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Biomedical subjects

M Bonora

Publications and source records attributed to M Bonora.

At least 55 records · Page 3Linked to original sources

Postnatal maturation of ventilation and breathing pattern in kittens: influence of sleep.

Ventilation and breathing pattern were studied in kittens at 1, 2, 3, 4, and 8 wk of life during quiet wakefulness (W), quiet sleep (QS), and active sleep (AS) with the barometric method. Tidal volume (VT), respiratory frequency (f), ventilation (VE), inspiratory time (TI), expiratory time (TE), mean inspiratory flow (VT/TI), and respiratory "duty cycle" (TI/TT) were measured. VT, VE, TI, TE, and VT/TI increased; f decreased and TI/TT remained constant during postnatal development in wakefulness and in both sleep states. No significant difference was observed between AS and QS for all the ventilatory parameters except TI/TT, which was greater in QS than in AS at 2 wk. VE was larger in W than in both AS and QS at all ages. This was mainly due to a greater f, TI/TT remaining constant. VT/TI, which represents an index of the central inspiratory activity, was larger in W than in sleep, VT not being significantly different whatever the stage of consciousness. The results of this study show that in the kitten 1) unlike in the adult cat, ventilation and breathing pattern are similar in QS and in AS; 2) in sleep, the central inspiratory drive appears to be independent of the type of sleep; and 3) in wakefulness, the increase of the central inspiratory activity could be related to important excitatory inputs.

Animals↗

Effects of hypoxia on ventilation during postnatal development in conscious kittens.

Effects of steady-state hypoxia (inspired O2 fraction = 0.11) on ventilation and breathing pattern were studied during postnatal development in unanesthetized kittens. Studies were done from 2 days to 8 mo of age, every week during the first month and every month thereafter. During the first 2 months, states of consciousness were determined. In the first month, minute ventilation (VE) was depressed in hypoxia compared with control values in air, whereas in the older kittens VE was increased in hypoxia, as in adult cats. The inhibitory effect of hypoxia was observed in all three states of consciousness in 7- and 14-day-old kittens. In the 21- and 28-day-old kittens, VE could not be reliably related to the state of consciousness. In the 2-mo-old kittens, VE increased in all states. Tidal volume (VT) was markedly decreased in kittens up to 14 days of age, and respiratory frequency increased. In the 21- and 28-day-old kittens, changes in breathing pattern were variable. In the oldest, the increase of VE was mainly due to an increase of VT. We conclude that in unanesthetized kittens, the ventilatory response to hypoxia is mature at 2 mo of age. The hypoxic tachypnea observed at 7 and 14 days resembles that previously seen in adult carotid-denervated cats, and may be due to a low level of carotid chemoreceptor drive and to a central excitatory effect of hypoxia on respiratory frequency. The complex response observed during the first month of life must reflect the development of peripheral and central mechanisms and their interactions.

Aging↗

Selective depression by ethanol of upper airway respiratory motor activity in cats.

We studied the effects of systemically administered ethyl alcohol on the respiratory motor activity of the phrenic, hypoglossal and recurrent laryngeal nerves in unanesthetized, decerebrate cats. Some of the cats were studied after carotid sinus nerve section. In addition, parallel studies were done in intact, awake cats with chronic electromyographic electrodes in the diaphragm, genioglossus, and posterior cricoarytenoid (PCA) muscles. In decerebrate animals, alcohol induced a significant reduction of hypoglossal and recurrent laryngeal nerve activities at doses that had little or no effect on the phrenic nerve discharge. Similar changes were observed in chemodenervated cats. In awake animals, genioglossal and PCA muscle activities were depressed by alcohol, whereas diaphragm activity showed no consistent change. Alcohol caused a significant increase in respiratory frequency in awake cats and reduced the responses of genioglossal and PCA muscle activities to hypercapnia and normocapnic hypoxia. We conclude that alcohol induces a selective reduction in upper airway respiratory motor activity by an action that does not require intact suprapontile structures, vagal afferents, or peripheral chemoreceptors. This reduction may contribute to the alcohol-induced exacerbation of obstructive sleep apnea.

