Biomedical subjects

M Bonora

Publications and source records attributed to M Bonora.

At least 37 records · Page 2Linked to original sources

PubMed1993

Ventilatory and metabolic responses to cold and CO2 in intact and carotid body-denervated awake rats.

We investigated in conscious rats the characteristics and modes of action of CO2 on thermoregulation and ventilatory control during cold stress. In a group of 10 rats studied intact and after carotid body denervation, measurements of metabolic rate (VO2), ventilation (V), shivering, and colonic temperature (Tc) were made at controlled ambient temperatures (Ta) of 25, 20, 15, 10, and 5 degrees C. Animals were exposed on different days to 1) normoxia, 2) normoxia and 4% CO2, 3) 12% hypoxia, or 4) 10.8% hypoxia and 4% CO2. The following results were obtained. 1) During CO2 exposure in normoxia or hypoxia, VO2 is increased at Ta of 25 degrees C and decreased for lower Ta. These effects are partly mediated by carotid body afferents. 2) Shivering and nonshivering thermogenesis and therefore Tc regulation are affected by CO2 exposure as shown by relationships between VO2-Tc and VO2-shivering intensity. 3) V is controlled by PO2 and PCO2 directly through their peripheral and central actions but also indirectly through their effects on VO2. Our conclusions are as follows. 1) Control of Tc is markedly dependent on PCO2 level. Carotid body afferents play a role, but direct central effects acting on the different sources of thermogenesis and possibly on thermolysis are most prominent. 2) As far as control of V is concerned, during hypercapnia in normoxia or hypoxia, several analogies may be formed between exposure to cold and muscular exercise, both of which increase VO2 and V, suggesting common integrative mechanisms at the central nervous system level.

Animals↗

PubMed1992

Control of metabolic and ventilatory responses to cold in anesthetized cats.

Interactions between the control of thermogenesis and ventilation were studied during normoxia, hyperoxia, and ambient or CO hypoxia in adult anesthetized intact or carotid-denervated cats. Shivering, metabolic and ventilatory responses to cold stress were studied. In addition, the effects of transient pharmacological stimulation (NaCN) or inhibition (Dopamine) of arterial chemoreceptor activity were studied under different levels of oxygenation. In intact animals, cold exposure provoked increases in VO2 and ventilation which were directly proportional to the intensity of shivering. During ambient or CO hypoxia, VO2 was less than in normoxia for all values of shivering intensity, suggesting that a non-shivering thermogenesis component may also be inhibited by hypoxia. The decrease in VO2 was associated with a smaller decrease in ventilation in ambient than in CO hypoxia because of the presence of the chemoreflex drive during ambient hypoxia. Pharmacological changes in chemoreceptor activity induced transient and opposite changes in ventilation and shivering intensity, confirming their role in the control of thermogenesis. After carotid denervation, when the drug effects were inconsistent or absent, changes in levels of oxygenation were still followed by changes in shivering activity and associated changes in VO2 and ventilation. We conclude that control of thermogenesis and ventilation and their interaction may be mediated by chemoreceptors as well as by direct effects upon central, possibly diencephalic structures.

Animals↗

PubMed1992

Diaphragmatic and ventilatory responses to alveolar hypoxia and hypercapnia in conscious kittens.

Ventilation and electromyographic (EMG) activity of the diaphragm were recorded in unanesthetized kittens 2 and 10 wk of age during normoxia, hypercapnia (2 and 4% CO2), and hypoxia (12 and 10% O2). We measured integrated diaphragmatic EMG activity at end inspiration (DIAI) and end expiration (DIAE); the difference (DIAI-E), which represents the phasic change of the diaphragmatic activity, was considered responsible for a given tidal volume (VT). During hypercapnia, the 2-wk-old kittens increased minute ventilation (V) by increases in both VT and respiratory frequency (f), whereas the 10-wk-old kittens increased V primarily by an increase in VT. At both ages, DIAI and DIAI-E increased during hypercapnia, whereas DIAE did not change significantly. During hypoxia, in the young kittens, V and VT decreased while f increased markedly; in the older kittens, V, VT, and f did not change significantly. In kittens of both ages, DIAI increased during hypoxia; because diaphragmatic activity persisted into expiration, DIAE also increased. DIAI-E, as well as VT, was decreased in the young kittens, whereas in the older ones DIAI-E was slightly increased despite an unchanged VT. Finally, the ventilatory and diaphragmatic response to hypoxia changes with maturation in contrast to the response to hypercapnia. It is concluded that 1) the hypoxia-induced reduction of VT may result from prolongation of diaphragmatic activity into expiration, inasmuch as it induces a reduction of the phasic change of the diaphragmatic activity, and 2) because DIAI-E indirectly reflects central inspiratory output, a central mechanism should be involved in the reduced VT and V in response to hypoxia in newborns.

