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

Rats were exposed to 11% CO2 in air for 15 min or 3 h and measurements made of ventilation, CSF acid-base values, and blood, CSF and brain electrolytes. Brain tissue HCO3- was studied by performing CO2 titration curves of tissue homogenates in vitro, the upward displacement of these curves reflecting the non-physico-chemical buffer mechanisms prominent in sustained hypercapnia. At 15 min, the CO2 induced increase in [HCO3-] was accompanied in CSF by an equimolar increase in [Na+] and in brain tissue by an increase in [K+]. At 3 h, the further increase in [HCO3-] was accompanied in CSF by a smaller increase in [Na+] and a decrease in [Cl-] and in brain tissue, there were no longer any significant changes in monovalent ions. In brain, the immediate pH regulatory response to hypercapnia appears to involve physico-chemical buffering and an ionic exchange with blood while by 3 h, the further increase in cell HCO3- must reflect altered cell metabolism. In CSF, the immediate increase in [Na+] and [HCO3-] is probably via choroid plexus while by 3 h, the CSF [HCO3-] increase could reflect exchange with blood at non-choroidal sites or to a less likely extent exchange with brain cells. CSF and brain cell pH regulation is reflected in ventilation which is lower at 3 h than at 15 min of CO2 exposure.
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PMID:Brain and cerebrospinal fluid ionic composition and ventilation in acute hypercapnia. 677 43

Using flat-surface pH electrodes we continuously measured changes in the brain surface pH during respiratory arrest in anesthetized and paralyzed dogs which were previously ventilated with pure oxygen. Respiratory arrest was induced by halting the respirator. The mean arterial PO2 fell from 502.7 +/- 15.9 (1 SD) to 23.7 +/- 18.5, and the mean arterial PCO2 rose from 36.4 +/- 3.5 to 80.4 +/- 7.1 mm Hg, 10 min after asphyxia. The arterial blood pressure increased gradually over several minutes but fell relatively abruptly and profoundly at the end, due to circulatory failure. Initially, and as long as the arterial blood pressure and, therefore, cerebral blood flow were upheld (phase 1), changes in the brain surface pH were small (delta pH/delta t= -0.026 pH unit/min) in spite of severe hypercapnia. When cerebral perfusion pressure fell due to circulatory failure (phase 2), cerebral ischemia occurred and there was an abrupt fall in brain surface pH (delta pH/delta t= -0.067 pH unit/min). Changes in cisternal CSF [H+] grossly underestimated the magnitude of brain surface acidosis during the period of respiratory arrest; the initial difference between the mean brain surface fluid and cisternal CSF [H+] which was 8.9, rose to 15.1 and 47.4 nmol/L, respectively, 5 and 10 min after asphyxia. Changes in sagittal venous blood acid-base variables were more pronounced than those observed in the arterial blood or cisternal CSF; 5 min after respiratory arrest, arterial and sagittal venous blood and cisternal CSF and brain surface pH were 7.20, 7.09, 7.19 and 7.11, respectively. We conclude that (1) in the course of respiratory arrest cerebral outcome can potentially be determined by circulatory failure as evidenced by simultaneous changes in the arterial blood pressure and brain surface pH; (2) cisternal CSF acid-base changes lag behind those on the brain surface and CSF analyses provide unreliable information about the severity of brain acid-base changes during asphyxia; (3) changes in cerebral venous blood acid-base variables best represent the severity of metabolic aberrations in the brain during respiratory arrest.
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PMID:Changes in the brain surface pH and cisternal cerebrospinal fluid acid-base variables in respiratory arrest. 683 98

