RESUMO
This study examined the location and distribution of O(2) chemoreceptors involved in cardio-respiratory responses to hypoxia in the neotropical teleost, the pacu (Piaractus mesopotamicus). Intact fish and fish experiencing progressive gill denervation by selective transection of cranial nerves IX and X were exposed to gradual hypoxia and submitted to intrabuccal and intravenous injections of NaCN while their heart rate, ventilation rate and ventilation amplitude were measured. The chemoreceptors producing reflex bradycardia were confined to, but distributed along all gill arches, and were sensitive to O(2) levels in the water and the blood. Ventilatory responses to all stimuli, though modified, continued following gill denervation, however, indicating the presence of internally and externally oriented receptors along all gill arches and either in the pseudobranch or at extra-branchial sites. Chemoreceptors located on the first pair of gill arches and innervated by the glossopharyngeal nerve appeared to attenuate the cardiac and respiratory responses to hypoxia. The data indicate that the location and distribution of cardio-respiratory O(2) receptors are not identical to those in tambaqui (Colossoma macropomum) despite their similar habitats and close phylogenetic lineage, although the differences between the two species could reduce to nothing more than the presence or absence of the pseudobranch.
Assuntos
Células Quimiorreceptoras/fisiologia , Peixes/fisiologia , Brânquias/fisiologia , Hipóxia/fisiopatologia , Animais , Pressão Sanguínea/fisiologia , Fenômenos Fisiológicos Cardiovasculares , Brânquias/inervação , Frequência Cardíaca/fisiologia , Oxigênio/metabolismo , Reflexo/fisiologia , Fenômenos Fisiológicos Respiratórios , Cianeto de Sódio/farmacologia , Especificidade da EspécieRESUMO
Experiments were carried out to test the hypothesis that ventilatory and cardiovascular responses to hypercarbia (elevated water P(CO2)) in the tambaqui Colossoma macropomum are stimulated by externally oriented receptors that are sensitive to water CO(2) tension as opposed to water pH. Cardiorespiratory responses to acute hypercarbia were evaluated in both the absence and presence of internal hypercarbia (elevated blood P(CO2)), achieved by treating fish with the carbonic anhydrase inhibitor acetazolamide. Exposure to acute hypercarbia (15 min at each level, final water CO(2) tensions of 7.2, 15.5 and 26.3 mmHg) elicited significant increases in ventilation frequency (at 26.3 mmHg, a 42% increase over the normocarbic value) and amplitude (128%), together with a fall in heart rate (35%) and an increase in cardiac stroke volume (62%). Rapid washout of CO(2) from the water reversed these effects, and the timing of the changes in cardiorespiratory variables corresponded more closely to the fall in water P(CO2) (Pw(CO2)) than to that in blood P(CO2) (Pa(CO2)). Similar responses to acute hypercarbia (15 min, final Pw(CO2) of 13.6 mmHg) were observed in acetazolamide-treated (30 mg kg(-1)) tambaqui. Acetazolamide treatment itself, however, increased Pa(CO2) (from 4.81+/-0.58 to 13.83+/-0.91 mmHg, mean +/-S.E.M.; N=8) in the absence of significant change in ventilation, heart rate or cardiac stroke volume. The lack of response to changes in blood P(CO2) and/or pH were confirmed by comparing responses to the bolus injection of hypercarbic saline (5% or 10% CO(2); 2 ml kg(-1)) into the caudal vein with those to the injection of CO(2)-enriched water (1%, 3%, 5% or 10% CO(2); 50 ml kg(-1)) into the buccal cavity. Whereas injections of hypercarbic saline were ineffective in eliciting cardiorespiratory responses, changes in ventilation and cardiovascular parameters accompanied injection of CO(2)-laden water into the mouth. Similar injections of CO(2)-free water acidified to the corresponding pH of the hypercarbic water (pH 6.3, 5.6, 5.3 or 4.9, respectively) generally did not stimulate cardiorespiratory responses. These results are in agreement with the hypothesis that in tambaqui, externally oriented chemoreceptors that are predominantly activated by increases in water P(CO2), rather than by accompanying decreases in water pH, are linked to the initiation of cardiorespiratory responses to hypercarbia.