Animals↗

PubMed1992

Ventilatory and metabolic responses to cold and hypoxia in intact and carotid body-denervated rats.

The effects of hypoxia on thermoregulation and ventilatory control were studied in conscious rats before and after carotid denervation (CD). Measurements of metabolic rate (VO2), ventilation (V), shivering intensity (SI), and colonic temperature (Tc) were made in groups of eight rats subjected to three protocols. In protocols 1 and 2, at ambient temperature (Ta) of 25 and 5 degrees C, respectively, rats were exposed to normoxia and hypoxia [inspired O2 fraction (FIO2) 0.13-0.11]. In protocol 3, Ta was decreased from 25 to 5 degrees C in 30-min steps of 5 degrees C. Recordings were made in normoxia and hypoxia (FIO2 0.12). The results show that in both intact and CD rats 1) in normoxia, cold exposure increased VO2, V, and SI, and these increases were proportional to the decrease in Ta; 2) hypoxia induced only a transient decrease in SI, and, for a given Ta, VO2 was reduced whereas V and SI were increased; and 3) in CD rats, V increased less during cold exposure in both normoxia and hypoxia; VO2 and Tc were more depressed during hypoxia. It is concluded that 1) the interaction between Ta and FIO2 in the control of V is partly dependent on the carotid body afferents, 2) shivering thermogenesis may be transiently affected by hypoxia independently of the carotid body afferents, and 3) nonshivering thermogenesis may be directly inhibited by hypoxia, especially during cold exposure.

Afferent Pathways↗

PubMed1991

Effects of hypoxia and cold acclimation on thermoregulation in the rat.

The effects of hypoxia (inspired O2 fraction = 0.12) on thermoregulation and on the different sources of thermogenesis were studied in rats before and after periods of 1-4 wk of cold acclimation. Measurements of metabolic rate (VO2) and body temperature (Tb) were made at 5-min intervals, and shivering activity was recorded continuously in groups of rats subjected to three protocols. In protocol 1, rats were exposed to normoxia to an ambient temperature (Ta) of 5 degrees C for 2 h. In protocol 2, at Ta of 5 degrees C, rats were exposed for 30 min to normoxia, then for 45 min to hypoxia, and finally for 30 min to normoxia. In protocol 3, in the non-cold-acclimated (NCA) rats, Ta was decreased from 30 to 5 degrees C in steps of 5 degrees C and of 30-min duration while in cold-acclimated (CA) rats at 5 degrees C for 4-wk, Ta was increased from 5 to 30 degrees C in steps of 5 degrees C and of 30-min duration. Recordings were made in normoxia and in hypoxia on different days in the same animals. The results showed that 1) in NCA rats, cold exposure in normoxia induced increases in VO2 and shivering that were proportional to the decrease in Ta; 2) in CA rats in normoxia, for a given Ta, VO2 and Tb were higher than in NCA rats, whereas shivering was generally lower; and 3) in both NCA and CA rats, hypoxia induced a transient decrease in shivering and a sustained decrease in nonshivering thermogenesis associated with a marked decrease in Tb that was about the same in NCA and CA rats. We speculate that hypoxia acts on Tb control to produce a general inhibition of thermogenesis. Nonshivering thermogenesis is markedly sensitive to hypoxia, especially demonstrable in CA rats; a recovery or even an increase in shivering can compensate for the decrease in nonshivering thermogenesis.

