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

Anesthetized spontaneously breathing rats, fitted with epicortical electrodes and catheters for sampling arterial, venous, and cerebral venous blood, were exposed to standardized progressive hypoxia. Three minutes of hypoxia sequentially caused hyperpnea, hypopnea, apnea, and cessation of electrocorticogram "spiking," of synchronization, and of background in electroencephalogram (EEG). Blood data and cerebral blood flow and metabolism were measured throughout and at "insults," i.e., at apnea and cessation events, to clarify their interdependence. Arterial and brain venous PO2 fell linearly with inspired oxygen (final value of 2% at 280 s). Hyperpnea induced arterial alkalosis; subsequent hypopnea led to near-normal PCO2 and pH when EEG ceased. Hypercapnia was more pronounced in cerebral than in systemic venous blood; time courses of pH changes were similar. Sagittal sinus blood pressure and outflow were linearly related and resembled the time course of local cerebral blood flow. Blood flow increased by 25% at apnea and only 60% at EEG silence. Cerebral metabolic rate of O2 rose during the hyperpnea phase and fell exponentially thereafter. Cerebral glucose uptake and lactate release increased within the first 3 min but fell abruptly when cortico-electric spiking ceased. Time courses of cerebral O2 consumption and spike rate were linearly related; both showed inverse linear relations to cerebral perfusion. The hypoxic insults were well defined by blood data; critical PO2 values were lower than previously assumed. This model is proving to be a useful, controlled method by which mechanisms of cerebral hypoxia tolerance may be studied in vivo.
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PMID:Progressive hypoxia until brain electrical silence: a useful model for studying protective interventions. 324 75

Symmetries and asymmetries in regional cerebral blood flow (rCBF) determinations are reported in eleven patients with symptomatic carotid artery occlusive disease. Flourine-18-fluoromethane rCBF values are obtained by means of a noninvasive positron emission tomographic (PET) technique during room air (RA) and following induced hypercapnia (CO2). Areas of abnormal CO2 reactivity predict both the hemodynamic significance of the vascular lesion in question and the areas most vulnerable for ischemic infarction. This data is intended to be preliminary in nature; future expansions of this data base will be made to include rCBF/CO2 estimations, rCBF/glucose metabolism determinations, and rCBF/"reserve" evaluations over time and following brain-specific therapies. Once established, the potential viability and reversibility of these ischemic, uninfarcted or minimally infarcted areas can then be reestablished over time, thus providing a quantitative measure of the natural history of flow/metabolic coupling or uncoupling.
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PMID:The study of cerebral ischemic reversibility: Part II. Preliminary preoperative results of fluoromethane positron emission tomographic determination of perfusion reserve in patients with carotid TIA and stroke. 350 24

The extreme elevation in plasma levels of free norepinephrine (NE) and free epinephrine (EP), which occurs during forced diving of ducks (Anas platyrhynchos), was studied before and after denervation of the adrenal glands. In intact animals both NE and EP concentration increased by up to two orders of magnitude in a 4-min dive but by a significantly lesser amount if the duck breathed O2 before the dive. Denervating the adrenal glands reduced the amounts of both catecholamines (CA) released during dives, plasma EP decreased to 10%, and NE to 50% of values obtained before denervation. Breathing O2 before a dive virtually eliminated CA release in denervates, indicating that hypoxia was the important non-neural releasing agent. Hypoxia was also the most important neural releasing agent compared with hypercapnia, acidosis, or hypoglycemia. Adrenal denervation did not cause significant changes in heart rate, blood pressure, arterial blood gas tensions, pH, or plasma glucose during dives, although denervation caused increased variation in some of these variables. In ducks CA release in dives is largely due to decreasing arterial O2 partial pressure, and full expression of the response is dependent on intact innervation of the adrenal gland.
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PMID:Adrenal gland denervation and diving in ducks. 359 85