Ventilatory adaptation to CO2 has been related to a return toward normal pH via an increase in CSF and arterial [HCO3(-)]. To examine whether the overall brain tissue can contribute HCO3(-) to surrounding fluids, we measured the in vitro CO2 buffer value (beta CO2) of control and hypercapnic rat brain homogenates and compared values with reported in vivo data. Hypercapnic rats were exposed to 7% CO2 for 3 days or 1 week. Brain homogenate was continuously tonometered for 3 h at 37 degrees C with 2%, 5% and 15% CO2 in O2. In addition, we used KOH to determine the brain buffering in the pH range 6.8-10.25. During CO2 titration, [HCO3(-)] increased gradually with time up to 90 min by about 10-15%, but the increase was blocked by a metabolic inhibitor, NaF, beta CO2, estimated per kg brain tissue from the dilute homogenate, ranged between 23.4 +/- 2.7 (SD) in controls and 26.0 +/- 1.3 meq/pH in the 7 day group, which were not significantly different. Over the same 7 days, CO2 dissociation curves were shifted upwards with similar slopes by about 6 ml/100 g tissue in association with a rise in pH of about 0.06, consistent with an accumulation of HCO3(-) without any change in buffers. No significant differences between groups were found from KOH titration curves, either in slope or position, consistent with lack of alteration in buffers as well. In vitro brain tissue beta CO2 (about 25) was less than reported in vivo values in the literature (around 40), possibly because H+ adjustments by whole body occur so rapidly in vivo. In addition, other investigators demonstrated that a major part of the increased brain cell [HCO3(-)] in prolonged hypercapnia could not be accounted for by the fixed acid production (Acta Physiol. Scand. 83: 344, 1971). By assuming the in vitro beta CO2 measures the available non-carbonic buffers, the data may be interpreted as showing that the overall brain tissue accumulates HCO3(-) from surrounding fluid during hypercapnia.
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PMID:In vitro buffer value of brain tissue during prolonged hypercapnia. 715 28

During most intracranial procedures, the microscope is used to allow the surgeon to work on structures which are deeply located in the brain. Under these circumstances, brain retraction is required for adequate exposure. It was rapidly suspected and later confirmed that brain retraction causes secondary brain damage. This is due not only to direct effect of the retractor on the cortical surface, but also because a pressure is generated under the retractor, on the brain tissue, which compromises local cerebral blood flow and local cerebral perfusion pressure, thus causing cerebral ischaemia. The need for retraction is increased if the lesion is located deeply and/or if the brain is tensed; thus the risk to generate ischaemic conditions is enhanced. These secondary surgical lesions are promoted and worsened by associated systemic conditions such as hypotension, hypoxaemia, hypercapnia. As an attempt to respond to the problem generated by surgical retraction, the "chemical brain retractor" concept is proposed. By compulsively rendering the brain as relaxed and compliant as possible, the chemical brain retractor should allow the surgeon to operate on without the use of a surgical brain retractor and, if such a retractor is still needed, to reduce the pressure under it. These goals are achieved with an osmotic agent like mannitol to improve brain compliance, and intravenous anaesthetic agents, moderate hypocarbia and a normal or elevated blood pressure, to minimize cerebral blood volume. In conjunction with the chemical brain retractor, two other manoeuvres should be used to enhance cerebral compliance: CSF drainage and moderate head up position during the procedure.
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PMID:[Neuro-anesthetic contribution to the prevention of complications caused by mechanical cerebral retraction: concept of a chemical brain retractor]. 767 88

Control of physiological parameters such as respiration, blood pressure, and arterial blood gases has been difficult in the mouse due to the lack of technology required to monitor these parameters in small animals. Here we report that anesthetized and artificially ventilated mice can be maintained under physiological control for several hours with apparently normal cerebrovascular reactivity to hypercapnia and mechanical vibrissal stimulation. SV-129 mice were anesthetized with urethane (750 mg/kg i.p.) and alpha-chloralose (50 mg/kg i.p.), intubated, paralyzed, and artificially ventilated. Respiratory control was maintained within physiological range by reducing the inspiratory phase of the respiratory cycle to < 0.1 s and by adjusting end-tidal CO2 to give a PCO2 of 35 +/- 3 mm Hg. In these mice, mean arterial pressure (95 +/- 9 mm Hg), heart rate (545 +/- 78 beats/min), and arterial pH (7.27 +/- 0.10) could be maintained for several hours. Body temperature was kept at 36.5-37.5 degrees C. We observed stable regional CBF (rCBF) measurements (as determined by laser-Doppler flowmetry) when systemic arterial blood pressure was varied between 40 and 130 mm Hg. Hypercapnia led to a 38 +/- 15% (5% CO2) and 77 +/- 34% (10% CO2) increase in rCBF. Mechanical stimulation of contralateral vibrissae for 1 min increased rCBF by 14 +/- 4%. Changes in rCBF compare favorably with those observed previously in another rodent species, the Sprague-Dawley rat. After placement of a closed cranial window, cerebrovascular reactivity to hypercapnia and whisker stimulation was intact and well maintained during 2-h superfusion with artificial CSF.
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PMID:Cerebrovascular responses under controlled and monitored physiological conditions in the anesthetized mouse. 779 Apr 12

