Cardiorespiratory responses to glutamatergic antagonists in the caudal ventrolateral medulla of rats.

The role of caudal ventrolateral medullary (CVLM) depressor neurons in influencing arterial pressure and ventilation as well as the baroreflex control of arterial pressure was investigated, and the part played by excitatory N-methyl-D-aspartate (NMDA) and non-NMDA receptors in mediating the responses was determined. In urethane-anesthetized, spontaneously breathing rats unilateral microinjections into the caudal depressor area of the broad-band glutamatergic antagonist kynurenic acid (KYN, 5 nmol or 1.58 nmol), or NMDA antagonist 2-amino-5-phosphonovaleric acid (2-APV, 2.7 nmol), or the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 0.257 nmol) caused a respiratory arrest within 4 min and the animals had to be artificially ventilated. Respiratory frequency increased on injecting KYN and CNQX while it did not change significantly with 2-APV. Apnea resulted from progressive decrease in tidal volume. During the apnea ventilation with 5% CO2 did not revive breathing. Mean arterial pressure (MAP) increased significantly with KYN and 2-APV injections but not with CNQX. The baroreflex decrease of MAP, elicited by left or right aortic depressor nerve stimulation, was significantly reduced or abolished after bilateral microinjections of all 3 antagonists. Ventilation as well as the baroreflex usually recovered after 1-1.5 h. Microinjections of the same doses of antagonists into the facial nucleus, as well as application of KYN (25 nmol) to the ventral medullary surface above the hypoglossal rootlets, had no significant effect. The results support previous findings that the CVLM neurons of the rat inhibit sympathetic neurons providing the vasomotor tone, and that an intact CVLM is obligatory for mediating the baroreflex decrease of arterial pressure. The results also indicate that: (1) the CVLM is essential for sustaining ventilation in the rat; (2) only NMDA receptors are involved in maintaining baseline blood pressure while both NMDA and non-NMDA receptors mediate the baroreceptor depressor reflex; and (3) both NMDA and non-NMDA receptor activation is necessary to sustain ventilation.

Adaptive control is enhanced by background estimation.

The automated control of physiological variables must often contend with an unknown and time-varying background (i.e., the output level corresponding to no input). To allow for simultaneous real-time identification of background as well as the parameters of an autoregressive moving average model with exogenous inputs (ARMAX model) during adaptive control, a "floating identifier" (FI) approach was developed which may be used with most recursive identification algorithms. This method separates input and output data into low- and high-frequency components. The high-frequency components are used to identify the ARMAX model parameters and the low-frequency components to identify background. This approach was evaluated in computer simulations and animal experiments comparing an adaptive controller coupled to the FI with the same controller coupled to two other standard least squares identifiers. In the animal experiments, sodium nitroprusside was used to control mean arterial pressure of anesthetized dogs in the presence of background changes. Results showed that with the FI, the controller performed satisfactorily, while with the other identifiers, it sometimes failed. It is concluded that the FI approach is useful when applying ARMAX-based adaptive controllers to systems in which a change in background is likely.

Cardiovascular and respiratory responses to slow ramp carotid sinus pressures in the dog.

The respiratory and mean arterial pressure (MAP) responses to slow ramp pressure stimulation of carotid baroreceptors were compared in pentobarbital-anesthetized vagotomized dogs breathing 100% O2. Carotid sinus pressure (CSP) was raised from 50 (control) to 220 mmHg and then returned to control as linear ramps (+/- 1 mmHg/s) in isolated sinuses. MAP, heart rate (HR), ventilation (VE), frequency (f), and tidal volume (VT) were expressed as percent of control. The maximum difference between responses to positive and negative ramps at a given CSP (MAX) and the average difference (AVG) served as indicators of the hysteresis for each response. In 27 dogs MAP changed monotonically with varying CSP with insignificant (P = 0.27, MAX) or barely significant (P = 0.03, AVG) hysteresis, monotonic function being one that is continuously nondecreasing or continuously nonincreasing. Similar responses were obtained for HR. VE decreased as CSP increased, but the change was not monotonic. During negative ramp, VE increased back to control with an overshoot. Hysteresis for VE was pronounced (P less than 0.0001, both measures). The VE response was primarily determined by f; VT increased with CSP. To eliminate secondary respiratory effects due to alterations in MAP, in seven dogs similar experiments were performed after ganglionic blockade with hexamethonium. Hysteresis in VE and f persisted. To assess the role of changing arterial PCO2 (PaCO2) on VE, the CSP was held constant (after a ramp rise) at 140, 150, or 180 mmHg before reducing it at -1 mmHg/s to 50 mmHg; however, a significant hysteresis in VE was still observed. Further experiments, to eliminate secondary reflexes due to altered PaCO2, were performed in seven dogs after ganglionic blockade and paralysis with Flaxedil, with phrenic nerve activity as an indicator of ("neural") respiration. The hysteresis in VE and f were no longer significant. In summary, the results indicate that 1) slow ramp carotid baroreceptor stimulation elicits both VE and cardiovascular responses, the VE response showing a dramatically higher hysteresis than the cardiovascular responses; 2) the ventilatory hysteresis is partially explained by the secondary changes in PaCO2 and perhaps by cardiovascular variables; and 3) the central processing of the baroventilatory reflex appears to be rate sensitive at a slower rate of pressure change than that which causes rate sensitivity in the baropressure reflex.

