapnic hypoxic and rebreathing hypercapnic ventilatory responses in 9 awake normal men, with and without artificial nasal occlusion. Resting breathing frequency was lower (P less than 0.05) with mouth (12.5 +/- 1.0 [SEM]) than with nose (15.1 +/- 1.3 b/min) breathing, due to prolongation (P less than 0.05) of expiratory time with mouth breathing (mouth 3.25 +/- 0.35, nasal breathing 2.41 +/- 0.37 sec). Resting tidal volume was similar for both routes, thus minute ventilation was lower (P less than 0.01) mouth breathing (8.43 +/- 0.44) compared with nose breathing (9.37 +/- 0.47 L/min). Ventilatory responses were greater with mouth than nose breathing both for hypercapnia (mouth 2.29 +/- 0.21, nose 1.58 +/- 0.18 L/min/mm Hg CO2; P less than 0.01) and for hypoxia (mouth 1.08 +/-0.16, nose 0.91 +/- 0.21 L/min/% SaO2; P = 0.10). In 6 subjects measurements were repeated before and after upper airway lignocaine anaesthesia, which abolished the differences in respiratory timing and drive between the breathing routes. It is suggested that there may be upper airway flow receptors which influence respiratory timing.
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PMID:Effect of breathing route on ventilation and ventilatory drive. 684 56

During rapid eye movement (REM) sleep, hypoxia and hypercapnia occur in conjunction with hypoventilation. Although the hypoxic ventilatory response has previously been shown to be reduced in REM sleep, the hypercapnic ventilatory response (HCVR) has not been studied during REM sleep in adult humans. We therefore measured the ventilatory response to hypercapnia in 12 sleeping adults using a modified rebreathing method. The HCVR was significantly reduced in all stages of sleep compared with that during wakefulness (1.60 +/- 0.19 SEM L/min/mmHg CO2), falling to less than half the waking HCVR during non-REM sleep (0.75 +/- 0.08 L/min/mmHg CO2), with a further significant drop during REM sleep when HCVR was less than a third of that during wakefulness (0.45 +/- 0.10 L/min/mmHg CO2). The decreased ventilatory responses to hypercapnia and hypoxia in REM sleep help explain REM-related hypoxemic episodes.
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PMID:Hypercapnic ventilatory response in sleeping adults. 714 40

To investigate the role of endorphins in central respiratory control, the effect of naloxone, a specific opiate antagonist, on resting ventilation and ventilatory control was investigated in a randomised double-blind, placebo-controlled study of normal subjects and patients with chronic airways obstruction and mild hypercapnia due to longstanding chronic bronchitis. In 13 normal subjects the ventilatory response to hypercapnia increased after an intravenous injection of naloxone (0.1 mg/kg), ventilation (VE) at a PCO2 of 8.5 kPa increasing from 55.6 +/- SEM 6.2 to 75.9 +/- 8.21 min-1 (p less than 0.001) and the delta VE/delta PCO2 slope increasing from 28.6 +/- 4.4 to 34.2 +/- 4.21 min-1 kPa-1 (p less than 0.05). There was no significant change after placebo (saline) injection. Naloxone had no effect on resting ventilation or on the ventilatory response to hypoxia in normal subjects. In all six patients naloxone significantly (p less than 0.02) increased mouth occlusion pressure (P 0.1) responses to hypercapnia. Although there was no change in resting respiratory frequency or tidal volume patients showed a significant (p less than 0.01) decrease in inspiratory timing (Ti/Ttot) and increase in mean inspiratory flow (VT/Ti) after naloxone. These results indicate that endorphins have a modulatory role in the central respiratory response to hypercapnia in both normal subjects and patients with airways obstruction. In addition, they have an inhibitory effect on the control of tidal breathing in patients with chronic bronchitis.
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PMID:Endogenous opiates and the control of breathing in normal subjects and patients with chronic airflow obstruction. 716 1

Arousal responses (AR) to hypercarbia and to hypoxia were ascertained in 25 N-M SIDS infants and 21 control infants in whom ventilatory responses to hypercarbia and hypoxia were also measured. Although the frequency of a positive AR to hypercarbia was not significantly less in the N-M SIDS compared to control group, the overall pattern was a generally absent AR in the lowest hypercarbic ventilatory response slope group progressing to a generally positive AR in the highest hypercarbic response slope group. Among the 25 infants having a positive hypercarbic AR, the Mean (+/- SEM) PACO2 at which arousal occurred was 48.5 +/- 1.6 in N-M SIDS versus 42 +/- 1.2 mmHg in control infants (p less than .001). The overall pattern for hypoxic AR was also a generally absent AR in the lowest hypoxic ventilatory response slope group progressing to a generally positive AR in the highest response slope group. Although the PAO2 level at which an AR occurred did not differ in the two groups, a positive hypoxic AR occurred in 76% of the control versus only 29% of the N-M SIDS group (p less than .01). In summary, infants with a clinical N-M SIDS history and diminished ventilatory response slopes have as a group a concomitant abnormality in hypercarbic and/or hypoxic arousal.
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PMID:Abnormal hypercarbic and hypoxic sleep arousal responses in Near-Miss SIDS infants. 730 67