Animals↗

Active and passive respiratory mechanics and control of breathing in kittens.

In five spontaneously breathing kittens (12-13 days old), anesthetized with pentobarbital sodium, we measured the passive and active elastances and resistances of the respiratory system and the decay of inspiratory muscle pressure (PmusI) during expiration. When normalized for body weight (BW), passive resistance (Rrs . BW) was smaller in kittens than in adult cats, whereas passive elastance (Ers . BW) did not differ significantly. As a result, passive time constant (tau rs = Rrs/Ers) was shorter in kittens (mean +/- SE: 0.073 +/- 0.011 s) than in cats (0.121 +/- 0.008 s). This, associated with a faster decay in PmusI in kittens, results in 2-3 times higher flows per kilogram body weight during spontaneous tidal expirations in kittens than in cats. As in the adult cats, the average values of active elastance and resistance were higher than the passive, the average percentage increase amounting to 59 and 49%, respectively. The greater active impedance reflects force-length and force-velocity properties of inspiratory muscles. Its price is higher work of breathing; its advantage is greater intrinsic load compensation.

Airway Resistance↗

Ventilatory response of intact cats to carbon monoxide hypoxia.

Adult intact conscious or anesthetized cats have been exposed to either hypoxia or low concentrations of CO in air. In addition, the ventilatory response to CO2 was studied in air, hypoxic hypoxia, and CO hypoxia. The results show that 1) in conscious cats, low concentrations of CO (0.15%) induce a slight decrease in ventilation and higher concentrations of CO (0.20%) induce first a small decrease in ventilation and then a characteristic tachypnea similar to the hypoxic tachypnea described in carotid-denervated cats; 2) in anesthetized cats, CO hypoxia induces only mild changes in ventilation; and 3) the ventilatory response to CO2 is increased in CO hypoxia in both conscious and anesthetized animals but differs from the increase observed during hypoxia. It is concluded that the initial decrease in ventilation may be caused by some brain stem depression of the respiratory centers with CO hypoxia, whereas the tachypnea originates probably at some suprapontine level. Conversely, the possible central acidosis may account for the potentiation of the ventilatory response to CO2 observed in either conscious or anesthetized animals.

Anesthesia, General↗

Dose effect of pentobarbital sodium on control of breathing in cats.

The dose effect of pentobarbital sodium on integrated ("moving time average") phrenic activity (EPHR), transdiaphragmatic pressure (Pdi), gastric pressure (Pga), changes in lung volume (V), and mechanical properties of the respiratory system was studied in six cats breathing room air. Increased pentobarbital dose from an initial value of 35 mg/kg ip, had no substantial effect on the relationship between EPHR and Pdi during both unoccluded and occluded inspirations, indicating that the diaphragmatic excitation-contraction coupling was not affected. Similarly, increased anesthetic dose had no effect on the relationship between EPHR and delta Pga during both occluded and unoccluded breaths, suggesting that the contribution of the diaphragm to the breathing movements did not change with increasing depth of anesthesia. Although the time course of phrenic activity showed substantial interanimal differences, the shape of the phrenic neurogram did not change substantially with increased pentobarbital dose in any of the cats studied. Increased anesthetic dose depressed, in the same proportion, the rate of rise of EPHR, Pdi, and V, but the mechanical properties of the respiratory system remained unchanged. The depression of ventilation with increased anesthetic dose was not proportional to the drop in central inspiratory activity, as quantified in terms of rate of rise of EPHR.

Airway Obstruction↗

Pattern of respiration in patients recovering from barbiturate overdose.

Ventilation has been recorded in seven patients who were unconscious following self-poisoning. Measurements were obtained on admission to the hospital and repeated daily until the patients regained consciousness. On admission, recordings were characterized by a low minute ventilation as a result of a low tidal volume in spite of a high frequency of respiration. During the period of recovery tidal volume and minute ventilation increased, whereas frequency decreased. The modifications observed during recovery were the reverse of those noted during the induction of anaesthesia wih barbiturates in man. However, these modifications differ from those observed during induction of anaesthesia in cats. Consequently, as far as respiratory control is concerned, models elaborated in animals cannot be extrapolated to deeply anaesthetized human subjects.