Species dependence of baroreceptor effects on ventilation in the cat and the dog.

Reflex respiratory responses to brief carotid baroreceptor stimuli in vagotomized pentobarbital-anesthetized cats were characterized and compared with those reported previously for chloralose-anesthetized dogs. To eliminate effects due to the anesthetic choice, dogs were reexamined under pentobarbital. Stimuli were applied to the isolated carotid sinus (CS) of both animals within a single respiratory phase. The stimuli were either steps triggered after one of four delays (5, 25, 50, and 75% of the control phase duration) and terminated at the end of the phase or pulses lasting 300-500 ms. In cats, 80-mmHg steps during inspiration shortened inspiratory duration by 23.2*, 25.0*, 20.4*, and 4.1% (*P less than 0.01) at the above four delays, respectively; inspired volume decreased by 21.4*, 18.0*, 8.0*, and 2.2%. Steps during expiration lengthened expiration by 38.4*, 37.1*, 21.9*, and 3.4%; expired volume changed less than 4%. Qualitatively, similar responses were obtained with steps 40 mmHg in amplitude. In dogs, 40-mmHg stimuli lengthened both inspiration (by 12.8*, 8.9*, -1.2, and -2.5%) and expiration (by 75.2*, 57.9*, 54.0*, and 61.4*%) but tidal volume did not change. Similar differences were observed when pulses were used. Selective baroreceptor denervation in the cat and occipital arterial occlusion in the dog confirmed that the responses were not chemoreceptor mediated. We conclude that although CS baroreceptor activity inhibits ventilation in both cats and dogs, the pattern of the responses is strongly species dependent.

Chemoreceptor stimulation on sympathetic activity: dependence on respiratory phase.

Experiments were performed on chloralose-anesthetized, vagotomized, paralyzed, and artificially ventilated cats breathing 100% O2. Peripheral chemoreceptors were stimulated by rapid injections of CO2-saturated NaHCO3 in different phases of the respiratory cycle. Responses of cardiac and renal sympathetic nerves were computed by digital integration. Spontaneous sympathetic activity was consistently modulated by respiration, the modulation being greater for cardiac than for renal nerves. Cardiac nerve responses to peripheral chemoreceptor stimulation depended on the respiratory phase for at least one experimental condition in four of seven animals: the responses were largest during late inspiration and smallest (or absent) during postinspiration and early expiration. Renal nerve responses depended on respiratory phase in only two of eight animals. An average end-tidal CO2 concentration increase from 4.6 +/- 0.8% (SD) to 6.7 +/- 0.9% enhanced the respiratory modulation of spontaneous activity but reduced the responses to peripheral chemoreceptor stimulation. The results indicate that the respiratory modulation of chemoreceptor-induced sympathetic responses was less prominent than the modulation of spontaneous activity. It is hypothesized that the phase dependence of the responses is caused by the spontaneously occurring expiratory diminution of sympathetic activity rather than by an inherent gating of the chemoreceptor reflex.

Tonic and baroreflex effects on arterial pressure and ventilation of pentobarbital and nicotine on the rat ventral medullary surface.

Unilateral aortic depressor nerve stimulation caused depression of arterial pressure (baropressure reflex) and ventilation (baro-ventilatory reflex) in urethane-anesthetized, spontaneously breathing Sprague-Dawley rats. Application of sodium pentobarbital to the ventral medullary surface (VMS) depressed baseline arterial pressure and ventilation, and attenuated the baro-pressure reflex, but not the baro-ventilatory reflex. Application of nicotine on the VMS decreased baseline arterial pressure and increased ventilation, but left both baro-pressure and baro-ventilatory reflexes unaltered. The results suggest that some of the structures that affect vasomotor tone may not be involved in the baroreflex inhibition of arterial pressure. Additionally, neither the neural structures near the VMS which modulate CO2 control of ventilation, nor those that affect tonic control of vasomotor tone are likely to be significantly involved in the baro-ventilatory reflex.