Acclimatization↗

PubMed1990

Effects of carotid denervation and decerebration on ventilatory response to CO.

To clarify the mechanisms involved in the ventilatory response to the inhalation of low concentrations of CO (0.18-0.22% in air), the roles of the arterial chemoreceptors and the forebrain structures have been investigated in unanesthetized adult cats. The ventilatory response was observed in conscious animals intact, after carotid denervation (CD), and after midcollicular decerebration. The results show that the initial small ventilatory depression was unaffected by CD but that the subsequent characteristic tachypnea was blunted after CD even after more prolonged exposure to CO. The CO tachypnea was not observed after decerebration, but a residual hyperventilation was noted with the higher concentration used. It may be concluded that carotid chemoreceptors do not mediate the CO tachypnea, which may then originate in suprapontine structures as shown by comparison of intact and decerebrate animals. The blunting of the tachypnea after CD may be caused by the relative hypercapnia observed in CD animals. The residual hyperventilation observed in decerebrate animals may be caused by central acidosis and/or some peripheral potentiation of chemoreceptor activity resulting from the decrease in arterial blood pressure that accompanied CO inhalation in decerebrate animals.

Animals↗

PubMed1990

Role of dopamine and arterial chemoreceptors in thermal tachypnea in conscious cats.

In mammals submitted to a warm environment, intracerebral injection of dopamine (DA) produces no change or an increase in body temperature accompanied by an increase in metabolic heat production, but its effect on heat loss mechanisms such as vasodilation and tachypnea is not clear. Because the principal mechanism of heat loss in the conscious cat is thermal tachypnea, we studied the influence of DA on thermal tachypnea in response to heat stress (ambient temperature = 33-36 degrees C) in five conscious cats. We first studied the steady-state response to a DA agonist, apomorphine, which crosses the blood-brain barrier. Intravenous injection of apomorphine greatly reduced thermal tachypnea by decreasing respiratory frequency (from 94.9 to 52.5 breaths/min) and increasing tidal volume (from 13.2 to 20.4 ml). The subsequent injection of the DA antagonist haloperidol, which also crosses the blood-brain barrier, restored the initial tachypnea. To further investigate the mechanism involved in thermal tachypnea, we studied the influence of peripheral chemoreceptors by transiently stimulating or inhibiting carotid body (CB) activity during tachypneic breathing. CB stimulation by intravenous injection of NaCN or domperidone reduced thermal tachypnea mainly by decreasing the respiratory frequency, whereas CB inhibition by DA tended to increase frequency and thus tachypnea. It is concluded that 1) in a warm environment, central DA receptors are also greatly involved in heat loss mechanisms, 2) arterial chemoreceptor input appears to counteract this tachypneic breathing, and 3) thermal and hypoxic tachypnea may be controlled by the same mechanism in which a DA-like system has a key role.

Animals↗

PubMed1989

Effects of hypoxia on metabolic rate of conscious adult cats during cold exposure.

Oxygen consumption (VO2) and shivering movements were recorded in adult, conscious cats in a thermoneutral (24-27 degrees C) and in a cold (3-8 degrees C) environment during normoxia, hypoxia, or hyperoxia for 55 min. In the cold environment, VO2 correlated with shivering index (SI) under conditions of normoxia or ambient hypoxia (FIO2 = 0.12). During normoxia, VO2 was 63% higher in the cold than the thermoneutral environment. Ambient hypoxia acutely reduced VO2 in cold and thermoneutral environments, the decrement being greater for the former than the latter. Similarly, the variation in VO2 for unit change in SI was greater in hypoxia than normoxic conditions, suggesting that hypoxia influenced nonshivering as well as shivering components of cold-induced VO2. Hypoxia induced by CO (FICO = 0.002) also reduced VO2 and SI, a result that is consistent with previous results indicating that carotid body chemoreceptors do not mediate the suppression of shivering by ambient hypoxia. Hyperoxia increased VO2 and SI in the cold, and the effects of both hypoxia and hyperoxia in the cold were antagonized by increasing FICO2 to 0.03. The results demonstrate that hypoxia suppresses VO2 in the cold by reducing the intensity of shivering and, probably, by an action on metabolic rate that is unrelated to cold-induced calorigenesis.

