Increase In Ventilation Research Articles

Maturation of baseline breathing and of hypercapnic and hypoxic ventilatory responses in newborn mice.

Breathing during the first postnatal hours has not been examined in mice, the preferred mammalian species for genetic studies. We used whole body plethysmography to measure ventilation (VE), breath duration (T(TOT)), and tidal volume (VT) in mice delivered vaginally (VD) or by cesarean section (CS). In experiment 1, 101 VD and 100 CS pups aged 1, 6, 12, 24, or 48 h were exposed to 8% CO2 or 10% O2 for 90 s. In experiment 2, 31 VD pups aged 1, 12, or 24 h were exposed to 10% O2 for 5 min. Baseline breathing maturation was delayed in CS pups, but VE responses to hypercapnia and hypoxia were not significantly different between VD and CS pups [at postnatal age of 1 h (H1): 48 +/- 44 and 18 +/- 32%, respectively, in VD and CS pups combined]. The VE increase induced by hypoxia was greater at H12 (46 +/- 27%) because of T(TOT) response maturation. At all ages, hypoxic decline was ascribable mainly to a VT decrease, and posthypoxic decline was ascribable to a T(TOT) increase with apneas, suggesting different underlying neuronal mechanisms.

COMPARISON OF TREADMILL MAX VALUES TO RESPONSES PULLING A VEHICLE 400 METERS

The purpose of this study was to examine the oxygen consumption (VO2), ventilation (VE), heart rate (HR) responses to pulling a 1960 kg vehicle 400 meters and compare these to maximum values achieved on a treadmill test (TMmaz). Seven strength trained subjects (male, n = 6, female, n = 1: age 27.8 ± 5.5 yr) volunteered for this study. Oxygen consumption and HR were measured continuously utilizing an Aerosport KB1-C portable analyzer and Polar Heart Rate monitor. Data was recorded every 50 meters. Results (M ± SD) are presented in Table 1. No significant increase in VO2, VE, or HR occurred after the first 100M of the Jeep Pull. These results may have important applications for coaches wishing to optimize pulling distance specific to a given sport. *Values at 50M significantly less (p ± 0.05) than 100, 200, 300, & 400M Percentages of TMmax values in parentheses.Table 1: Descriptive comparison of TMmax values to pulling values

Ventilatory Response to Sustained Hypoxia in Carotid Body Denervated Rats

Hypoxia stimulates ventilation, but when it is sustained, a decline in the ventilatory response is seen. The mechanism responsible for this decline lies within the CNS, but still remains unknown. In this study, we attempted to elucidate the possible role of hypoxia-induced depression of respiratory neurons by comparing the ventilatory response to hypoxia in intact rats and those with denervated carotid bodies. A whole-body plethysmograph was used to measure tidal volume, frequency of breathing and minute ventilation (VE) in awake and anesthetized intact rats and rats after carotid body denervation during exposure to hypoxia (FIO2 0.1). Fifteen-minute hypoxia induced an initial increase of VE in intact rats (to 248 % of control ventilation in awake and to 227 % in anesthetized rats) followed by a consistent decline (to 207 % and 196 % of control VE, respectively). Rats with denervated carotid bodies responded with a smaller increase in VE (to 134 % in awake and 114 % in anesthetized animals), but without a secondary decline (145 % and 129 % of control VE in the 15th min of hypoxia). These results suggest that afferentation from the carotid bodies and/or the substantial increase in ventilation are crucial for the biphasicity of the ventilatory response to sustained hypoxia and that a central hypoxic depression cannot fully explain the secondary decline in VE.

Role of central adenosine in the respiratory and thermoregulatory responses to hypoxia.

No reports are available about the role of central adenosine in the respiratory and thermoregulatory responses to hypoxia in conscious rats. We therefore measured ventilation (VE) and body temperature (Tb) before and after intracerebroventricular injection of saline or aminophylline (adenosine antagonist), followed by a 30-min period of hypoxia exposure. Aminophylline did not change VE or Tb during normoxia; however, during hypoxia, it caused a significant increase in VE, and significantly attenuated hypoxic hypothermia. The present data indicate that central adenosine has an inhibitory effect on hypoxic hyperventilation and partially causes hypoxic hypothermia, suggesting that the ventilatory and metabolic interaction during hypoxia does not involve opposing mechanisms.