We have extracellularly recorded single neuron activity in the ventral medulla of the isolated brain stem-spinal cord preparation of the neonatal rat (37 preparations) in order to test their sensitivity to changes in CO2/H+. Search for neuronal activity was performed when the preparation was superfused with control mock CSF (equilibrated with 2% CO2, 90% O2 in N2; pH = 7.8 at 27 degrees C). Neurons, found down to about 500 microns from the surface, could be classified as R neurons when they showed rhythmic discharge in phase with phrenic activity, recorded from C4 ventral roots; or as Non-R neurons when they did not exhibit such phasic discharge. Among the 89 Non-R neurons, 20 responded to rapidly replacing the control CSF by hypercapnic CSF (8% CO2, 90% O2 in N2; pH = 7.2) with increased, 44 with reduced activity, while 25 did not respond to hypercapnia. Five Non-R neurons became phasic with respiration during hypercapnia. Of the 14 R neurons, 10 fired predominantly in expiration (R-E), 4 in inspiration (R-I). Only one R-E and two R-I neurons were excited by hypercapnia, the remaining were either inhibited or did not respond. Excited Non-R and R neurons were mainly encountered in rostral parts of those areas in the ventral medulla that have been reported as chemosensitive.
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PMID:Hypercapnia and medullary neurons in the isolated brain stem-spinal cord of the rat. 823 31

The central chemoreceptor drive to ventilation was assessed in unanesthetized toads, Bufo paracnemis, exposed to three different temperatures: 15, 25 and 35 degrees C. The acid-base status of the fourth ventricle was manipulated by mock CSF perfusion. In additional experiments, arterial pH was varied by inspiration of hypercapnic gas mixtures. Ventilation was measured directly by pneumotachography and arterial blood samples were analyzed using electrodes for pH and PO2. Regardless of temperature, the ventilatory control of acid-base status was predominantly central. Moreover, an increase in temperature was accompanied by a proportional increase in the ventilatory response to chemoreceptor stimulation by either lowered mock CSF pH or hypercapnia. The alphastat hypothesis could not adequately account for the temperature effects on the ventilatory responses to hypercapnia or on air convection requirements in the toad.
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PMID:Temperature and central chemoreceptor drive to ventilation in toad (Bufo paracnemis). 823 32

We tested the hypothesis that the CBF response to extracellular acidosis is mediated by nitric oxide (NO). A closed cranial window, superfused with artificial CSF (aCSF), was implanted over the parietal cortex in anesthetized and ventilated Wistar rats. Regional cerebral blood flow (rCBF) was measured continuously with laser-Doppler flowmetry (LDF). The reaction of rCBF to hypercapnia (PaCO2 from 30.5 +/- 1.8 to 61.3 +/- 5.8 mm Hg by adding CO2 to the inspiratory gas) was 2.9 +/- 1.4%/mm Hg, and the reaction of rCBF to H+ (superfusion of acidic aCSF, pH 7.07 +/- 0.05) was 101.7 +/- 24.7%/pH unit. The regional NO synthase (NOS) activity was blocked by superfusing aCSF containing 10(-3) M N omega-nitro-L-arginine (L-NA, n = 10). After 30 min of L-NA superfusion, rCBF was reduced to 80.1 +/- 6.5% of baseline, and the rCBF responses to hypercapnia (PaCO2 from 30.9 +/- 2.9 to 58.8 +/- 7.7 mm Hg) and extracellular acidosis (aCSF pH 7.08 +/- 0.06) were reduced to 0.8 +/- 1.1%/mm Hg and 10.1 +/- 23.0%/pH unit, respectively (both p < 0.001). This effect was stereospecific since aCSF containing 10(-3) M N omega-nitro-D-arginine affected neither baseline rCBF nor the response to H+ (n = 5). The NOS blockade did not affect the vasodilatation by the NO donor sodium nitroprusside (n = 5, 114.3 +/- 25.1% before vs. 130.2 +/- 24.7% after NOS blockade). The results confirm the involvement of NO in the CBF reaction to hypercapnia and demonstrate for the first time that NOS blockade also strongly attenuates the H+ response of the cerebral vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blockade of nitric oxide synthesis in rats strongly attenuates the CBF response to extracellular acidosis. 847 12