The intrinsic processes involved in the initiation and arrest of seizures are not completely understood. Cortical and cerebellar inhibitory mechanisms, accumulation of metabolic products, and glial uptake of extracellular potassium (K+o), anions, and released neurotransmitters are all important processes that limit focal firing and terminate a seizure once it has been initiated. Of these, the intrinsic cortical inhibitory mechanisms--i.e., recurrent and surround inhibition--appear to be the most important. Active cation and anion transport processes are two metabolic events that have yet to be elucidated but clearly could be involved in terminating a seizure discharge. For example, without an active mechanism to transport chloride, opening of the chloride channel by the inhibitory transmitter GABA would not result in increased chloride permeability. The transient hypoxia and hypercapnia and lactic acidosis that follows a severe tonic-clonic seizure produces a mixed systemic metabolic and respiratory acidosis. In experimental animals, the hypercapnia that results is sufficient to block seizure discharges. Increasing the CO2 concentration significantly reduces the extension to flexion (E/F) ratio of mice given maximal electroshock seizures (MES) and increases the time required for 50% of the animals to recover sufficiently from a first MES to be able to have another MES. The decreased E/F ratio and the increased recovery time (RT50) are both indicative of a decrease in seizure activity. Since the extent to which CO2 is allowed to accumulate in the brain is regulated by the glial specific enzyme carbonic anhydrase (CA), it follows that the glial cell has an integral role in the mechanisms involved in arresting seizure activity. In contrast, hypoxia increased the E/F ratio and decreased the RT50, evidence that seizure activity was enhanced. Another metabolic factor affecting duration of seizure activity, susceptibility to seizures, and recovery from seizures is glucose. Recovery from seizures depends in part on an adequate supply of this energy source. An inverse correlation (R = 0.95) between RT50 and blood sugar was found when the blood sugar was altered experimentally by treatments that altered the endocrine status (pancreatectomy, treatment with alloxan, cortisol, insulin, glucagon, and dextrose). Since glial cells contain (as glycogen) the small amount of glucose present in the brain, they probably hasten the ability of the brain to recover normal function following a seizure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of glial cation and anion transport mechanisms in etiology and arrest of seizures. 370 23

The relative importance of pCO2 versus pH in regulating myocardial blood-flow (MBF) is not settled. Therefore, the influence of hypocapnia, hypercapnia and sodium carbonate infusion, on MBF and myocardial metabolism, has been investigated in 10 closed-chest pentobarbital anaesthetized dogs. The animals were hyperventilated, and CO2 was added to the inspiratory gas to induce normocapnia and hypercapnia. A mass spectrograph continuously measured the ventilatory gas components, and MBF was measured by the hydrogen desaturation technique with a catheter positioned in the coronary sinus. During the experiments, there were no significant alterations in heart rate, mean aortic blood-pressure, myocardial oxygen consumption or uptake of glucose and free fatty acids. During hypocapnia MBF was insignificantly reduced, while myocardial oxygen extraction increased significantly. During hypercapnia, however, MBF increased more than 40%. This increase in MBF was abolished following an infusion of sodium carbonate. Thus, in the present study, increased MBF, observed during hypercapnia, was due to the reduction in pH and not to the increase in pCO2.
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PMID:Effects of carbon dioxide and pH on myocardial blood-flow and metabolism in the dog. 393 53