Evolution of inspiratory and expiratory muscle pressures during endurance exercise.

We investigated the relationship between minute ventilation (VE) and net respiratory muscle pressure (Pmus) throughout the breathing cycle [Total Pmus = mean Pmus, I (inspiratory) + mean Pmus, E (expiratory)] in six normal subjects performing constant-work heavy exercise (CWHE, at approximately 80% maximum) to exhaustion on a cycle ergometer. Pmus was calculated as the sum of chest wall pressure (elastic + resistive) and pleural pressure, and all mean Pmus variables were averaged over the total breath duration. Pmus, I was also expressed as a fraction of volume-matched, flow-corrected dynamic capacity of the inspiratory muscles (P(cap, I)). VE increased significantly from 3 min to the end of CWHE and was the result of a significantly linear increase in Total Pmus (Delta = 43 +/- 9% from 3 min to end exercise, P < 0.005) in all subjects (r = 0. 81-0.99). Although mean Pmus, I during inspiratory flow increased significantly (Delta = 35 +/- 10%), postinspiratory Pmus, I fell (Delta = -54 +/- 10%) and postexpiratory expiratory activity was negligible or absent throughout CWHE. There was a greater increase in mean Pmus, E (Delta = 168 +/- 48%), which served to increase VE throughout CWHE. In five of six subjects, there were significant linear relationships between VE and mean Pmus, I (r = 0.50-0.97) and mean Pmus, E (r = 0.82-0.93) during CWHE. The subjects generated a wide range of Pmus, I/P(cap, I) values (25-80%), and mean Pmus, I/P(cap, I) increased significantly (Delta = 42 +/- 16%) and in a linear fashion (r = 0.69-0.99) with VE throughout CWHE. The progressive increase in VE during CWHE is due to 1) a linear increase in Total Pmus, 2) a linear increase in inspiratory muscle load, and 3) a progressive fall in postinspiratory inspiratory activity. We conclude that the relationship between respiratory muscle pressure and VE during exercise is linear and not curvilinear.

RESISTIVE UNLOADING IN OLDER MEN AND WOMEN WITH MILD CHRONIC AIRFLOW LIMITATION

1031 We had previously observed an increase in maximal ventilation (VE) with resistive unloading (HeO2 breathing) in healthy elderly subjects. To investigate the effects of resistive unloading in elderly individuals with mild chronic airflow limitation (CAL, FEV1/FVC: 61 ± 4%), we studied ten Elderly (70 ± 3 yr) men and women. These subjects performed graded cycle ergometry to exhaustion, once breathing room air and once breathing a HeO2 gas mixture (79% He, 21% O2). Pulmonary mechanics and PetCO2 were measured during each 1 min increment in work rate. Data were analyzed by paired T-test at rest, ventilatory threshold (VTh), and maximal exercise. VE was significantly (p<0.05) increased at VTh (3.4 ± 4.0 L/min, 12 ± 15%) and maximal exercise (15.2 ± 9.7 L/min, 22 ± 13%) while breathing HeO2. Concomitant to the increase in VE, PetCO2 was decreased at all levels (p<0.01), while total work of breathing against the lung (WOBT) was not different. End expiratory lung volume was decreased at rest, VTh, and maximal exercise (p<0.05), although tidal volume was only increased (p<0.01) during maximal exercise. Despite the significant increase in maximal VE while breathing HeO2, there were no significant differences in maximal work rate, or exercise time between the room air and HeO2 tests. We conclude that VE is increased during HeO2 breathing due to resistive unloading of the airways and the maintenance of the relationship between WOBT and exercise level. Supported by NIA AG-11805

Ventilatory responses to dynamic exercise elicited by intramuscular sensors.