Animals↗

PubMed1989

Effects of hypoxia on thermal polypnea in intact and carotid body-denervated conscious cats.

The effects of the level of oxygenation on the respiratory response to heat exposure have been studied in conscious cats during normoxia, severe or mild hypocapnic hypoxia [inspired O2 fraction (FIO2) = 0.11 or 0.13], or hyperoxia. Several cats were also studied during severe normocapnic hypoxia. Experiments were repeated while the same animals were chronically carotid body denervated (CBD). The increase in respiratory frequency (f) leading to thermal tachypnea occurred at a lower body temperature (Tb) in severe hypocapnic hypoxia than in ambient air, but this effect was less pronounced when hypocapnia was corrected. No significant changes were observed during mild hypoxia or hyperoxia compared with normoxia in intact animals. After CBD, thermal tachypnea occurred at lower Tb in air than it did with intact animals in three of five cats, and it also occurred at lower Tb in mild hypocapnic hypoxia compared with air. It appears, therefore, that in conscious cats exposed to heat load 1) severe hypoxia enhances thermal tachypnea, 2) this effect persists after CBD, which suggests that it originates from a central action of hypoxia, and 3) the chemoreceptor afferents, to some degree, inhibit the onset of thermal tachypnea, as was previously observed for hypoxic tachypnea, which appears only in CBD cats (J. Appl. Physiol. 49: 769-777, 1980). Therefore, triggering of thermal and hypoxic tachypnea may involve common central mechanisms, probably located in the diencephalic structures under the control of afferents from arterial chemoreceptors.

Animals↗

PubMed1989

Pneumomediastinum not associated with lesion of mediastinal organs.

A review of 2,092 patients who had sustained closed thoracic trauma or undergone mechanical ventilation was made in order to clarify the incidence, clinical picture, pathogenesis and prognosis of pneumomediastinum without pneumothorax or lesion of mediastinal organs. Air in the mediastinal space was observed in ten patients (0.5% of cases). Bronchial and esophageal lesions were excluded at bronchoscopy and esophagoscopy. The clinical presentation included subcutaneous emphysema of the neck, without signs of mediastinitis. No patient had pain or dyspnoea. Trauma or barotrauma were assumed to have caused sudden rise in the intrapulmonary pressure, leading to passage of air from the parahilar alveoli into the mediastinum along the peribronchial and perivascular spaces. Management was conservative and the prognosis good, with normalization of the chest radiogram usually within a week.

Adolescent↗

PubMed1988

Influence of dopamine and norepinephrine on the central ventilatory response to hypoxia in conscious cats.

The effects of intravenous administration of agonists and antagonists of dopamine (DA) and norepinephrine (NE) on the central ventilatory response to hypoxia were studied in unanesthetized cats. The experiments were performed in intact animals exposed to CO-hypoxia and in carotid-body denervated animals breathing a hypoxic mixture. The DA agonist, apomorphine (APO) significantly decreased minute ventilation in response to central hypoxia, whereas the opposite effect occurred with the DA antagonist, haloperidol (HAL). Indeed, the characteristic tachypnea elicited by CO or hypoxic hypoxia was inhibited by APO as the respiratory frequency markedly decreased while tidal volume concomitantly increased. Conversely, HAL administration enhanced the tachypnea during milder hypoxia or reversed the inhibitory action of APO. In contrast, the NE agonist, clonidine (CLO) and antagonists propranolol (PRO) and phenoxybenzamine (PHE) did not cause significant changes in minute ventilation and breathing pattern although CLO tended to attenuate the hypoxic tachypnea. This study confirms, therefore, that catecholamines are involved in the central ventilatory response to hypoxia and suggests that the brain dopaminergic system plays a major role in the CO or hypoxic tachypnea.

