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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regional cerebral blood flow (CBF) was measured in isoflurane-anesthetized turtles (Pseudemys scripta) by the hydrogen clearance method. Teflon-coated platinum electrodes (25 microns) were implanted in the olfactory bulbs, midcerebral cortex and cerebellum in eight adult turtles. The electrodes were voltage clamped at +0.30 V relative to a Ag-AgCl electrode implanted in the dorsal neck muscles. Washout kinetics of H2 gas administered via controlled ventilation was used to calculate local blood flow for electrodes exhibiting monoexponential washout kinetics of hydrogen (92 of 104 determinations). Data were obtained in animals with body temperatures of 15, 25, and 35 degrees C under normocapnic conditions during ventilation with 21% O2 and during ventilation with 100% N2. During normoxia, mean blood flows were 1.9 +/- 0.8, 5.0 +/- 1.9, and 6.1 +/- 1.3 (+/- SD) ml.100 g-1.min-1 at 15, 25, and 35 degrees C, respectively. There were no differences between CBF values in the different brain regions. During 1-3 h of anoxia, CBF was 3.0 +/- 2.1, 7.0 +/- 3.7, and 6.6 +/- 2.9 ml.100 g-1.min-1 at 15, 25, and 35 degrees C, respectively (normoxia-anoxia difference not statistically different). Hypercarbia (ventilation with 10-20% CO2 in air or N2), or the transition from anoxia to normoxia, increased CBF up to 80% at each of these temperatures. Maintenance of CBF during anoxia likely contributes to the anoxia tolerance of the turtle brain.
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PMID:Effects of temperature and anoxia on regional cerebral blood flow in turtles. 155 24

The widespread, heterogeneous distribution of opiate receptors and their endogenous ligands in the nervous system are reflective of the variety of central and systemic effects seen after opiate administration. Most neurons respond to either systemic or local opiate application with a decrease in firing rate, although increased neuronal activity has also been reported in such regions as the caudate, amygdala, ventral tegmentum, and substantia nigra. While regional metabolic studies have consistently reported neuronal suppression, some portion of this might be secondary to systemic hypercapnia. Using a brief blood flow marker, we recently reported a heterogenous increase in activity in more than half of the brain regions examined. To extend that study, we report herein the results of a dose-response and antagonist challenge experiment. Rats received an acute injection of one of the following: heroin (0.1, 0.3 or 1.0 mg/kg), naloxone (1.0 mg/kg), a cocktail of heroin (0.3 mg/kg) plus naloxone or saline. One min after drug administration, 160 muCi/kg [1-14C] octanoate, a marker for cerebral blood flow, was delivered IV. Rats were sacrificed two min later, brains removed and prepared for autoradiography. Of the fifty-eight areas analyzed, heroin caused an increase in blood flow in the caudate, claustrocortex, laterodorsal thalamus and dentate gyrus. Decreases were found for the bed nucleus of the stria terminalis, preoptic area, basolateral nucleus of the amygdala, dorsomedial and paraventricular hypothalamus, entorhinal and cingulate cortices and dorsal raphe. Naloxone resulted in significant increases in the olfactory tubercle and paraventricular nucleus while decreases were seen in the cingulate and basolateral amygdala.
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PMID:Effects of heroin and naloxone on cerebral blood flow in the conscious rat. 180 37

Breathing was monitored during normocarbia, hypercarbia (6% CO2 in air), and the period immediately after the return to normocarbic conditions in intact, olfactory-denervated, and vagotomized bullfrogs. In intact frogs, ventilation increased during hypercarbia, but the breathing pattern remained episodic. Immediately upon return to air, there was a further paradoxical increase in breathing frequency, and breathing became continuous in most frogs. Results obtained from animals after olfactory receptor denervation indicate that tonic stimulation of olfactory receptors by airway CO2 inhibited breathing during hypercarbia. Measurements of the kinetics of changes in airway and arterial blood CO2 levels support the suggestion that the sudden release of this inhibition on the return to normocarbic conditions was responsible for the posthypercarbic hyperpnea. Vagotomy increased ventilation during normocarbia. Hypercarbia now caused a change in breathing pattern but had no net effect on total ventilation, suggesting that pulmonary vagal feedback inhibited ventilation during normocarbia but stimulated ventilation during hypercarbia. Although olfactory and pulmonary receptor feed-back shape the breathing pattern, they were not responsible for initiating or terminating the episodes of breathing.
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PMID:CO2-sensitive olfactory and pulmonary receptor modulation of episodic breathing in bullfrogs. 876 95

