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

To evaluate the effects of succinylcholine on cardiac arrhythmias and serum levels of potassium and catecholamines, dogs with hypoxia alone and with hypoxia and hypercarbia were studied during anesthesia with halothane or enflurane. After the injection of succinylcholine (0.3 mg/kg), cardiac arrhythmias occurred in all halothane:hypoxia dogs and in 70% of dogs given halothane during hypoxia:hypercarbia. No dogs given enflurane anesthesia developed arrhythmias. Serum potassium levels increased significantly 3 and 5 min after succinylcholine in all groups. Serum epinephrine levels increased in the halothane-hypoxia:hypercarbia and enflurane:hypoxia groups and, after the injection of succinylcholine, epinephrine levels increased further in dogs in the halothane:control, halothane:hypoxia, halothane-hypoxia:hypercarbia, enflurane:hypoxia, and enflurane-hypoxia:hypercarbia groups. Norepinephrine levels increased with enflurane-hypoxia:hypercarbia and after the succinylcholine in the halothane:hypoxia, halothane-hypoxia:hypercarbia, and enflurane-hypoxia:hypercarbia groups. The results suggest that succinylcholine induces arrhythmias by sympathetic stimulation and that halothane sensitizes the myocardium to arrhythmias at the same levels of serum catecholamines and potassium in the presence of hypoxia or hypoxia:hypercarbia more than does enflurane.
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PMID:Mechanisms of succinylcholine-induced arrhythmias in hypoxic or hypoxic:hypercarbic dogs. 368

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

Studies of acutely induced hyperammonemia and chronic hyperammonemia associated with liver dysfunction suggest that cerebral blood flow (CBF) and O2 consumption (CMRO2) become uncoupled and that CMRo2 may depend on arterial CO2 tension (PaCO2). We examined CBF (radiolabeled microspheres) and CMRO2 during hypercapnia (PaCO2 congruent to 74 Torr) and hypocapnia (PaCO2 congruent to 21 Torr) both before and during intravenous ammonium acetate infusion in pentobarbital-anesthetized dogs. Continuous infusion over 120 min produced stable increases of arterial ammonia levels (1,400 mumol/l) by 30 min, whereas CBF, CMRO2, and O2 extraction (measured at sagittal sinus) remained unchanged when PaCO2 was held constant (congruent to 35 Torr). Acute hyperammonemia attenuated the increase in CBF during hypercapnia by 44% and abolished the decrease in CBF during hypercapnia. Regional blood flow to pons and midbrain increased under normocapnic conditions, and midbrain blood flow increased further during hypocapnia. Sodium acetate infusion did not affect CBF responses to CO2. Thus we failed to observe an uncoupling of global CBF and CMRO2 during normocapnic hyperammonemia, or an interaction of CO2 and ammonia on CMRO2, although the increased pons and midbrain blood flow may reflect regional effects of ammonia on reticular activating system metabolism. On the basis of the literature, we suggest that the attenuated hypercapnic CBF response may arise from impaired glial regulation of extracellular potassium and bicarbonate concentrations and that lactic acid production, enhanced by combined alkalosis and hyperammonemia, may contribute to the abolition of hypocapnic vasoconstriction.
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PMID:Interaction of CO2 and ammonia on cerebral blood flow and O2 consumption in dogs. 392 Sep 20

1. The effects of asphyxia, hypoxia, hypercapnia, stimulation of peripheral chemoreceptors, pneumothorax and breathing through resistances have been investigated on laryngeal resistance to airflow in anaesthetized cats, with and without bilateral vagotomy below the origin of the recurrent laryngeal nerves.2. Resistance to airflow of the innervated larynx was usually measured with the larynx isolated in situ with constant flow from the trachea to a pharyngeal opening, and expressed by the relationship between translaryngeal pressure and airflow.3. Asphyxia, hypoxia and hypercapnia each stimulated breathing and decreased laryngeal resistance to airflow, in both the inspiratory and expiratory phases. After vagotomy the effect was reduced, abolished or (usually) reversed to a laryngeal constriction, especially in expiration.4. Intra-arterial injections of potassium cyanide (to stimulate carotid body chemoreceptors) caused a short apnoea or an augmented breath followed by hyperpnoea, concurrently with expiratory constrictions of the larynx. The responses were usually stronger after bilateral vagotomy.5. Pneumothorax caused tachypnoea, inspiratory dilatations and expiratory constrictions of the larynx. The responses were abolished by vagotomy.6. Imposition of respiratory resistances dilated the larynx, in inspiration and expiration, while complete closure of trachea caused expiratory constrictions of the larynx. These changes did not depend on intact vagal pathways.7. The results are discussed in terms of nervous control of the larynx in the different conditions.
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PMID:Studies on laryngeal calibre during stimulation of peripheral and central chemoreceptors, pneumothorax and increased respiratory loads. 441 40