Effects of antihistamines and local anesthetics on excess tachycardia in conscious dogs.

Atropine produces cardioacceleration in conscious dogs partly by reversing the pre-existing parasympathetic cardioinhibition and partly by inducing "excess tachycardia" (ET). Because ET occurs independently of adrenergic mechanisms, the present study sought to determine whether ET is generated by a positive chronotropic action of endogenous histamine on pacemaker cell H1 receptors. ET was antagonized in conscious dogs by the H1-receptor antagonists pyrilamine, diphenhydramine, chlorpheniramine and promethazine (1-5 mg/kg i.v.), but not the H2-receptor antagonist cimetidine (2-10 mg/kg i.v.). Pyrilamine (0.1 mg/kg i.v.), but not cimetidine (4 mg/kg i.v.), also eliminated a histamine tachycardia (31 +/- 4.1 beats/min) produced by injecting histamine (22 +/- 14.2 micrograms) into the sinus node artery after pharmacological autonomic blockade. The 30-fold greater dose of pyrilamine required to antagonize ET than histamine tachycardia suggests a nonantihistaminic, and possibly a local anesthetic mechanism of action on ET. Indeed, lidocaine, procaine, propranolol and pyrilamine antagonized ET in doses corresponding to the known relative local anesthetic potencies of these agents. The same doses of pyrilamine, lidocaine and procaine had significantly less effects on a comparable beta adrenergic tachycardia produced by intravenous isoproterenol infusion (0.1-0.5 micrograms/kg/min i.v.) after hexamethonium (10 mg/kg i.v.). The results indicate that H1-receptor blockers antagonize ET because of their local anesthetic effects and not their antihistaminic properties. The results also suggest that the ionic pacemaker mechanisms generating ET and beta adrenergic tachycardia are different.

Respiratory effects of brief baroreceptor stimuli in the anesthetized dog.

To quantify the immediate isocapnic respiratory response to baroreceptor stimulation, pressure in the isolated externally perfused carotid sinuses (CS) of 24 vagotomized alpha-chloralose-anesthetized dogs was increased selectively during either inspiration or expiration as a step (from time of onset to end of respiratory phase) or a pulse (500 ms). The rise time (150 ms), base-line pressure (80 mmHg), and stimulus magnitude (40 mmHg) were similar for the two stimuli. The time of stimulus onset (delay), expressed as a percent of control time of inspiration (TI) or expiration (TE), was varied. TI, TE, and tidal volume (VT) were expressed as percent changes from control. Stimuli delivered early in inspiration lengthened TI [23.5 +/- 6.4% (SE) for step and 11.7 +/- 6.3% for pulse stimuli at 5% delay] more effectively than late stimuli. VT was essentially unaltered. In contrast, step stimuli delivered during expiration caused a lengthening of TE (32.7 +/- 6.3% at 5% delay) that did not depend on the delay (up to 75%). Very late (85%) pulse stimuli lengthened TE (15.2 +/- 5.7%) more effectively than early stimuli. For both stimuli, the expiratory VT was unaltered. When the responses are compared before and after separation of the blood supply of the carotid bodies from the CS region and when they are compared before and after inhibition of reflex systemic hypotension by ganglionic blockade, the observed responses were shown to be due solely to CS baroreceptor stimulation and not to alterations in carotid body blood flow or reflex changes in systemic cardiovascular variables.

Effectiveness of sodium nitroprusside as a function of total peripheral resistance in the anesthetized dog.

To determine the influence of background vasomotor tone on the effectiveness of sodium nitroprusside in decreasing total peripheral resistance, experiments were performed on 12 open-chest dogs under halothane anesthesia. In the first experiment, the vasomotor condition of six dogs was changed by altering the background infusion rate of phenylephrine (0,40, and 0 microgram/min). Increasing background phenylephrine infusion from 0 to 40 micrograms/min significantly enhanced the effectiveness of nitroprusside in decreasing total peripheral resistance. In contrast, the effectiveness of nitroprusside in decreasing arterial pressure was not altered significantly. In a second experiment on six other dogs, phenylephrine was infused continuously at 40 micrograms/min, and the vasomotor condition was changed by the infusion of phentolamine (0, 60-100, 0 microgram/min). Phentolamine significantly diminished the effectiveness of nitroprusside in decreasing peripheral resistance. In contrast, the effectiveness of nitroprusside in decreasing arterial pressure was not altered significantly. Stepwise linear regression analysis indicated that the background peripheral resistance was the hemodynamic variable that could account partially for the changes in nitroprusside effectiveness. Increasing background total peripheral resistance significantly enhanced the effectiveness of nitroprusside in decreasing total peripheral resistance.