Animals↗

PubMed1987

Maturational changes in body temperature and ventilation during hypoxia in kittens.

Developmental changes in body temperature (Tb) and minute ventilation (V) were studied in unanesthetized kittens of 1, 2, 4, 6 and 8 weeks of postnatal age while breathing either air, 11% O2, or 11% O2 + 2.5% CO2. Experiments were mainly carried out at the ambient temperature (Ta) of 26-28 degrees C at which Tb was similar to that measured in the nesting box with the mother and littermates. In air, Tb progressively rose with increasing age to approach adult values by the age of 8 weeks. In hypoxia, Tb significantly decreased relative to room air values at all ages. However, the greatest decline occurred during the first month after birth, whereas by 6 and 8 weeks Tb was only slightly affected by hypoxia. The hypoxic-induced fall in Tb was partially prevented by the addition of 2.5% CO2 to the hypoxic mixture at 1, 2 and 4 weeks and slightly enhanced in the oldest kittens. On the other hand, V was consistently depressed by hypoxia relative to room air in the 1- and 2-week-old kittens. After 4 weeks of age, hypoxia induced a marked and sustained increase in V as in adult cats. Therefore, the depressant effect of hypoxia on body temperature which becomes progressively less effective during the first two months after birth appears to follow a similar postnatal evolution as the ventilatory response to hypoxia. It is suggested that maturity may be a contributing factor to the hypoxic-induced fall in Tb and that the maturational changes in V and Tb in response to hypoxia may be under the influence of the same central mechanisms.

Air↗

PubMed1987

Hypoxia-induced changes in shivering and body temperature.

Experiments were carried out on conscious cats to evaluate the general characteristics and modes of action of hypoxia on thermoregulation during cold stress. Intact and carotid-denervated (CD) conscious cats were exposed to ambient hypoxia (low inspired O2 fraction) or CO hypoxia in prevailing laboratory (23-25 degrees C) or cold (5-8 degrees C) environments. In the cold, both groups promptly decreased shivering and body temperature when exposed to either type of hypoxia. Small increases in CO2 concentration reinstituted shivering in both groups. At the same inspired concentration of O2, CD animals decreased shivering and body temperature more than intact cats. While this difference resulted, in part, from a lower alveolar PO2 in CD cats, a difference between intact and CD cats was apparent when the two groups were compared at the same alveolar PO2. During more prolonged hypoxia (45 min), shivering returned but did not reach normoxic levels, and body temperature tended to stabilize at a hypothermic value. Exposure to various levels of hypoxia produced graded suppression of shivering, with the result that the change in body temperature varied directly with inspired O2 concentration. Hypoxia appears to act on the central nervous system to suppress shivering and sinus nerve afferents appear to counteract this direct effect of hypoxia. In intact cats, this counteraction appears to be sufficient to maintain body temperature under hypoxic conditions at room temperature but not in the cold.

Animals↗

PubMed1987

Influence of halothane on control of breathing in intact and decerebrated cats.

The effects of halothane anesthesia have been investigated in intact and in decerebrated cats. Pulmonary ventilation and breathing pattern were studied during room-air breathing, hypercapnia, and O2 inhalation. The following results have been demonstrated. First, halothane anesthesia does not modify pulmonary ventilation, but a tachypnea much more intense in intact than in decerebrated cats is observed. This indicates that halothane-induced tachypnea originates mainly in structures rostral to the brain stem. Second, decerebrated animals exhibit a breathing pattern and a ventilatory response to CO2 similar to those of intact conscious cats, suggesting that forebrain facilitatory and inhibitory influences on brain stem are cancelled out by decerebration. However, the tidal volume vs. inspiratory duration relationship observed in decerebrated cats differs from that in conscious cats. Finally, during halothane anesthesia, ventilatory response to CO2 is markedly depressed. Third, during O2 inhalation, except in decerebrated, anesthetized animals, ventilation is only slightly depressed. This suggests that central stimulatory effect of O2 is enhanced and/or that peripheral chemoreceptor drive is reduced.