Eight subjects, aged 27.0+/-1.6 yr, performed incremental workload cycling to investigate the contribution of skeletal muscle mechano- and metaboreceptors to ventilatory control during dynamic exercise. Each subject performed four bouts of exercise: exercise with no intervention (CON); exercise with bilateral thigh cuffs inflated to 90 mm Hg (CUFF); exercise with application of lower-body positive pressure (LBPP) to 45 torr (PP); and exercise with 90 mm Hg thigh cuff inflation and 45 torr LBPP (CUFF+PP). Ventilatory responses and pulmonary gas exchange variables were collected breath-by-breath with concomitant measurement of leg intramuscular pressure. Ventilation (VE) was significantly elevated from CON during PP and CUFF+PP at workloads corresponding to > or = 60% CON peak oxygen uptake (VO2peak) and during CUFF at workloads > or = 80% CON VO2peak, P < 0.05. The VO2 at which ventilatory threshold occurred was significantly reduced from CON (2.17+/-0.28 L x min(-1)) to 1.60+/-0.19 L x min(-1), 1.45+/-0.15 L x min(-1), and 1.15+/-0.11 L x min(-1) during CUFF, PP, and CUFF+PP, respectively. The slope of the linear regression describing the VE/CO2 output relationship was increased from CON by approximately 22% during CUFF, 40% during PP, and 41% during CUFF+PP. As intramuscular pressure was significantly elevated immediately upon application of LBPP during PP and CUFF+PP without a concomitant increase in VE, it seems unlikely that LBPP-induced increases in VE can be attributed to activation of the mechanoreflex. These findings suggest that LBPP-induced reductions in perfusion pressure and decreases in venous outflow resulting from inflation of bilateral thigh cuffs may generate a metabolite sensitive intramuscular ventilatory stimulus.

Protein kinase C modulation of ventilatory response to hypoxia in nucleus tractus solitarii of conscious rats.

This study aimed to determine the role of protein kinase C (PKC) in signal transduction mechanisms underlying ventilatory regulation in the nucleus tractus solitarii (NTS). Microinjection of phorbol 12-myristate 13-acetate into the commissural NTS of nine chronically instrumented, unrestrained rats elicited significant cardiorespiratory enhancements that lasted for at least 4 h, whereas administration of vehicle (n = 15) or the inactive phorbol ester 4alpha-phorbol 12,13-didecanoate (n = 7) did not elicit minute ventilation (VE) changes. Peak hypoxic VE responses (10% O2-balance N2) were measured in 19 additional animals after NTS microinjection of bisindolylmaleimide (BIM) I, a selective PKC inhibitor (n = 12), BIM V (inactive analog; n = 7), or vehicle (Con; n = 19). In Con, VE increased from 139 +/- 9 to 285 +/- 26 ml/min in room air and hypoxia, respectively, and similar responses occurred after BIM V. BIM I did not affect room air VE but markedly attenuated hypoxia-induced VE increases (128 +/- 12 to 167 +/- 18 ml/min; P < 0. 02 vs. Con and BIM V). When BIM I was microinjected into the cerebellum (n = 4), cortex (n = 4), or spinal cord (n = 4), VE responses were similar to Con. Western blots of subcellular fractions of dorsocaudal brain stem lysates revealed translocation of PKCalpha, beta, gamma, delta, epsilon, and iota isoenzymes during acute hypoxia, and enhanced overall PKC activity was confirmed in the particulate fraction of dorsocaudal brain stem lysates harvested after acute hypoxia. These studies suggest that, in the adult rat, PKC activation in the NTS mediates essential components of the acute hypoxic ventilatory response.

THE RELATIONSHIP BETWEEN PLASMA K+ AND THE VENTILATORY DRIFT DURING STEADY STATE EXERCISE

238 Recently, potassium has been investigated as a possible metabolite involved in the control of exercise ventilation. Graded and incremental cycle tests using healthy subjects show a strong positive correlation between plasma K+ and ventilation (VE). During steady state exercise, there is an upward drift in ventilation which cannot be accounted for by lactate or expired CO2. The purpose of this study was to examine the relationship between plasma K+ levels and the ventilatory drift during steady state exercise. Participants cycled at 60% VO2 max for 30 min. VO2, VCO2, VE, plasma K+, and plasma lactate were measured each min. There was an 8% increase in both VO2 (P<0.02) and VE (P<0.03), and a 16% increase in K+ (P<0.04) between 6 and 30 min of continuous exercise. VCO2 and lactate remained unchanged. There was a significant correlation between VE and K+ (r =.97) and between VO2 and K+ (r =.97) during steady state exercise. VE and lactate over the same duration were not correlated (r =.47). These results suggest a positive relationship between increases in K+ and ventilation during steady state exercise. Whether K+ is the causative agent of the ventilatory drift, however, remains to be determined.