Extracellular pH changes were measured in the superfused cat carotid body with double barreled pH glass microelectrodes, under constant pH (7.45 +/- 0.02), temperature (35 degrees C) and flow (3.6 ml/min) of the superfusion medium. Changes of pO2 in the medium from about 188 Torr (30% O2) to 35 or 12 Torr (5% and 2% respectively) called hypoxia, induced a change of the pH signal of about 0.1 units indicating acidification of the tissue. Medium pH monitored with a pH macroelectrode did not change during hypoxic stimulation. An increase of pCO2 in the medium from about 20 Torr (3% CO2, pH 7.45 +/- 0.02) to 70 Torr (12% CO2, pH 6.98 +/- 0.01) called hypercapnia, under constant pO2 (188 +/- 2 Torr), temperature (35 degrees C) and flow (3.6 ml/min) resulted in acidification of the tissue of about 0.3 pH units. Extracellular pH changes during hypoxia did not occur when the superfusion medium had no glucose; however, pH changes during hypercapnia persisted under these conditions. The hypoxic and hypercapnic chemosensory response of the sinus nerve were decreased or abolished during glucose deprivation in a time-dependent manner. Replacement of glucose with 2-deoxyglucose in the medium led to a similar pattern, i.e. inhibition of the hypoxic and hypercapnic chemosensory nerve response and of the extracellular hypoxic pH changes. These results indicate that glycolysis takes place and contributes to O2 and CO2-chemoreception in the carotid body.
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PMID:Extracellular pH changes in the superfused cat carotid body during hypoxia and hypercapnia. 404 28

To examine the possible contribution of active H+ secretion mediated by brush border enzymes to proximal tubule HCO-3 absorption, paired reperfusions of surface proximal convoluted tubules were performed with the inhibitor dicyclohexylcarbodiimide (DCCD). In control studies using a solution devoid of HCO-3 but containing 5.5 mM glucose, 1 mM DCCD had no effect on glucose or fluid (Na+) absorption, suggesting that this inhibitor did not interfere with sodium entry at the brush border or mitochondrial energy production (ATP synthesis). In experiments using a perfusion solution containing 18-25 mM HCO-3, DCCD caused a fall in absolute CO2 absorption of approximately 15% under eucapneic conditions and 30% during acute hypercapnia. One millimole per liter amiloride (an inhibitor of the passive Na+-H+ exchanger) caused a 15% inhibition of CO2 absorption during acute hypercapnia and a disproportionately large reduction in fluid (Na+) absorption. The latter was not due to cell poisoning, since 1 mM amiloride had no inhibitory effect on fluid or glucose absorption when a HCO-3-free perfusion solution was used. Addition of 1 mM DCCD to a perfusion solution containing either 10(-3) M amiloride or 10(-4) M acetazolamide caused a significant inhibition of CO2 absorption compared with amiloride or acetazolamide alone. The observations are consistent with the view that in addition to passive Na+-H+ exchange, active transport mediated by either a H+-ATPase or a redox-driven H+ pump in the brush border contributes significantly to HCO-3 absorption in the proximal tubule.
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PMID:Evidence for a DCCD-sensitive component of proximal bicarbonate reabsorption. 406 52

1. In closed-chest dogs anaesthetized with trichlorethylene, the inhalation of carbon dioxide sufficient to increase the arterial P(CO2) from 40 to about 100 mm Hg, increased myocardial blood flow (measured using a (133)Xe clearance technique) and right atrial pressure. There were no consistent changes in mean arterial blood pressure, heart rate or cardiac output.2. The effect of hypercapnia on myocardial blood flow was not influenced by the previous administration of atropine and propranolol or of bretylium. It can be concluded, therefore, that the elevated arterial P(CO2) has a direct vasodilator effect on the myocardial microcirculation.3. During hypercapnia the coronary sinus P(O2) was increased and the coronary arteriovenous oxygen content difference, and calculated myocardial oxygen consumption, reduced. It is suggested that this latter effect may be the result of myocardial depression produced by the decrease in arterial blood pH.4. There was no evidence of myocardial glucose uptake either before or during hypercapnia. The myocardial extraction of lactate and pyruvate at rest varied between 0 and 55%. During acute hypercapnia the extraction of lactate usually fell.5. When the arterial P(CO2) was maintained at 100 mm Hg for a period of 1 hr the effects on myocardial blood flow and on oxygen consumption were not sustained.6. Stepwise increments and decrements in arterial P(CO2) of 10-20 mm Hg produced corresponding increases and decreases in myocardial blood flow and demonstrated that changes in arterial P(CO2) of 20-30 mm Hg can markedly affect blood flow in the myocardium.
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PMID:The effect of hypercapnia on myocardial blood flow and metabolism. 550 Aug 24