The self-tuning controller: comparison with human performance in the control of arterial pressure.

A self-tuning controller was implemented for the automated infusion of sodium nitroprusside to lower mean arterial pressure in anesthetized dogs. The system incorporated a recursive least-squares parameter identifier and a modified minimum-variance controller. The onset delay was estimated on-line, the performance criterion included the cost of control, and requested step-changes were automatically translated into five successive smaller steps to reduce overshoot. The performance of the system in lowering mean arterial pressure was quantitatively compared with that of a well-trained anesthesiologist. In 10 runs in four animals, the automated system performed as well as the physician who devoted 100% of his attention to the task. Since the stability of the self-tuning controller cannot be guaranteed, such a system should be operated only in the presence of appropriate supervisory algorithms.

Excess tachycardia: heart rate after antimuscarinic agents in conscious dogs.

In conscious dogs the heart rate after atropine is higher than after bilateral vagotomy; we have termed the additional heart rate with atropine "excess tachycardia" (ET). In six dogs the cervical vagosympathetic trunks were exteriorized in skin tubes, and arterial and venous catheters were chronically implanted. Atropine sulfate (0.1 mg/kg iv) injected during cold blockade of the vagi increased the heart rate by only 6 +/- 4 (SE) beats/min (NS) but rewarming the vagi in five of the six dogs after atropine resulted in an additional heart rate increase (ET) of 26 +/- 6 beats/min (P less than 0.005). The ET (41 +/- 11 beats/min) tended to be larger when the animals were pretreated with 1 mg/kg propranolol (P = 0.09). Similar results were obtained when atropine methylbromide, a charged derivative of atropine sulfate, or glycopyrrolate, a synthetic antimuscarinic agent, was substituted for atropine sulfate (ET: 51 +/- 6 and 51 +/- 16 beats/min, respectively). Raising the arterial blood pressure with phenylephrine increased the heart rate further; lowering the blood pressure with sodium nitroprusside attenuated or abolished the ET. Our results show that ET is produced by antimuscarinic agents in general and is not mediated by the beta-adrenergic system. Furthermore, ET is present only when the cervical vagi are intact, probably because ET is mediated by cholinergic vagal efferent fibers via a mechanism that has not yet been recognized in cardiac rate control.

The role of spinal cord transmission in the ventilatory response to electrically induced exercise in the anaesthetized dog.

1. The ventilatory response to electrically induced ;exercise' was studied in six chloralose-anaesthetized dogs. The on-transient and steady-state responses to ;exercise' were compared in the same dogs before and after spinal cord transection at T8/9 (dermatome level T6/7) on fifteen occasions.2. Phasic hind limb ;exercise' was induced for periods of 4 min by passing current (2 Hz modulated 50 Hz sine wave) between two needles inserted through the hamstring muscles. The maximum current used was 30 mA. This was below the level previously found to produce an artifactual stimulation of breathing with the cord intact.3. Cord transection produced no significant change in either the resting values of ventilation ( V(I)) and CO(2) production ( V(CO) (2)) or the ventilatory equivalent for CO(2) during ;exercise' ( big up tri, open V(I)/ big up tri, open V(CO) (2)).4. During the steady state of exercise P(a, CO) (2) was on average significantly lower than at rest with the cord intact (mean big up tri, openP(a, CO) (2), - 2.1 mmHg; range - 5.7 to + 1), and higher, though not significantly, with the cord cut (mean P(a, CO) (2), + 1.2 mmHg; range - 1.5 to + 4.3). However, even in the absence of spinal cord transmission, the ventilatory response to exercise could not be accounted for on the basis of CO(2) sensitivity; the big up tri, open V(I)/ big up tri, openP(a,CO) (2) obtained with exercise (apparent sensitivity) was significantly greater than that obtained with CO(2) inhalation (true sensitivity) both before and after cord section.5. V(I) and V(CO) (2) increased more slowly with the cord cut than with the cord intact. This was thought to be due to a slower increase in venous return in the absence of sympathetic innervation of the lower half of the body following cord transection.6. Similar experiments were performed during muscle paralysis (following gallamine triethiodide). Ventilation was maintained with a respirator controlled by phrenic nerve activity. These experiments showed an increase in ventilation, independent of muscle contraction, which was only present when the cord was intact and which was confined to the on-transient. Only in the absence of spinal cord transmission could there be certainty that the dynamics of the ventilatory response to electrically induced ;exercise' was free of artifact.7. It was concluded that spinal cord transmission is not necessary for the steady-state ventilatory response to electrically induced exercise of the hind limbs.8. The dog with spinal cord transection provides a suitable model for the study of the chemical control of breathing during electrically induced exercise.