Adult↗

Mechanical properties of the lungs during acclimatization to altitude.

Mechanical properties of the lung were studied in nine healthy lowlanders during a 6-day sojourn at an altitude of 3,457 m. In comparison to sea-level values, it was found at altitude that 1) lung volumes measured by plethysmography including total lung capacity, vital capacity, and functional residual capacity (FRC) presented small changes not exceeding 300 ml; 2) static and dynamic lung compliances were not modified but static pressure-volume curves of lungs were shifted progressively to the left (the decrease in lung elastic recoil averaged about 2 cmH2O on days 4-6); and 3) maximal midexpiratory flow, forced expiratory volume in 1 s, and maximal expiratory and inspiratory flows were increased and, conversely, airways and pulmonary flow resistances were decreased on most days at altitude. The unchanged FRC in the face of a decreased lung recoil may be explained by an increase in thoracic blood volume at altitude, but other possible mechanisms are discussed. The decrease in resistances and increase in maximal flows may be partly explained by the decreased air density at altitude, but another contributing factor such as a bronchodilatation is also suggested. It is proposed that changes in lung mechanics at altitude may account for some of the changes in the pattern of breathing and mouth occlusion pressure (P0.1) observed during acclimatization of lowlanders to altitude.

Acclimatization↗

Phrenic activity, respiratory pressures, and volume changes in cats.

In eight anesthetized cats we measured the integrated ("moving time average") phrenic activity [using phrenic electroneurogram (EPHR)] and the active transdiaphragmatic pressure [Pdi(mus)] during room air breathing, hypoxia, and hypercapnia. The relationship between Pdi(mus) and EPHR was unaffected by either hypoxic or hypercapnic stimulation of breathing, suggesting that in spontaneously breathing cats the pressure losses are negligible. In all cats, however, there was a substantial volume-related decrease in Pdi(mus), indicating that with increasing lung volume the effectiveness of the diaphragm as a pressure generator decreases. In addition, we have developed a model that allows prediction of the time course changes in lung volume for different morphology of inspiratory driving pressure. This model explains many of the features of control of breathing found experimentally in our cats.

Animals↗

Time course of phrenic activity and respiratory pressures during airway occlusion in cats.

The morphology of integrated ("moving time average") phrenic electroneurograms (EPHR) and of tracheal (Ptr) and transdiaphragmatic (Pdi) pressure waves during occluded inspirations was studied in eight anesthetized cats breathing air and various hypercapnic and hypoxic mixtures. The shape of the rising part of EPR-, Ptr-, and Pdi-time profiles varied between animals (from convex to concave), but in each animal it remained virtually unchanged by hypoxia and hypercapnia. The shape of the Ptr and Pdi occlusion waves reflected the shape of EPHR. The relationship of EPHR to Pdi and Ptr did not change with chemical drive. It is concluded that central inspiratory activity (CIA) (as reflected by EPHR and its mechanical transforms Pdi and Ptr) increases in amplitude with stimulation of breathing but that the profile of CIA remains essentially unchanged. However, substantial differences in the time course development of phrenic activity, Pdi, and Ptr exist between cats. The fixed interrelationships among EPHR, Pdi, and Ptr indicate a proportional increase in activity among all inspiratory muscles with increased chemical drive.

Airway Obstruction↗

Breuer-Hering inflation reflex and breathing pattern in anesthetized humans and cats.

In nine cats and nine human subjects anesthetized with alfaxalone, respiratory activity and tracheal pressure were recorded prior to and during occlusion of the airway at end inspiration or end expiration. Lung inflations at the end of expiration were also performed. In addition, the ventilatory pattern was analyzed during hypercapnia. The results show that occlusions at the end of inspiration or inflations provoked an apnea in both cats and humans. However, concomitant with increases in tidal volume during hypercapnia, inspiratory duration decreased in cats and did not change in human subjects. These results indicate that the Breuer-Hering reflex, which delays the onset of inspiration during inflation was equally operative in cats and humans. In contrast, the "Breuer-Hering threshold curve," which accounts for the off-switch" of inspiration was different in cats and humans. Thus, in summary, the Breuer-Hering inflation reflex is operative in human subjects, but it does not seem to be involved in the control of the inspiratory off-switch mechanism during increases respiratory activity resulting from hypercapnia.