The effects of hyperlactatemia on cerebral glucose metabolism of normoglycemic 20-day-old rats were studied in animals breathing air or 20% CO2:21% O2:59% N2. Sodium lactate or sodium bicarbonate were given intraperitoneally, together with a mixture of [3H]deoxyglucose and [2-14C]glucose. Animals were sacrificed in a freeze-blowing apparatus at intervals of 2-15 min after injection. Blood lactate levels in the lactate-injected rats were 4-6 mM. Hyperlactatemia caused a gradual decline in the brain rate of glucose utilization in air-breathing animals to 50-70% of control rates. Results with both tracers were similar. Concentrations of Krebs cycle intermediates and glutamate did not decrease. These findings indicate that lactate can partially replace glucose as an oxidative fuel for developing rat brain. Hypercapnia depressed the rate of glucose utilization by developing brain and rates were 30-40% lower still in lactate-injected hypercapnic rats. Decreases in levels of Krebs cycle intermediates and glutamate were similar in both groups. Thus, lactate and CO2 are additive in their depressant effects on brain glucose utilization. The observation that lactate did not prevent the decreases in Krebs cycle intermediates and glutamate caused by hypercapnic acidosis suggests an inhibition of flux through pyruvate dehydrogenase during hypercapnia. The data from this study, coupled with data on lactate transport across the blood-brain barrier, indicate that the direction of movement of lactate and its rate of utilization by developing brain are functions of its concentration on blood relative to brain. Physiological and pathological conditions which elevate blood lactate levels above those in brain will, then, have a sparing effect upon brain glucose utilization.
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PMID:Effects of lactate on glucose metabolism of developing rat brain. 632 76

Modern ultrasound techniques enable dynamic studies of fetal activity in utero to be studied and quantified. Real-time B-mode scanning has become the method of choice for this purpose because of its ease of use and precision. Fetal movements can be visualized as early as in the seventh week of pregnancy and the development of the movement patterns can be followed throughout the pregnancy. Up to 16 types of movements have been described by several research groups. In early pregnancy, the finding of normal fetal movements is a good prognostic sign in cases of threatened abortion. A decrease in the movement incidence or a qualitative change of the movements are associated with poor outcome. In late pregnancy, the mean incidence of general fetal movements has been found on average to be 9 to 18 per cent of observation time. Fetal breathing movements, mainly with typical "see-saw' configurative changes of the fetal trunk, occur episodically: both long-term and short-term periodicity have been revealed. For recognition of the time incidence pattern of fetal movements or breathing, a sufficiently long observation time (80 to 100 minutes) is necessary. The incidence of fetal breathing movements increases with gestational age and breathing movements become more regular in mature fetuses. Fetal motor activity is subject to several external influences: glucose given to the mother causes an increase in the fetal breathing movement incidence; maternal hypercarbia stimulates the fetal breathing movements; alcohol administered to the mother abolishes fetal breathing; maternal smoking changes the time spacing of breathing and increases the fetal breathing rate; and exposure of the fetus to sound causes an increase in the number of movements. Real-time ultrasonography enables detection and recording of several other fetal activities: hiccups, swallowing and changes in the stomach volume, micturition, and fetal eye movements. The latter fetal activity is used together with fetal movements, fetal mouth movements and fetal heart rate for the identification of the fetal behavioural states. Quantification of fetal activity as a clinical test of fetal well-being was expected to give an alarm signal in cases of fetal hypoxia and imminent asphyxia. In general, the predictive value of a negative result (i.e., a finding of normal fetal activity) was high; the predictive value of decreased or abnormal fetal activity was found to be much less predictive of fetal compromise.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Ultrasonic assessment of fetal activity. 636 Apr 64


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