NMDA receptors mediate peripheral chemoreceptor afferent input in the conscious rat.

N-methyl-D-aspartate (NMDA) glutamate receptors mediate critical components of cardiorespiratory control in anesthetized animals. The role of NMDA receptors in the ventilatory responses to peripheral and central chemoreceptor stimulation was investigated in conscious, freely behaving rats. Minute ventilation (VE) responses to 10% O2, 5% CO2, and increasing intravenous doses of sodium cyanide were measured in intact rats before and after intravenous administration of the NMDA receptor antagonist MK-801 (3 mg/kg). After MK-801, eupcapnic tidal volume (VT) decreased while frequency increased, resulting in a modest reduction in VE. Inspiratory time (TI) decreased, whereas expiratory time remained unchanged. The VE responses to hypercapnia were qualitatively similar in control and MK-801 conditions, with slight reductions in respiratory drive (VT/TI) after MK-801. In contrast, responses to hypoxia were markedly attenuated after MK-801 and were primarily due to reduced frequency changes, whereas VT was unaffected. Sodium cyanide doses associated with significant VE increases were 5 and 50 microg/kg before and after MK-801, respectively. Thus 1-log shift to the right of individual dose-response curves occurred with MK-801. Selective carotid body denervation reduced VE during hypoxia by 70%, and residual hypoxic ventilatory responses were abolished after MK-801. These findings suggest that, in conscious rats, carotid and other peripheral chemoreceptor-mediated hypoxic ventilatory responses are critically dependent on NMDA receptor activation and that NMDA receptor mechanisms are only modestly involved during hypercapnia.

Effectiveness of Controlled and Spontaneous Modes in Nasal Two-Level Positive Pressure Ventilation in Awake and Asleep Normal Subjects

The purpose of the present study was to compare in awake and asleep healthy subjects, under nasal intermittent positive pressure ventilation (nIPPV) with a two-level intermittent positive pressure device (two-level nIPPV), the efficacy of the controlled and spontaneous modes, and of different ventilator settings in increasing effective minute ventilation (VE). Eight healthy subjects were studied. In the controlled mode, inspiratory positive airway pressure (IPAP) was kept at 15 cm H2O, expiratory positive airway pressure (EPAP) at 4 cm H2O, and the inspiratory/expiratory (I/E) time ratio at 1. The respirator frequencies were 17 and 25/min. In the spontaneous mode experiment, IPAP was started at 10 cm H2O and progressively increased to 15 and 20 cm H2O; EPAP was kept at 4 cm H2O. We measured breath by breath the effective tidal volume (VT with respiratory inductive plethysmography), actual respiratory frequency (f), and effective VE. Using the controlled mode, effective VE was significantly higher on nIPPV than during spontaneous unassisted breathing, except in stage 2 nonrapid eye movement sleep at 17/min of frequency; increases in f from 17 to 25/min led to a significant decrease in VT reaching the lungs, during wakefulness and sleep; effective VE was higher at 25 than at 17/min of frequency only during sleep; periodic breathing was scarce and apneas were never observed. Using the spontaneous mode, with respect to awake spontaneous unassisted breathing, two-level nIPPV at 10 and 15 cm H2O of IPAP did not result in any significant increase in effective VE either in wakefulness or in sleep; only IPAP levels of 20 cm H2O resulted in a significant increase in effective VE; during sleep, effective VE was significantly lower than during wakefulness; respiratory rhythm instability (ie, periodic breathing and central apneas) were exceedingly common, and in some subjects extremely frequent, leading to surprisingly large falls in arterial oxygen saturation. It appears that two-level nIPPV should be used in the controlled mode rather than in the spontaneous mode, since it seems easier to increase effective VE with a lower IPAP at a high frequency than at a high pressure using the spontaneous mode. We suggest that the initial respirator settings in the controlled mode should be an f around 20/min, an I/E ratio of 1, 15 cm H2O of IPAP, and EPAP as low as possible.