The osphradium of the pond snail Lymnaea stagnalis was studied to determine the stimuli to which this organ responds. The following stimuli were tested: hypoxia, hypercapnia, a mixture of amino acids, a mixture of citralva and amyl acetate and a mixture of lyral, lilial and ethylvanillin. The mean nerve activity consistently increased with elevated PCO2, whereas hypoxia produced variable effects. The nerve activity became rhythmic upon application of citralva and amyl acetate, but it increased in a non-rhythmic way upon application of the other two odorant mixtures tested. Whole-cell patch-clamp recordings were made from a group of 15 neurones that lay next to the issuing osphradial nerve, to determine whether ganglion cells were involved in olfactory signal processing. All neurones tested responded to at least one of the three mixtures of odorants. Both excitatory and inhibitory responses occurred. Our results indicate that the osphradium of the pond snail Lymnaea stagnalis is sensitive to elevated PCO2 as well as to three different classes of odorants. In addition, at least some neurones within the osphradium are involved in the processing of olfactory information.
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PMID:Chemosensitivity of the osphradium of the pond snail Lymnaea stagnalis 931 49

In a previous study, complete denervation of the gills in the tambaqui Colossoma macropomum did not eliminate the increase in breathing amplitude seen during exposure of this species to hypoxia. The present study was designed to examine other sites of putative O(2)-sensitive receptors that could be involved in this reflex action. Superfusion of the exposed brain of decerebrate, spinalectomized fish did not reveal the presence of central chemoreceptors responsive to hyperoxic, hypoxic, hypercarbic, acidic or alkaline solutions. Subsequent central transection of cranial nerve IX and X, removing not only all innervation of the gills but also sensory input from the lateral-line, cardiac and visceral branches of the vagus nerve, did not eliminate the increase in breathing amplitude that remained following peripheral gill denervation alone. Administration of exogenous catecholamines (10 and 100 nmol kg(-1) adrenaline) to fish with intact brains and minimal surgical preparation reduced both respiratory frequency and amplitude, suggesting that humoral release of adrenaline also could not be responsible for the increase in breathing amplitude that remained following gill denervation. Denervation of the mandibular branches of cranial nerve V and the opercular and palatine branches of cranial nerve VII in gill-denervated fish (either peripheral gill denervation or central section of cranial nerves IX and X), however, did eliminate the response. Thus, our data suggest that hypoxic and hyperoxic ventilatory responses as well as ventilatory responses to internal and external injections of NaCN in the tambaqui arise from O(2)-sensitive receptors in the orobranchial cavity innervated by cranial nerves V and VII and O(2)-sensitive receptors on the gills innervated by cranial nerves IX and X. Our results also revealed the presence of receptors in the gills that account for all of the increase in ventilation amplitude and part of the increase in ventilation frequency during hyperoxic hypercarbia, a group or groups of receptors, which may be external to the orobranchial cavity (but not in the central nervous system), that contribute to the increase in ventilation frequency seen in response to hyperoxic hypercarbia and the possible presence of CO(2)-sensitive receptors that inhibit ventilation frequency, possibly in the olfactory epithelium.
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PMID:Extrabranchial chemoreceptors involved in respiratory reflexes in the neotropical fish Colossoma macropomum (the tambaqui). 1204 35

In many species of air-breathing vertebrates CO2-sensitive airway receptors play an important role in ventilatory control. In ectotherms, olfactory receptors often inhibit breathing and prolong breath holding when environmental CO2 levels are high. CO2/H+ sensitive pulmonary receptors (intra pulmonary chemoreceptors (IPC) and pulmonary stretch receptors (PSR)) regulate breathing patterns in all vertebrates in a manner that reduces dead space ventilation and enhances the efficiency of CO2 excretion under conditions of environmental hypercarbia, and/or reduces CO2 loss from hyperventilation. The greater CO2 sensitivity of IPC may allow them to also serve as a venous CO2 receptor (at least transiently when levels of metabolically produced CO2 begin to rise), prevent alkalosis during hyperpnea/polypnea, and may have contributed to the evolution of the extremely thin air/blood barrier and increased diffusion capacity associated with the rigid avian lung. The presence of all three receptor groups with different degrees of CO2 sensitivity in most reptiles, however, gives rise to what appear to be anomalous responses to environmental CO2.
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PMID:Evolutionary trends in airway CO2/H+ chemoreception. 1555 2

The hypercapnic drive to breathe in amphibians is generally greater than hypoxic ventilatory drive and a variety of interdependent control systems function to regulate both the hypoxic and hypercapnic ventilatory responses. During exposure to hypercapnic conditions, breathing increases in response to input from central chemoreceptors (sensitive to CSF pH/CO(2) levels) and peripheral chemoreceptors (sensitive to arterial blood O(2) and CO(2)). On the other hand, olfactory CO(2) receptors in the nasal epithelium inhibit breathing during exposure to acute hypercapnia. Further complexity arises from the CO(2)-sensitive nature of the pulmonary stretch receptors (PSR) which provide both tonic (stimulates lung inflation at low lung volumes; deflation at higher volumes) and phasic (generally excitatory) feedback. This review focuses on interactions between the various populations of chemoreceptors and interactions between chemoreceptors and PSR. Differences between various levels of experimental reduction (i.e., in vitro; in situ; in vivo) are highlighted as are the effects of chronic respiratory challenges on acute hypoxic and hypercapnic chemoreflexes.
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PMID:Chemoreceptor and pulmonary stretch receptor interactions within amphibian respiratory control systems. 1650 4

