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

Recent information appears to solidify the concept that the left ventricle hypertrophies with age in normal adult man. The stimulus for this moderate increase in wall thickness has not been precisely determined but an attractive hypothesis suggests that the stimulus may be an increased load imposed by the peripheral vascular resistance. The mechanism for the well-documented diminished cardiovascular response to maximal exercise in normal aged man still remains unclear. Evidence in the canine model indicates that a diminished chronotropic response to catecholamines could in part explain a limitation in maximal heart rate response. The reflex change in heart rate in respone to hypercapnia, hypoxia, and sustained isometric handgrip in normal man is diminished with age. The precise mechanism of this age-associated phenomenon remains to be elucidated, but the chronotropic responsiveness to catecholamines is likely a contributing factor. Finally, there is evidence of slowed myocardial relaxation in hearts of aged animals and man. A decrement in the speed at which the sarcoplasmic reticulum from hearts of aged rats accumulates calcium has been demonstrated and appears to be involved in the mechanism of prolonged contraction in aged myocardium.
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PMID:Alterations in the cardiovascular system that occur in advanced age. 15 53

One subject was exposed for six days to increasing levels of CO2, rising at a constant rate from 0.03 to 3.0% CO2 within a 15-h period followed by 9 h of air breathing. To assess acid-base parameters, arterialized capillary blood was taken from a finger twice daily (at 8 a.m. and 11 p.m.) at times corresponding to the beginning and end of the intermittent exposure to CO2. Venous blood samples were obtained on alternate days at the same times. Urine specimens were collected twice daily. The subject was on a liquid diet. Resting respiratory minute volume (VE), oxygen consumption (VO2), carbon dioxide excretion (VCO2), alveolar carbon dioxide and oxygen tension (PACO2) and PAO2) were measured twice daily. PACO2 and PAO2 were also determined at the end of breath-holding twice daily; CO2 tolerance tests and lung function tests were also carried out. In contrast to the effects of chronic exposure to 3% CO2, the CO2 tolerance tests showed an increased sensitivity (increase of slope) and breath-holding PACO2 did not change, indicating that acclimatization to CO2 did not develop. The ventilatory response to CO2 was not sufficient to prevent CO2 accumulation in the body; this accumulation was eliminated during the nightly air-breathing periods on the fourth and fifth days, indicated by higher values of PaCO2 and PACO2. The known renal response to hypercapnia, consisting of an increased excretion of titratable acidity, ammonia, and hydrogen ion excretion, occurred but was interrupted after the first day and was triggered again on the fourth and fith days when accumulated CO2 was released from body CO2 stores. The second renal response was associated with a marked calcium excretion, which suggests that bone CO2 stores were involved.
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PMID:Effect of intermittent exposure to 3% CO2 on respiration, acid-base balance, and calcium-phosphorus metabolism. 50 20

Effect of increased concentrations of Ca++ and Mg++ in the fluid perfusing the cerebral ventricles, and hypoxia on evoked tongue jerks. Acta Physiol. Pol., 1978, 29 (1): 27-36. The infraorbital nerve, the sensory part of the trigeminal nerve, was stimulated in rats under chloralose anaesthesia. Electric stimuli of 0.2 Hz caused retractive movements of the stretched tongue. These evoked tongue jerks (ETJ) were recorded directly on a kymograph or on a linear recorder. Using a stereotaxic apparatus cannulas were inserted into both lateral ventricles of the brain for infusion of McIlwain-Rodnight's fluid at a rate of about 50 microliter/minute. The cannula for outflow of the perfusing fluid was inserted into the cerebellomedullary cistern. The ETJ was enhanced by 43%, on the average, during perfusion of the cerebral ventricles with solutions with fivefold increased concentration of calcium ions, and decreased by a mean value 24% when the perfusing solution contained a higher concentration of magnesium ions. After 10 min of breathing with increased respiratory dead space, which caused hypoxia and hypercapnia, the amplitude of ETJ diminished by 65%, on the average.
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PMID:Effect of increased concentrations of ca++ and mg++ in the fluid perfusing the cerebral ventricles, and hypoxia on evoked tongue jerks. 66 47