Assuntos
Dióxido de Carbono/análise , Células Quimiorreceptoras/metabolismo , Peixes/fisiologia , Água Doce/análise , Acetazolamida/farmacologia , Análise de Variância , Animais , Pressão Sanguínea/efeitos dos fármacos , Dióxido de Carbono/sangue , Inibidores da Anidrase Carbônica/farmacologia , Células Quimiorreceptoras/fisiologia , Frequência Cardíaca/efeitos dos fármacos , Concentração de Íons de Hidrogênio , Fenômenos Fisiológicos Respiratórios/efeitos dos fármacos , Volume Sistólico/efeitos dos fármacosRESUMO
To study the effects of environmental hypercarbia on ventilation in snakes, particularly the anomalous hyperpnea that is seen when CO(2) is removed from inspired gas mixtures (post-hypercapnic hyperpnea), gas mixtures of varying concentrations of CO(2) were administered to South American rattlesnakes, Crotalus durissus, breathing through an intact respiratory system or via a tracheal cannula by-passing the upper airways. Exposure to environmental hypercarbia at increasing levels, up to 7% CO(2), produced a progressive decrease in breathing frequency and increase in tidal volume. The net result was that total ventilation increased modestly, up to 5% CO(2) and then declined slightly on 7% CO(2). On return to breathing air there was an immediate but transient increase in breathing frequency and a further increase in tidal volume that produced a marked overshoot in ventilation. The magnitude of this post-hypercapnic hyperpnea was proportional to the level of previously inspired CO(2). Administration of CO(2) to the lungs alone produced effects that were identical to administration to both lungs and upper airways and this effect was removed by vagotomy. Administration of CO(2) to the upper airways alone was without effect. Systemic injection of boluses of CO(2)-rich blood produced an immediate increase in both breathing frequency and tidal volume. These data indicate that the post-hypercapnic hyperpnea resulted from the removal of inhibitory inputs from pulmonary receptors and suggest that while the ventilatory response to environmental hypercarbia in this species is a result of conflicting inputs from different receptor groups, this does not include input from upper airway receptors.
Assuntos
Dióxido de Carbono/análise , Crotalus/fisiologia , Hipercapnia/metabolismo , Ventilação Pulmonar/efeitos dos fármacos , Análise de Variância , Animais , Gasometria , Pressão Sanguínea/efeitos dos fármacos , Dióxido de Carbono/administração & dosagem , Dióxido de Carbono/farmacologia , Células Quimiorreceptoras/efeitos dos fármacos , Células Quimiorreceptoras/fisiologia , Crotalus/metabolismo , Ventilação Pulmonar/fisiologia , América do Sul , Volume de Ventilação Pulmonar/efeitos dos fármacosRESUMO
We examined the magnitude of the hypoxic metabolic response in golden-mantled ground squirrels to determine whether the shift in thermoregulatory set point (T(set)) and subsequent fall in body temperature (T(b)) and metabolic rate observed in small mammals were greater in a species that routinely experiences hypoxic burrows and hibernates. We measured the effects of changing ambient temperature (T(a); 6--29 degrees C) on metabolism (O(2) consumption and CO(2) production), T(b), ventilation, and heart rate in normoxia and hypoxia (7% O(2)). The magnitude of the hypoxia-induced falls in T(b) and metabolism of the squirrels was larger than that of other rodents. Metabolic rate was not simply suppressed but was regulated to assist the initial fall in T(b) and then acted to slow this fall and stabilize T(b) at a new, lower level. When T(a) was reduced during 7% O(2), animals were able to maintain or elevate their metabolic rates, suggesting that O(2) was not limiting. The slope of the relationship between temperature-corrected O(2) consumption and T(a) extrapolated to a T(set) in hypoxia equals the actual T(b). The data suggest that T(set) was proportionately related to T(a) in hypoxia and that there was a shift from increasing ventilation to increasing O(2) extraction as the primary strategy employed to meet increasing metabolic demands under hypoxia. The animals were neither hypothermic nor hypometabolic, as T(b) and metabolic rate appeared to be tightly regulated at new but lower levels as a result of a coordinated hypoxic metabolic response.