The ph oscillations in arterial blood during exercise; a potential signal for the ventilatory response in the dog.

1. The effect of electrically induced ;exercise' on the respiratory oscillation of arterial pH was studied in chloralose-anaesthetized dogs with spinal cord transection at T8/9 (dermatome level T6/7).2. Respiratory oscillations of arterial pH (presumed to be due to oscillations of arterial P(CO2)) were sensed with a fast-responding electrode in one carotid artery. Breath-by-breath estimates of the maximum rate of change of pH of the downstroke of the pH oscillation (dpH/dt downward arrowmax) were obtained by differentiating the pH signal.3. Consistent with the findings of the previous paper (Cross et al. 1982), the ventilatory response to exercise could not be explained on the basis of sensitivity to CO(2); the Delta V(I)/DeltaP(a, CO2) was significantly greater for ;exercise' than for CO(2) inhalation.4. On average, the amplitude of the pH oscillations decreased during ;exercise'. The change in the phase relationship (varphi) between respiratory and pH cycles, although significant from the second breath onwards, was not thought to be responsible for the increased ventilation V(I); the direction of the change was opposite to that previously found to increase V(I).5. Inspiratory duration (t(i)), expiratory duration (t(e)), V(I) and the dpH/dt downward arrowmax changed significantly by the third breath of ;exercise'. A significantly linear relationship was obtained between t(e) and dpH/dt downward arrowmax during the on-transient (first ten breaths) of ;exercise'. This relationship was maintained throughout ;exercise'. V(I) and dpH/dt downward arrowmax were also linearly related during the on-transient, although the same relationship did not hold true throughout ;exercise'.6. The dpH/dt downward arrowmax was related to CO(2) production ( V(CO2)) lending support to the prediction that the slope of the downstroke of the pH oscillation is a function of V(CO2).7. It was concluded that the dpH/dt downward arrowmax (dpCO(2)/dt upward arrowmax) is a potential humoral signal in ;exercise' and could account totally for the shortening of t(e). Since there was a late rise in V(I) (due to an increase in tidal volume V(T)) in the absence of a change in dpH/dt downward arrowmax, it was considered unlikely that the dpH/dt downward arrowmax was the only humoral signal present during ;exercise'.

Sympathetic and parasympathetic cardiac control in athletes and nonathletes at rest.

A simple model to characterize sympathetic and parasympathetic effects on heart rate (R) was tested during rest in 10 nonathletes and 8 world-class oarsmen. The model states that R = mnR0, where R0 is the intrinsic cardiac rate, and m and n depend only on sympathetic and parasympathetic activity, respectively. The multipliers, m and n, were determined by dual pharmacological blockade in two sessions under similar conditions, but in one session propranolol and in the other atropine was given first. In agreement with the model, when corrections were made for atropine-induced blood pressure changes, m and n did not depend on which blocking agent was administered first. In athletes the control heart rate [55 +/- 3.3 (SD) beats/min] and R0 (81 +/- 8.3 beats/min) were lower than in nonathletes (62 +/- 6.0, P less than 0.01 and 102 +/- 11, P less than 0.001, respectively). The sympathetic multiplier, m, was similar (1.18 +/- 0.06 vs. 1.20 +/- 0.05, P greater than 0.4) in the two groups, but n, the parasympathetic multiplier, was closer to 1 in the athletes (0.57 +/- 0.03 vs. 0.51 +/- 0.05, P less than 0.01). We conclude that the model is suitable for the quantitative study of sympathetic/parasympathetic heart rate control in humans, and that the lower resting heart rate in oarsmen is solely due to a reduction in intrinsic cardiac rate, and not to an increase in parasympathetic tone.