The resistance of the larynx to airflow was measured during hypercapnia, hypoxemia, and stimulation of peripheral chemoreceptors by sodium cyanide and phenyl diguanide in 15 dogs anesthetized with alpha-chloralose (80 mg/kg). Laryngeal airway resistance (R1x) was obtained by measuring the pressure difference between the subglottic region and the mouth while a constant flow of humidified air was passed through the larynx. During spontaneous respiration, R1x varies with the phase of the respiratory cycle: R1x is high during expiration (mean +/- SEM = 0.79 +/- 0.19 cm H2O/L/sec) and falls just before inspiration (0.49 +/- 0.14 cm H2O/L/sec) and remains low until the end of inspiration. Hypercapnia, hypoxemia, and chemoreceptor stimulation each stimulated respiration and simultaneously decreased R1x during both inspiration and expiration. Chemoreceptor stimulation with phenyl diguanide (100 microgram/kg) and sodium cyanide (100 microgram/kg) produced similar decreases in R1x whether injected into the right atrium or left ventricle, indicating that these agents are not stimulating pulmonary receptors. The decrease in R1x during stimulation of chemoreceptors will decrease the work of ventilation. This study suggests that the control of ventilation involves the active regulation of the resistance of the laryngeal airway.
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PMID:Laryngeal regulation of airway resistance. I. Chemoreceptor reflexes. 741 65

Chronic metabolic acidosis typically results in hypercalciuria and negative calcium balance. The impact of chronic respiratory acidosis on calcium metabolism has been less well studied. To address this issue, metabolic balance and static bone histomorphometric data were obtained during a 14-day exposure of rats to 10% CO2 (blood pH 7.33, PaCO2 83 mm Hg) and were compared with pair-fed controls. All rats were fed a 0.8% calcium diet. Urinary calcium excretion (mg/period, mean +/- SEM) was increased during both week 1 and week 2 (16 +/- 3 vs 9 +/- 1 and 16 +/- 2 vs 9 +/- 1, CO2 group vs controls, respectively [p < 0.05]). Net intestinal calcium absorption (intake minus fecal excretion) was increased throughout the period of hypercapnia (week 1, 213 +/- 19 mg vs 135 +/- 15 mg; week 2, 135 +/- 16 mg vs 43 +/- 14 mg; and cumulatively, 344 +/- 27 mg vs 178 +/- 20 mg, CO2 group vs controls [p < 0.01]). As a consequence of the marked increment in intestinal calcium absorption during hypercapnia, mean net calcium balance was more positive than that of controls throughout the study (week 1, 197 +/- 18 mg vs 126 +/- 15 mg; week 2, 120 +/- 15 mg vs 34 +/- 15 mg; and cumulatively, 317 +/- 25 mg vs 159 +/- 20 mg, CO2 group vs controls, respectively [p < 0.01]). There were no significant differences in calcium intake, plasma total calcium, immunoreactive parathyroid hormone, 25-hydroxyvitamin D, or creatinine clearance between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of chronic respiratory acidosis on calcium metabolism in the rat. 760 39

We measured regional cerebral blood flow (rCBF) in young and old Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats by a minimally invasive microsphere technique. Blood flows to the cerebrum, diencephalon, mesencephalon, cerebellum and pons-medulla during normocapnia were determined. To test the ability of the vessels to dilate, rCBF was also measured during hypercapnia. Reactivity to CO2 was calculated as delta rCBF/delta paCO2. In the old SHR, blood flow to the pons-medulla (88 +/- 8 ml/min/100 g, mean +/- SEM) was markedly lower than that in the young SHR (107 +/- 4 ml/min/100 g, p < 0.05), whereas the difference of those values in the old and young WKY rats was slight (0.05 < p < 0.1). There were no differences in the values of blood flow to the cerebrum, diencephalon, mesencephalon or cerebellum between the young and old rats in both species. Cerebrovascular CO2 reactivity was markedly impaired in the old SHR (p < 0.05) compared to that in the young SHR, but the difference in reactivity in the WKY rats was not significant. The results indicate that blood flow to the pons-medulla is reduced in association with age, particularly in the hypertensive animals, and that the ability of the cerebral vessels to dilate is impaired homogeneously by the combination of chronic hypertension and aging.
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PMID:Effects of aging and chronic hypertension on cerebral blood flow and cerebrovascular CO2 reactivity in the rat. 773 29

L-Glutamate was microinjected into the nucleus tractus solitarii (NTS) in anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, and spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres. Unilateral chemical stimulation of the NTS (n = 13) significantly decreased SCBF in the cervical cord from 43 +/- 6 (mean +/- SEM) to 28 +/- 4 (P < 0.05), in the thoracic cord from 35 +/- 3 to 24 +/- 4 (P < 0.01), and in the lumbar cord from 49 +/- 3 to 40 +/- 3 ml min-1 (100 g)-1 (P < 0.05). The decrease in SCBF was not due to the decrease in arterial blood pressure (ABP) because the SCBF during the chemical stimulation of the NTS was significantly smaller (P < 0.05) than the SCBF during controlled hemorrhagic hypotension (n = 11). Chemical stimulation of the NTS did not affect the reactivity of the spinal cord vessels to hypercapnia (n = 5). Microinjection of the vehicle solution into the NTS had no effects on spinal cord circulation (n = 9). These results suggest that the cell bodies within the NTS may play a role in the control of spinal cord circulation.
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PMID:Chemical stimulation of the nucleus tractus solitarii decreases spinal cord blood flow in anesthetized rats. 774 99


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