Nitric oxide inhalation reduces pulmonary tidal volume during exercise in severe chronic heart failure

Multiple mechanisms have been proposed to explain the hyperventilation and the limited exercise capacity in congestive heart failure (CHF) including increased intrapulmonary pressures, total pulmonary resistance, and airway abnormalities. We investigated the hypothesis that inhalation of nitric oxide could influence the maximum exercise capacity and excessive ventilatory response to exercise in CHF. Fifteen patients in CHF (mean age 48 ± 12 years) underwent a control and a nitric oxide inhalation progressive treadmill exercise test with 30 ppm. We determined the maximum oxygen consumptiom (peak VO 2 ), CO 2 production (VCO 2 ), minute pulmonary ventilation (VE), respiratory rate, tidal volume (VT), ventilatory equivalent for oxygen (VE/VO 2 ), ventilatory equivalent for carbon dioxide (VE/VCO 2 ), estimated physiologic dead space/tidal volume ratio (VD/VT), VE/VCO 2 slope, heart rate, systemic arterial pressure, VE/exercise time slope, and VT/exercise time slope during every incremental exercise. Mean maximum exercise values of heart rate, systolic systemic arterial pressure, diastolic systemic arterial pressure, VD/VT, respiratory rate, peak VO 2 , VO 2 /heart rate, VE/CO 2 , and maximum exercise time were unchanged by inhalation of nitric oxide. There was a strong trend toward reduction of VE/VO 2 from 53 ± 15 to 47 ± 12 ( p = 0.051) and in maximum VE from 58 ± 21 to 48 ± 17 L × min -1 ( p = 0.059). Maximum VT decreased from 1639 ± 556 to 1406 ± 479 ml ( p = 0.04). The VE/VCO 2 slope was reduced from 43 ± 12 to 35 ± 8 ( p = 0.018). Two patients had signs of pulmonary congestion during peak exercise or the recovery period with inhalation of nitric oxide. The VE/exercise time slope and VT/exercise time slope during incremental exercise were reduced by inhalation of nitric oxide, demonstrating a statistically significant minor increase in VE and VT. Inhalation of nitric oxide attenuated the excessive increase in VT response to exercise in CHF. The l -arginine-nitric oxide pathway may be involved in mechanisms contributing to hyperventilation during exercise in CHF. (Am Heart J 1997;134:737-44.)

Cardiorespiratory response patterns to afferent stimulation of muscle nerves in the rabbit.

The aim of this study was to test the hypothesis that stimulation of thin fiber muscle afferents is capable of matching the cardiovascular and ventilatory responses. In 46 anesthetized rabbits, the central end of the gastrocnemius nerves was electrically stimulated at 3 [low-frequency stimulation (LFS)] and 100 Hz [high-frequency stimulation (HFS)]. Intensities up to 200 times motor threshold were used. LFS induced a decrease in both mean arterial pressure (-19.9 +/- 2.9%) and systemic vascular resistance (-23.9 +/- 3.2%) an increase in cardiac output (CO) (6.4 +/- 1.7%), stroke volume (7.3 +/- 3.0%) and pulmonary ventilation (VE) (26.7 +/- 2.3%); heart rate and central venous pressure were not changed significantly. HFS induced an increase in mean arterial pressure (11.1 +/- 4.9%), CO (15.8 +/- 5.4%), stroke volume (13.4 +/- 5.4%), and VE but no significant changes in heart rate, systemic vascular resistance and central venous pressure. In both response patterns, arterial and end-tidal CO2 did not change significantly. The patterns of cardiorespiratory responses to both LFS and HFS were characterized by an increase in Co and VE without concomitant decreases in arterial and end-tidal PCO2 (isocapnic hyperpnea).

Cardiovascular and ventilatory response to isocapnic hypoxia at sea level and at 5,050 m.