Standardized volume-pressure craniospinal system loadings based on physiological loadings were developed in order to study the CSF outflow route efficiency and to evaluate the intracranial volume-pressure relations. The study was carried out on 10 cats. Standardized abdominal compression was applied in order to produce a central venous pressure increased and subsequently ICP increase to the level of 20 and 30 mmHg for 2 minutes. The abdominal compression test seems to be useful in the CSF outflow route evaluation. The orthostatic changes were studied in control animals and in cats with an epidural balloon. The animal body was evaluated to an angle of 50 degrees and 80 degrees with the head directed upwards and downwards. This test was found suitable for the intracranial volume reserve estimation. Similar application, especially in experimental conditions can be found in the hypercapnia test. PaCO2 concentration was increased by means of respiration with a gas mixture containing 5% CO2. A steady increase of ICP of 9 +/- 1 mmHg was obtained. Vascular dilatation resulted in an intracranial volume loading. The ICP response in subjects with normal CO2 response can be related to the intracranial volume reserve. The studies performed show the usefulness of the standardized volume-pressure loadings. The loadings applied are more physiological than lumbar infusion tests used so far.
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PMID:Evaluation of craniospinal system condition using standardized volume-pressure loadings. 874 65

Endogenous opioid peptides are present in cerebral perivascular nerves and in the CSF, and their concentrations are changing in response to stimuli that activate regulatory mechanisms of the cerebral circulation (e.g., alterations of the perfusion pressure or changes of the arterial O2 tension). Opiate receptors are expressed in the cells of the CNS and the cerebrovascular bed, and their activation modulates the function of other vasoregulatory mechanisms (i.e., the autonomic nervous system, nitric oxide, prostanoids, vasopressin) that are involved in the control of the cerebrovascular tone. The direct vasomotor effects of opioid peptides and opiates on the cerebral arteries under in vitro or in situ conditions appear to be weak or absent in several species. However, Met- and Leu-enkephalin induce pial arterial vasodilation in the newborn pig. In this species, beta-endorphin acts as a constrictor, whereas dynorphin may induce either dilation or constriction depending on the experimental conditions. The influence of exogenously applied natural and synthetic opioids on the cerebral blood flow (CBF) is determined mainly by their metabolic, neuronal, and respiratory effects. Hypothalamic and pituitary circulations are especially sensitive to opioids. Under resting conditions, endogenous opioid peptides do not participate in the regulation of the cerebrovascular tone and CBF. On the other hand, mu and delta opiate receptor stimulation by endogenous opioid peptides, interacting with other vasoactive factors, obviously contributes to the hypoxia- and hypercapnia-induced cerebral vasodilation. Furthermore, endogenous opioid mechanisms are involved in the autoregulation of the hypothalamic blood flow. Thus, the endogenous opioid system may well represent a latent regulatory mechanism, which is of limited importance under basal conditions, but becomes more important under conditions of stress. Synthetic exogenous opioids do not appear to influence the hypoxic or hypercapnic CBF responses or the cerebral autoregulatory process.
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PMID:Opiate receptor-mediated mechanisms in the regulation of cerebral blood flow. 896 68


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