The role of the skeleton in electrolyte equilibrium, well known for various diseases, remains difficult to understand during chronic hypercapnia. An experimental study of normoxic (O2:21%) hypercapnia (CO2:8 +/- 1%) was carried out for two, four and six weeks, followed by a systematic quantitative determination, in thigh-bone samples of Na+, K+, Ca++, PO4--, N2 and CO2 in 72 rats, and of total H2O and extracellular H2O (H2Oe) in 129 rats. Considering the mean values of groups (from 16 to 42 subjects for each group), at various times of hypercapnia, bone K+ was increased during hypercapnia (+3 to 4 X 10(-3) mEq/g fresh tissue), Ca++ diminished (--12.5 to 15.4 mEq). PO4-- and Na+ temporarily decreased at two and four weeks of hypercapnia. On account of the scatter of individual results, only the variation of K+ was statistically significant (at two weeks). This increase in bone K+, accompanying a partially compensated acidaemia, is to compare with the significant hyperkaliemia observed at two and four weeks, whereas this period is characterized by a decrease in K+ in skeletal muscle, as shown in a previous work. In a group of 72 rats, the analysis of correspondances and correlations points out the bone CO2 as a very significant variable, opposite to the variable H2Oe. PO4--is positively correlated to Na+. The complexity of the results does not permit a decisive interpretation of the phenomenon. On the other hand, this study corroborates the bone calcium loss and reveals the gain in bone potassium during hypercapnia.
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PMID:[Bone electrolytes in experimental chronic hypercapnia (author's transl)]. 101 78

To ascertain whether any routine practices or clinical manipulations in a neonatal intensive care unit could induce intraventricular hemorrhage (IVH) in preterm infants, we performed ultrasonic monitoring of the germinal layer continuously for 48 hours in 33 extremely premature infants with respiratory distress. Intraventricular hemorrhage developed in 16 of these infants. In four infants the timing of the germinal layer hemorrhage was confirmed with ultrasonic monitoring. Three of the four cases were apparently associated with clinical events occurring at the moment of IVH: manual ventilation for improvement of hypercapnia associated with primary pulmonary hypertension of the newborn; correction of hyperkalemia, which was causing an arrhythmia, with administration of calcium gluconate and sodium bicarbonate; and administration of surfactant-TA to improve respiratory failure caused by pulmonary hemorrhage. In these three infants it appeared that one of the basic factors inducing IVH might be an increase in blood pressure with or without hypercapnia, causing cerebral reperfusion after ischemic damage of the germinal layer.
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PMID:Clinical events in association with timing of intraventricular hemorrhage in preterm infants. 140

Recent investigations have shown that the calcium channel blocker verapamil attenuated the hypoxic ventilatory chemosensitivity of carotid body in animals. To determine whether this is also the case in humans, transient physiological chemodenervation by O2 breaths (withdrawal test) during sustained hypoxia (N = 7), and ventilatory and circulatory responses to progressive hypoxia and hypercapnia (N = 8) were examined after oral administration of verapamil. During sustained hypoxia after verpamil, there was a significant reduction of withdrawal response from 5th to 25th min value (p < 0.01), but not after placebo. On the other hand, no significant difference in ventilatory responses to progressive hypoxia and hypercapnia was observed after verapamil. Verapamil run reveals similar features with placebo run in circulatory parameters except blood pressure response, which tended to be suppressed by verapamil. We conclude that verapamil attenuates peripheral chemoreceptor activity with time during sustained mild hypoxia in normal adult humans and this may be explained by delayed depletion in intracellular Ca2+ for chemotransduction of the peripheral chemoreceptors.
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PMID:Effect of verapamil on ventilatory and circulatory responses to hypoxia and hypercapnia in normal subjects. 149 1

Malignant hyperthermia is a rare syndrome that occurs in genetically susceptible individuals who are exposed to frequently used inhalation anesthetics. The disorder is most common in children and young adults. It is triggered through a defect in the ability of skeletal muscles to concentrate and release calcium. Signs of malignant hyperthermia include hypercarbia, muscle rigidity and tachycardia. Temperature elevation is often a late sign of the syndrome. Treatment begins with stopping all inhaled anesthetics at the earliest sign of the syndrome. The use of dantrolene has significantly reduced mortality from malignant hyperthermia. No simple screening test exists. Family members or those with a suspicious history need to be counseled and should consider muscle biopsy and testing prior to surgery.
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PMID:Malignant hyperthermia. 157 19