To assess the effect of chronic hypoxic conditions on ventilatory, heart rate (HR), and blood pressure (BP) responses to acute progressive isocapnic hypoxia, we studied five healthy Caucasian subjects (3 men and 2 women). Each subject performed one rebreathing test at sea level (SL) and two tests at the Pyramid laboratory at Lobuche, Nepal, at the altitude of 5,050 m, 1 day after arrival (HA1) and after 24 days of sojourn (HA2). The effects of progressive isocapnic hypoxia were tested by using a standard rebreathing technique. BP, electrocardiogram, arterial oxygen saturation, airflow and end-tidal CO2 and O2 were recorded. For each subject, the relationships between arterial oxygen saturation and HR, systolic BP and minute ventilation (VE), respectively, were evaluated. At HA1, the majority of subjects showed a significant increase in VE and BP response and a decrease in HR response to progressive isocapnic hypoxia as compared to SL. At HA2, VE and BP responses further increased, whereas the HR response remained similar to that observed at HA1. A significant relationship between hypoxic ventilatory responses and both systolic and diastolic BP responses to progressive hypoxia was found. No significant correlation was found between hypoxic ventilatory and HR responses.

Effects of physical conditioning on endogenous nitric oxide output during exercise

Nitric oxide (NO) has been detected in the expiratory air of normal animals and human subjects. Recent experiments revealed that expiratory NO production rises during exercise and correlates well with O2 consumption (VO2) and heart rate. Whether physical conditioning influences expiratory NO output production remains unclear. In this study, NO concentration in expired gas was measured in 18 healthy male volunteers subdivided into three groups (sedentary, intermediate, and athletic) on the basis of the subjects' state of physical conditioning. Measurements were taken at rest and during two steady-state exercise bouts on a bicycle ergometer designed to elicit VO2 of 1 and 2 l/min with the athletes performing an additional bout at VO2 of 4 l/min. In the sedentary and intermediate groups, expired NO concentrations declined significantly with increasing VO2. In contrast, expired NO levels declined only slightly with increasing VO2 in the athletes. At a VO2 of 2 l/min, expired NO concentrations were significantly higher in the athletes compared with values in the other groups. When correlated with minute ventilation (VE), expired NO concentrations declined linearly with the increase in VE in sedentary and intermediate groups but not in the athletes. Only the athletes had a significant linear increase in NO output (expired NO x VE) with increasing VO2 (P < 0.001). These results support the notion that physical conditioning increases expiratory NO output during exercise. We speculate that the rise in expiratory NO output in the athletes might be due to increased vascular and/or epithelial production of NO. Enhanced vascular NO production may be the result of increased shear stress and/or upregulation of endothelial NO synthase gene expression.

A field study of the ventilatory response to ambient temperature and pressure in sport diving.

This study reports on the relationship between minute ventilation (VE) and environmental variables of temperature (T) and pressure (P) during open water diving. The author conducted a total of 38 dives involving either a light (20 dives) or a moderate (18 dives) level of physical activity. Within each of these groups, P and T taken together accounted for about two thirds of the variance in the VE data. A very significant increase in VE was observed as T decreased (1 < T(degrees C) < 22), and the magnitude of this increase at a given pressure level was similar in the 'light' and the 'moderate' data sets. A second order observation, particularly notable at lower temperature, was the decrease in VE with increasing pressure under conditions of light work. Empirical functions of the from VE = A+B/P n[1 + exp(T - 8)/10], where A, B, and n are adjustable variables, could accommodate both data sets over the whole range of T and P. These results are the first obtained under actual diving conditions to provide evidence for interactions between P, T, and VE. Understanding the physiological mechanisms by which these interactions occur would assist in appreciation of the limitations imposed on scuba divers by the environmental conditions as they affect their ventilatory responses.

Peripheral Chemoreceptor Function in Children With Myelomeningocele and Arnold-Chiari Malformation Type 2

Blunted rebreathing hyperoxic hypercapnic ventilatory and arousal responses are frequent in older children with myelomeningocele (MMC) and Arnold-Chiari malformation type 2 (ACM). In contrast, isocapnic hypoxic rebreathing ventilatory responses are only occasionally affected. Thus, regions mediating the hypoxic ventilatory response appear usually preserved in children with MMC and ACM. Peripheral chemoreceptor function (PCR), however, has not been critically assessed in these children. To study this, PCR was measured in ten children and adolescents with MMC and ACM with normal alveolar ventilation during wakefulness, and in ten sex- and age-matched controls by measuring the ventilatory responses induced by 100% O2 breathing, five tidal breaths of 100% N2, and vital capacity breaths of 15% CO2 in O2. In general, tidal breathing of 100% O2 resulted in smaller decreases in minute ventilation (VE) responses in patients with MMC, although absent VE responses to hyperoxia were found in four patients. Vital capacity breaths of 15% CO2 elicited similar increases in VE in five patients and in ten controls, but no changes in VE were found in the remaining five patients (p < 0.02). Acute hypoxia induced by N2 tidal breathing resulted in significant linear regression correlations between VE and SpO2 in five patients with MMC, while absent responses were measured in those same five patients with absent hypercapnic responses. We conclude that PCR, when assessed by acute hypoxia, hyperoxia, or hypercapnia is abnormal in some children with MMC and ACM, particularly in those demonstrating abnormal ventilation during sleep. We postulate that the large interindividual variability of PCR is dependent on the severity of brainstem involvement of PCR afferents or central respiratory integration sites.