Automated control of physiological variables and clinical therapy.

Improved transducers and low-cost computational power make the development of on-line systems to control physiological variables and clinical therapy feasible. This review deals only with systems that provide control by the infusion of chemical agents or by changing the concentration of respiratory gases; control provided by electrical stimulation or mechanical means (orthotic and prosthetic devices) are not considered. Applications reviewed include drug dosage planning by computer, insulin infusion, automated anesthesia, control of respiratory variables, and control of blood pressure by vasoactive agents. There is a general need for the development of new sensors for physiological variables, algorithms for adaptive control, and controllable miniature activators for delivering therapeutic agents. Proposed control systems should be thoroughly evaluated in a realistic environment, preferably by comparing them with systems that they were designed to replace.

Maturation of cardiac control in full-term and preterm infants during sleep.

ECG and respiration were recorded from 13 full-term and 8 preterm infants at 2-5 week intervals during sleep at home in the first year of life. Average pulse interval in both quiet and active sleep was minimum at postnatal ages between 4 and 10 weeks, with the minimum during quiet sleep being significantly smaller for preterm (409 +/- 22 (SE) msec) than for full-term (445 +/- 9 msec) infants. The minimum average pulse interval of preterm infants was smaller than the pulse interval of full-term infants at any post-conceptional age, and a smaller average pulse interval and smaller variations in pulse interval in preterm infants during quiet sleep persisted until a postnatal age of 7 months. The pulse interval variations attributable to respiration varied substantially with age. The results indicate that developmental changes in cardiac rate control are functions of both postnatal and post-conceptional age, with the post-conceptional age at birth setting the mean level of pulse interval, a level which is then altered by development linked to postnatal age.

Development of autonomic heart rate control in the kitten during sleep.

Development of cardiac rate control was studied in 34 kittens aged 4 days to 6 wk during quiet and active sleep, using atropine and propranolol to quantitatively assess the degree of tonic parasympathetic and sympathetic control, with the analysis based on the Rosenblueth and Simeone model. The order of blocking agent administration did not significantly affect the results if a correction was made for the baroreceptor-mediated heart rate change after the blockade of a single autonomic branch. During the first 4 wk, the heart rate in quiet sleep was lower than in active sleep due to a significantly higher parasympathetic tone. The heart rate decreased with age in both sleep states: the decrease in quiet sleep was accompanied by a transition from sympathetic to parasympathetic dominance. The intrinsic rate of the pharmacologically denervated heart was maximum at about 2 wk and decreased steadily thereafter. The observed changes may help explain some features of the development in heart rate previously reported for sleeping human infants.

Effect of lung volume on expiratory time in the newborn infant.

The effect of an increased end-expiratory lung volume on inspiratory and expiratory duration was examined in 13 term infants at 4, 30, and 70 h of age. This was accomplished by the administration of a continuous positive airway pressure (CPAP) of 0, 3, and 6 cmH2O by use of a face mask connected to a pneumotachometer, and by measurement of the timing of the respiratory cycle over 1-min intervals. At increasing functional residual capacity (FRC) there was a progressive increase in expiratory time (TE) and fall in respiratory rate, with a variable effect on inspiratory time (TI). As CPAP increased from 0 to 6 cmH2O, the TI/TE ratio fell from 0.75 to 0.62 (P less than 0.01), 0.90 to 0.66 (P less than 0.001), and 0.87 to 0.64 (P less than 0.001) at 4, 30, and 70 h, respectively. We conclude that alterations in end-expiratory lung volume significantly alter expiratory duration in the newborn infant at term. This may be analogous to the vagally mediated tonic control of expiratory time with changing FRC recently described in anesthetized animals.

Heart rate and respiratory rate differences between preterm and full-term infants during quiet sleep: possible implications for sudden infant death syndrome.

The heart rate and respiratory rate of eight preterm (average gestational age, 33.3 +/- 2.2 weeks) and 13 full-term infants were determined during quiet sleep at home during the first year of life. Both heart rate and respiratory rate were greater in preterm infants throughout the first six months. The difference was maximum at age 10 weeks (21.2 beats per minute and 13.7 breaths per minute), with the difference being statistically significant, at least at the P less than .01 level at ages 10, 12 and 14 weeks, while P greater than or equal to .01 at all other ages. The 10- to 14-week period is precisely the same period during which the incidence of sudden infant death syndrome (SIDS) has been reported to be maximum. These results support the concept that SIDS is linked to a vulnerable phase of cardiorespiratory maturation.