Assuntos
Regulação da Temperatura Corporal/fisiologia , Metabolismo Energético , Hipóxia , Consumo de Oxigênio/fisiologia , Sciuridae/fisiologia , Animais , Dióxido de Carbono/análise , Eletromiografia , Frequência Cardíaca , Masculino , Mamíferos , Músculo Esquelético/inervação , Músculo Esquelético/fisiologia , Valores de Referência , Respiração , Fatores de TempoRESUMO
It now appears that at least some members of all classes of vertebrates exhibit ventilatory responses to changes in CO2/pH per se, including fishes. With the transition from aquatic to aerial respiration, there is an increase in the sensitivity of animals to this complex of stimuli, an increase in the variety of putative receptors possibly involved in eliciting ventilatory responses and an increase in the relative importance of this complex of stimuli in the genesis of resting ventilation. The variety of CO2-sensitive chemoreceptors present in air-breathing lower vertebrates adds considerable complexity to experimental studies of ventilatory responses to CO2/pH. Because of the locations, discharge characteristics and reflex effects of the different receptor groups, most air-breathing lower vertebrates show different responses to increases in CO2/[H+] due to cerebral ischemia, anoxia, metabolic acidosis and environmental hypercarbia. In some cases the differences are only quantitative, while in other cases the responses are qualitatively very different. These differences appear to reflect differences in the relative strength of the reflexes elicited by the various receptor groups and the net sum of their modulating influences when CO2/pH are altered via different routes. Although the situation is simpler in the higher vertebrates, in all cases the input from all of the CO2/[H]-sensitive receptors appears to act as a biasing input which summates with other afferent information to modulate respiratory motor output, even in those species that breathe intermittently.
Assuntos
Animais , Células Quimiorreceptoras/fisiologia , Consumo de Oxigênio/fisiologia , Dióxido de Carbono/fisiologia , Mecânica Respiratória/fisiologia , Ventiladores Mecânicos , Acidose Respiratória/fisiopatologia , Peixes/fisiologia , Filogenia , Répteis/fisiologiaRESUMO
It now appears that at least some members of all classes of vertebrates exhibit ventilatory responses to changes in CO2/pH per se, including fishes. With the transition from aquatic to aerial respiration, there is an increase in the sensitivity of animals to this complex of stimuli, an increase in the variety of putative receptors possibly involved in eliciting ventilatory responses and an increase in the relative importance of this complex of stimuli in the genesis of resting ventilation. The variety of CO2-sensitive chemoreceptors present in air-breathing lower vertebrates adds considerable complexity to experimental studies of ventilatory responses to CO2/pH. Because of the locations, discharge characteristics and reflex effects of the different receptor groups, most air-breathing lower vertebrates show different responses to increases in CO2/[H+] due to cerebral ischemia, anoxia, metabolic acidosis and environmental hypercarbia. In some cases the differences are only quantitative, while in other cases the responses are qualitatively very different. These differences appear to reflect differences in the relative strength of the reflexes elicited by the various receptor groups and the net sum of their modulating influences when CO2/pH are altered via different routes. Although the situation is simpler in the higher vertebrates, in all cases the input from all of the CO2/[H+]-sensitive receptors appears to act as a biasing input which summates with other afferent information to modulate respiratory motor output, even in those species that breathe intermittently.