Ventilatory and metabolic responses to hypoxia during moderate hypothermia in anesthetized rats

In resting euthermic mammals, hypoxia elicits a hyperventilation that results from a combination of hyperpnea and hypometabolism. Often accompanying the hypoxia-induced hypometabolism is a drop in body temperature. To separate the synergic effects of hypothermia per se from the direct effects of hypoxia on metabolic rate, ventilation (VE), and O2 consumption (VO2) were measured in anesthetized rats fitted with abdominal heat exchangers and maintained at either normothermic (37.5 degrees C) or hypothermic (35 degrees C) body temperatures while exposed to either normoxia or hypoxia (7% O2). Hypothermia induced parallel decreases in VE and VO2, thereby maintaining VE/VO2. Hypoxia resulted in a hyperventilation achieved with the same relative decrease in VO2 and increase in VE in both normothermic and hypothermic rats. The results suggest that 1) the changes in metabolic rate and VE during hypothermia reflect a direct effect of cold and, 2) because of similar levels of hypoxic hyperventilation in the hypothermic and normothermic rats, relative to metabolic rate, respiratory gain has not been depressed in hypothermic rats.

Ventilatory and Pulmonary Vascular Responses to Acute Hypoxia Are Nonuniform in Healthy Man

The present study was undertaken to examine the pulmonary vascular and ventilatory responses to acute hypoxia in healthy individuals. Pulmonary hemodynamics and minute ventilation (VE) were serially measured during inhalation of 13% O2 for 15 min. There was a wide variability in the pulmonary vascular response to acute hypoxia, and a significant negative correlation between the initial increase in VE after the start of hypoxia (delta VE) and the percent increase in mean pulmonary arterial pressure (r = -0.646; p < 0.01). The fall in arterial oxygen tension significantly decreased in response to an increase in delta VE. These results support the view that a blunted ventilatory response to acute hypoxic stimulation enhances alveolar hypoxia, thereby favoring the constriction of pulmonary vasculature. Thus, our results suggest that the ventilatory response to acute hypoxia plays a significant role in the pulmonary vascular response to acute hypoxia.

The Effects of Incline on Cardiopulmonary Function during Exercise in the Horse.

We investigated the effects of incline on cardiopulmonary function in five trained 2-year-old Thoroughbred horses during exercise on a high-speed treadmill. The horses began exercise at 1.5 m/s for 2 min followed by 1 min step increments at 4.0, 7.0, 8.0, 9.2, and 10.4 m/s. Each horse performed the exercise test on separate days with at least 2 days interval at four different inclines (0, 3, 6 and 10%). The sequence of exercise test was randomized. The major findings were: 1) Oxygen uptake (Vo2), carbon dioxide production (Vco2), minute ventilation (VE), tidal volume (VT), heart rate (HR), cardiac output (Qt), and % O2 extraction increased linearly with speed and incline, however the regression estimates of the change in Vo2/change in speed (ΔVo2/ΔSp) increased with increasing incline. 2) VE increased linearly with speed and was a function of increased VT and respiratory frequency (f), however the linear increase in VE with incline was solely due to increased VT as f was unchanged. 3) The VE/Vo2 slope for 0% incline was greater than the slope 3%, 6%, 10% incline. 4) The increase in arterio-mixed venous oxygen content difference (Ca-vDO2) with speed and incline was mainly due to the decrease in CvO2, whereas CaO2 increased only slightly with incline and speed. 5) The increased Qt with speed and incline was due to increases in HR, as stroke volume was unchanged with speed and incline.