This study was carried out to define some of the cellular ionic mechanisms controlling cerebral arterial muscle. Muscle cells were enzymatically dispersed from cat cerebral arteries. Cells were dialyzed and voltage-clamped using patch pipettes and whole-cell currents measured. Using pipette solutions allowing us to record K+ currents we identified an outward current elicited by depolarizing voltage steps beyond -20 mV. This outward current exhibited properties of delayed outward rectification having a peak macroscopic current at +90 mV of 504 +/- 236 pA. The current was sensitive to 4-aminopyridine, but was sensitive to tetraethylammonium only at very high doses. When CsCl was in the recording pipette, macroscopic outward currents could not be recorded. Variations in the extracellular Ca2+ concentration from 0.5 to 5.0 mM had no effect on current amplitude or voltage dependence; similarly the Ca2+ channel blockers nifedipine and Mn2+ were without effect on this outward current. The current inactivated slowly with no decay seen even with 3-s command pulses. Repetitive voltage pulses from -60 to +90 mV at a frequency of 1 Hz resulted in "cumulative reduction", depressing peak current by 60% after ten pulses. Upon reduction of pH from 7.43 to 7.20 we observed a 350% increase in peak outward current in 7 of 12 cells studied in this regard. Thus, the cellular mechanism responsible for cerebral vascular dilation to acidosis and/or hypercapnia may involve an increase in outward K+ current.
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PMID:Characterization of an outward K+ current in freshly dispersed cerebral arterial muscle cells. 185 36

1. Cerebral blood flow (CBF) in the rat was monitored by a venous outflow technique with an extracorporeal circulation which allowed for continuous monitoring of flow over the several hours of the study. 2. Brief challenges with carbon dioxide (CO2) increased the CBF. 3. Nifedipine (1.00 mg/kg), a dihydropyridine calcium antagonist, attenuated the response of the animal to hypercapnia, while leaving the basal flow rate unchanged. 4. This study may have significant implications as to the effect of nifedipine on CBF. 5. Since similar results have been obtained with nifedipine in anoxia, this study suggests that the responses to anoxia and hypercapnia are interrelated and that the resulting hyperemia may be governed by the same mechanisms.
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PMID:Nifedipine reduces the increases in cerebral blood flow during hypercapnic episodes. 190 50

Endothelial modulation of norepinephrine (NE)-induced constriction of the isolated rat aorta was studied at normal (PCO2, 41 +/- 0 mmHg) and high CO2 tensions (PCO2, 91 +/- 1 mmHg). In preparations with intact endothelium, increased CO2 tension resulted in rightward shift of the NE dose-response curve with attenuation of maximal contraction. This effect of CO2 was not modified by indomethacin. Treatment with hemoglobin or rubbing of the endothelium meant that increased CO2 tension still resulted in rightward shift of the NE dose-response curve but without altering the maximal contractile response. The basal guanosine 3',5'-cyclic monophosphate (cGMP) levels in control and NE-treated aortic preparations were not affected by increasing the CO2 tension. Thus the inhibitory action of CO2 on NE-induced contraction in the presence of endothelium may not be derived from facilitation of endothelium-derived relaxation factor (EDRF)-induced cGMP synthesis. Increasing the CO2 tension attenuated the sustained contraction induced by the addition of NE and Ca2+ (2.5 mM) to intact endothelium preparations previously bathed in Ca2(+)-free solution. Further addition of Ca2+ (total 5.0 mM) did not increase the contraction. These findings suggest that the intrinsic activity of NE is greatly modified by endothelium at a high CO2 tension. Vasodilation during hypercapnia may be induced at least in part by synergistic actions of EDRF and CO2 on smooth muscle cells.
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PMID:Endothelial modulation of norepinephrine-induced constriction of rat aorta at normal and high CO2 tensions. 210 38


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