Adult↗

Possible alterations in brain monoamine metabolism during hypoxia-induced tachypnea in cats.

In carotid body-denervated cats, moderate hypoxia, or even normoxia when compared to hyperoxia, provokes a significant depression of the respiratory output. This is observed in conscious or anesthetized or decerebrated animals. On the other hand, more severe hypoxia induces tachypnea (hypoxic tachypnea of Miller and Tenney, Respir. Physiol. 23: 31-39, 1975) in conscious cats, whereas the same hypoxia is followed by marked respiratory depression or apnea in the anesthetized or decerebrated animals. Hypoxic tachypnea can be partly or completely reversed by injection of dopa or xanthines such as caffeine or aminophylline. This suggests that alterations in brain monoamine metabolism by hypoxia may be responsible for the alterations in suprapontine respiratory control systems, resulting the tachypnea. Mild hypercapnia can also reverse hypoxic tachypnea. It is concluded that the ventilatory response to hypoxia of conscious animals results from stimulation of peripheral chemoreceptors, inhibition of brain stem neurons, and finally involvement of suprapontine structures that seems to be mediated by depletion of monoamines.

Aminophylline↗

[Vagus nerves and pulmonary artery pressure in the conscious and anesthetized cats using different levels of oxygenation (author's transl)].

Pulmonary artery pressure (PAP systolic and diastolic) and heart rate (HR) have been recorded in conscious or anesthetized cats. Experiments have been carried out before and after bilateral vagotomy or section of vagal afferents at the level of the nodose ganglion. Animals were exposed to different levels of oxygenation using FIO2 from 0.11 to 1.00. The results show that: 1 Anesthesia with sodium pentobarbital did not affect PAP for a given level of FIO2 : changes in PAP caused by modifications of FIO2 were not affected by anesthesia. Heart rate was independent of FIO2, but remained always higher in the anesthetized animals (Fig. 4). 2 In anesthetized animals, pulmonary de-afferentation or vagotomy affected neither PAP, nor its variations with FIO2 nor HR (Fig. 5). 3 In conscious animals, PAP and its variations with FIO2 were not affected by vagotomy (Fig. 6 and 7) or pulmonary de-afferentation (Fig. 8). On the other hand, heart rate was always decreased after either vagotomy or pulmonary deafferentation. It is concluded that (1) PAP and its control by FIO2 are independent of the vagal innervation; (2) the pulmonary edema observed after vagotomy cannot be caused by an increase in lung vascular pressure; (3) anesthesia, on the one hand, and pulmonary afferents, on the other hand, can play a role in the control of the cardiovascular activity.

Anesthesia, General↗

[Is d-tubocurarine dangerous for the fetus and the newborn infant?].

A survey of a series of caesarean section done under general anesthesia with the aid of muscle relaxation obtained by repeated doses of d-tubocurarine evidenced a tendency to worsen the Apgar index. In the light of the cases and from the literature some hypotheses are here discussed; the most reliable are based upon the fact that injections of the curare before the plasma half life of the drug end by increasing the materno foetal gradients permitting the transplacentar passage of the d-tubocurarine.

Adult↗

Effects of carotid body denervation on respiratory pattern of awake cats.

Eight awake cats have been studied before and after carotid denervation during air and oxygen breathing, and during hypercapnia. Analysis of the variables that characterize the spirogram shows that carotid denervation consistently results in a decrease of the mean inspiratory flow (VT/TI), causing a decrease in tidal volume (VT) and ventilation with a relative alveolar hypercapnia. In carotid-denervated animals, inhalation of oxygen results in an increase in ventilation due to an augmentation of VT/TI and VT and a relative hypocapnia. TI does not significantly change in the different conditions whereas TE is significantly affected. TE seems therefore to be more closely related to the rate of rise of inspiratory activity than to inspiratory duration.

Animals↗