Anuran amphibians have multiple populations of pH/CO2-sensitive respiratory-related chemoreceptors. This study examined in cane toads (Bufo marinus) whether chronic hypercapnia (CHC) altered the pH/CO2 sensitivity of central respiratory-related chemoreceptors in vitro and whether CHC altered the acute hypercapnic ventilatory response (HCVR; 5% CO2) in vivo. Toads were exposed to CHC (3.5% CO2) for 9 days. In vitro brainstem-spinal cord preparations were used to examine central respiratory-related pH/CO2 chemosensitivity. CHC augmented in vitro fictive breathing as the pH of the superfusate was lowered from 8.2 to 7.4. Midbrain transection in vitro (at a level known to reduce the clustering of breaths) did not alter this augmentation. In vivo, CHC did not alter the acute HCVR but midbrain transection changed the breathing pattern and increased the overall level of ventilation. CHC did not alter the effect of olfactory CO2 chemoreceptor denervation on the acute HCVR in vivo but did alter the response when returned to normal air. The results indicate that CHC increases the response of central pH/CO2 chemoreceptors to changes in cerebrospinal fluid pH in vitro yet this increase is not manifest as an increase in the HCVR in vivo.
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PMID:Chronic hypercapnia modulates respiratory-related central pH/CO2 chemoreception in an amphibian, Bufo marinus. 1651 40

The goal of this study was to examine the role of respiratory-related afferent input on the chronic hypercapnia (CHC)-induced increase in central respiratory-related pH/CO2 chemosensitivity in cane toads (Bufo marinus). Toads were exposed to CHC (3.5% CO2) for 10 days, following which in vitro brainstem-spinal cord preparations were used to assess central respiratory-related pH/CO2 chemosensitivity. Motor output from the vagus nerve root was used as an index of breathing (fictive breathing). Olfactory denervation (OD), prior to exposure to CHC, was used to remove the influence of CO2-sensitive olfactory chemoreceptors, which inhibit breathing. Exposure to chronic hyperoxic hypercapnia (CHH) was used to reduce the level of arterial chemoreceptor input compared with CHC alone. In vivo experiments examined the effects of CHC, CHH and OD on the acute hypercapnic ventilatory response of intact animals. In vitro, a reduction in artifical cerebral spinal fluid (aCSF) pH increased fictive breathing in preparations taken from control and CHC animals. CHC caused an increase in fictive breathing compared with controls. OD and CHH abolished the CHC-induced augmentation of fictive breathing. In vivo, CHC did not cause an augmentation of the acute hypercapnic ventilatory response. CHH reduced the in vivo acute hypercapnic ventilatory response compared with animals exposed to CHC. In vivo, OD reduced breathing frequency and increased breath amplitude in both control and CHC animals. The results suggest that afferent input from olfactory and arterial chemoreceptors, during CHC, is involved in triggering the CHC-induced increase in central respiratory-related pH/CO2 chemosensitivity.
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PMID:Afferent input modulates the chronic hypercapnia-induced increase in respiratory-related central pH/CO2 chemosensitivity in the cane toad (Bufo marinus). 1721 Sep 60

Cerebral hypoxia has been proposed as a mechanism by which prenatal ethanol exposure causes fetal alcohol spectrum disorder (FASD) in children, but no study had tested this hypothesis using a chronic exposure model that mimicks a common human exposure pattern. Pregnant sheep were exposed to ethanol, 0.75 or 1.75 g kg(-1) (to create blood ethanol concentrations of 85 and 185 mg dl(-1), respectively), or saline 3 days per week in succession (a 'binge drinking' model) from gestational day (GD) 109 until GD 132. Fetuses were instrumented on GD 119-120 and studied on GD 132. The 1.75 g kg(-1) dose resulted in a significant increase in fetal biventricular output (measured by radiolabelled microsphere technique) and heart rate, and a reduction of mean arterial pressure and total peripheral resistance at 1 h, the end of ethanol infusion. The arterial partial pressure of CO(2) was increased, arterial pH was decreased and arterial partial pressure of O(2) did not change. Fetal whole-brain blood flow increased by 37% compared with the control group at 1 h, resulting in increased cerebral oxygen delivery. The elevation in brain blood flow was region specific, occurring preferentially in the ethanol-sensitive cerebellum, increasing by 44% compared with the control group at 1 h. There were no changes in the lower dose group. Assessment of regional differences in the teratogenic effects of ethanol by stereological cell-counting technique showed a reduced number of cerebellar Purkinje cells in response to the 1.75 g kg(-1) dose compared with the control brains. However, no such differences in neuronal numbers were observed in the hippocampus or the olfactory bulb. We conclude that repeated exposure to moderate doses of ethanol during the third trimester alters fetal cerebral vascular function and increases blood flow in brain regions that are vulnerable to ethanol in the presence of acidaemia and hypercapnia, and in the absence of hypoxia.
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PMID:Chronic ethanol increases fetal cerebral blood flow specific to the ethanol-sensitive cerebellum under normoxaemic, hypercapnic and acidaemic conditions: ovine model. 1782 57


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