Metabolic balance studies were carried out in normal dogs to define the renal mechanisms responsible for the adaptation to, and recovery from, chronic hypocapnia. A chronic reduction in arterial CO(2) tension (Pa(CO2)) of some 15 mm Hg was achieved by means of chronic exposure of the animals to 9% oxygen in an environmental chamber. The development of hypocapnia was associated with a marked suppression of net acid excretion which, together with a slight accumulation of organic acids, produced a reduction in plasma bicarbonate concentration (8 mEq/liter) that led to nearly full protection of extracellular pH (DeltaH(+) = - 2.5 nmoles/liter). When Pa(CO2) was returned to control levels, an augmentation of acid excretion restored plasma composition to normal after a brief period of "posthypocapneic metabolic acidosis."The changes in renal acid excretion during both adaptation and recovery were accomplished in a fashion notably different from that previously observed in chronic hypercapnia, being linked to changes in cation rather than chloride excretion. Thus, in dogs ingesting a normal NaCl diet, suppression of hydrogen ion excretion during adaptation to hypocapnia was associated with an increased excretion of sodium rather than with a retention of chloride. The fact that this loss of sodium occurred without a concomitant loss of potassium strongly suggests that the hypocapneic state specifically depressed distal sodium reabsorption; if distal sodium reabsorption had not been depressed, a reduction in proximal sodium reabsorption or a diminution in distal hydrogen ion secretion (or both) should have produced an increase in potassium excretion. The interpretation that chronic hypocapnia diminished sodium reabsorption was supported by the finding that when renal sodium avidity was enhanced by restriction of sodium intake, acid retention was accomplished by a loss of potassium rather than of sodium. The accompanying reduction in plasma bicarbonate concentration was slightly less than that observed in dogs ingesting a normal NaCl diet, a finding probably accounted for by a slight difference in the availability of cation for excretion under the two experimental circumstances. These findings, taken together with the observation that augmented acid excretion during recovery from hypocapnia is linked to cation retention, suggest that an adequate intake of cation during both adaptation and recovery from chronic hypocapnia may be critical to the physiologic regulation of acid-base equilibrium.
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PMID:The nature of the renal adaptation to chronic hypocapnia. 503 22

The present studies evaluate the effect of acute hypercapnia on distal nephron H+ secretion (DNH+S) in vivo by means of the urine-blood PCO2 difference (U-B PCO2) in alkaline urine. Bicarbonaturia was induced by either a sodium bicarbonate infusion or L-lysine administration. Our results demonstrate that the U-B PCO2, as a function of the urinary bicarbonate concentration, was significantly lower during acute respiratory acidosis; this effect was not dependent on changes in glomerular filtration rate and/or fractional excretion of sodium, potassium, and chloride. Infusion of the sodium salts of sulfate, a nonreabsorbable anion, did not correct the diminished U-B PCO2. Amiloride caused the U-B PCO2 to fall in normocapnic dogs but not in hypercapnic dogs. When hypercapnia was superimposed in dogs with extracellular fluid volume contraction, there were no changes in the U-B PCO2. This study indicates that acute hypercapnia in the intact dog decreases DNH+S and is compatible with an effect of hypercapnia on the voltage-dependent component of urine acidification. The mechanism appears to be direct rather than secondary to factors that influence the rate of sodium delivery to the distal nephron.
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PMID:Decreased distal acidification in acute hypercapnia in the dog. 629 83

The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.
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PMID:Respiratory muscle failure. 634 27

Hypokalemia has been previously reported as a cause for respiratory impairment complicating therapy for diabetic ketoacidosis. A case is presented with a short interval of hypoventilation documented by hypercapnia. A reversal from hypercapnia to hypocapnia occurred when the serum potassium level became normal after potassium replacement. Causes of muscular weakness other than hypokalemia were considered unlikely on the basis of clinical and laboratory data. The present report records the occurrence of hypoventilation associated with hypokalemia in diabetic ketoacidosis and serves to underscore the need for adequate potassium replacement during the treatment of this disorder.
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PMID:Hypokalemic hypoventilation complicating severe diabetic ketoacidosis. 676 71

A study on two groups of patients in acute respiratory failure with hypercapnia (18 subjects) and in hypercapnic coma (18 subjects) has been carried out to determine the related changes in sodium ion, potassium ion, chloride ion, urea and osmolality in blood and cerebrospinal fluid. There were significant differences between the two pathological states and particularly in coma, changes in transmembrane active transport of electrolytes are significantly related to high concentrations of CO2 in the brain.
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PMID:Changes in plasma and cerebrospinal fluid electrolytes in hypercapnia. 678 28

Rats were tested in the forced swim test in 35 or 20 cm of water or in an open field to evaluate the effects of different intensities of stress on blood gases, electrolytes, and metabolic indices, compared to nontested controls. Animals tested in the open field did not differ from controls on any measure. Immersion in deep water resulted in a greater mixed metabolic and respiratory acidemia (low pH, low bicarbonate, high pCO2), higher glucose and higher lactate levels than immersion in shallow water which in turn resulted in greater metabolic acidemia (low pH, low bicarbonate), and higher glucose and lactate levels than occurred in open field or control animals. In contrast to immersion in deep water, immersion in shallow water resulted in an initial hypocapnia followed by a hypercapnia. Immersion in deep water also resulted in higher potassium levels, lower bicarbonate and total carbon dioxide levels, and a higher anion gap than immersion in shallow water, testing in the open field, or in controls. In a second study, lactate infusion resulted in a metabolic alkalemia (increased pH and bicarbonate levels) and an increase in total carbon dioxide levels. These results indicate that test parameters from forced swim testing (e.g., water depth) can significantly affect the rat's physiological response to testing. The effects of forced swim testing are not simply due to general stress; and the physiological changes seen in conjunction with forced swim testing (e.g., acidemia) are not due to lactate alone.
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PMID:A further analysis of physiological changes in rats in the forced swim test. 780 Jul 51


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