Anesthesia↗

PubMed1986

Ventilatory response of the conscious or anesthetized cat to oxygen breathing.

In conscious intact cats, oxygen breathing for up to 1 h does not modify ventilation, and the ventilatory response to CO2 in hyperoxia is not consistently decreased. However, oxygen breathing induces sustained hyperventilation in conscious cats after carotid body denervation. In anesthetized cats, oxygen breathing provokes a hypoventilation which is transient under light anesthesia but more sustained under deeper levels of anesthesia. At all levels of anesthesia, the ventilatory response to CO2 is decreased in hyperoxia as compared with normoxia. These results suggest that: the effects of hyperoxia include a central stimulating component, seen only in conscious animals, which offsets the decreased ventilatory drive from peripheral chemoreceptors; this central component is sensitive to anesthesia, thus allowing an explanation for the permanent decrease in ventilation and decrease in ventilatory response to CO2 observed when oxygen is given during deep anesthesia; and anesthesia may help to purposefully unmask factors involved in the control of breathing, but it markedly alters the normal functioning of the respiratory network.

Anesthesia↗

PubMed1985

Changes in upper airway muscle activity related to head position in awake cats.

The influence of head position on the respiratory activity of the diaphragm (DIA), posterior cricoarytenoid (PCA) and genioglossus (GG) muscles was studied in conscious cats with chronically implanted electromyographic electrodes. Tracheal pressure was also recorded through a small implanted catheter. Spontaneous or passive downward movements of the head resulted in sustained increases in the respiratory excursions of tracheal pressure and in PCA and GG activities. Conversely, these variables all decreased when the head was raised. Activity of the DIA was little affected. In animals with chronic tracheostomies, which greatly diminished tracheal pressure excursions and their changes with head movements, the postural responses of PCA and GG activities persisted, but were attenuated. The responses also persisted after bilateral superior laryngeal nerve section. These findings demonstrate responses that act to maintain the patency of the upper respiratory tract, probably by reflex mechanisms. Receptors in the upper airway contribute to the responses, but other afferents - possibly from vestibular or joint receptors - are also involved.

Animals↗

PubMed1985

Differential elevation by protriptyline and depression by diazepam of upper airway respiratory motor activity.

Effects of systemically administered protriptyline and diazepam on the respiratory activity of the phrenic, hypoglossal, and recurrent laryngeal nerves were investigated in vagotomized, decerebrate cats. Both hypoglossal and recurrent laryngeal nerve activities were consistently increased after protriptyline administration, whereas the phrenic nerve discharge was not systematically altered. Similar changes were observed in cats with bilateral carotid sinus nerve sections. Diazepam induced a reduction of hypoglossal and recurrent laryngeal nerve activities at doses that did not alter phrenic nerve discharge. These results with diazepam were the same in carotid chemodenervated cats. We conclude that neural mechanisms controlling upper airway muscles are much more sensitive to protriptyline and diazepam than are those of the bulbospinal-phrenic system. The selective augmentation of hypoglossal and recurrent laryngeal discharges by protriptyline could account for the reported decrease in the frequency of obstructive sleep apneas in patients receiving this antidepressant. In contrast, diazepam, by depressing motor activity to upper airway muscles, may exacerbate oropharyngeal obstruction during sleep.

Animals↗

PubMed1984

Developmental changes in ventilation and breathing pattern in unanesthetized kittens.

Ventilation and the breathing pattern of 12 intact, unanesthetized, unrestrained kittens, were recorded at intervals from the second postnatal day to the end of the eighth month. Five of the animals were also studied at 12 months of age. Ventilation (VE) became stable by the 5th month, whereas body weight was still increasing. The relationship between tidal volume (VT) and breathing rate (BR) changed with age. During the 1st month, BR fell and VT increased, VE increasing slowly. From 1 to 5 months, BR remained nearly constant while VT increased. Finally, from 5 to 12 months, BR decreased slightly, VT increased slightly, and VE did not change. The results are compared with relevant data from the literature, especially those derived from interspecific analyses.

Aging↗