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

Widely distributed throughout the heart is a network of fibers connected to the medullary cardiovascular centers by nonmedullated vagal afferent fibers. When the traffic in these fibers is interrupted by vagal cooling, and the input from the arterial baroreceptors is prevented, the arterial blood pressure increases. Thus, these receptors act to inhibit tonically the vasomotor center. The receptors in the atria alter their rate of discharge with changes in atrial transmural pressure and contractility and are most active during end-inspiration and early expiration when the transmural pressure is maximal. The receptors in the ventricles respond to changes in ventricular end-diastolic pressure (preload), to the pressure generated during systole (afterload) and to changes in ventricular contractility. The cardiac mechanoreceptors have an equal or greater effect on the renal bed than the arterial mechanoreceptors and this effect is enhanced by hypercapnia. In animals, the cardiac mechanoreceptors have less control of the muscle vessels than the arterial mechanoreceptors, but the reverse is true in man. Both the cardiac and arterial mechanoreceptors can modulate the output of renin from the kidney, but the cardiac mechanoreceptors are more sensitive to small changes in blood volume. During coronary occlusion, in association with the bulging of the ischemic myocardium, the rate of discharge of these cardiac receptors is greatly increased.
Am J Cardiol 1979 Oct 22
PMID:Cardiac receptors: normal and disturbed function. 38 68

The cerebral blood flow is maintained at a constant level in spite of blood pressure variations, because of a very performing auto-regulation phenomenon: vasoconstriction in case of elevated blood pressure, vasodilatation in case of blood pressure drop. The upper limit of the mean blood pressure beyond which nothing can prevent the cerebral blood flow from increasing, ranges between 150 and 170 mmHg. The lower limit, from which the dilatation of the cerebral blood vessels is not able to prevent the decreased cerebral blood flow, has been set between 50 and 70 mmHg. The auto-regulation of the cerebral blood flow is influenced by numerous factors: hypercapnia, hypoxia and ischemia complete inhibit it, making the cerebral blood flow directly related to the blood pressure; the sympathetic stimulation shifts the entire curve toward the right, because of the constriction of the pia-mater arteries, followed with a reactional vasodilatation of the small cerebral vessels. In the course of chronic arterial hypertension, the same shift of the auto-regulation curve toward high pressures is observed, related to structural alterations of the vascular wall; this make them more prone to constriction than dilatation: when these alterations are reversible, antihypertensive treatment may sometimes bring the auto-regulation curve in its initial position.
Ann Cardiol Angeiol (Paris) 1989 May
PMID:[The brain and arterial hypertension. 1. Physiologic and physiopathologic aspects]. 266 Jul 35

The ability of different substrates to affect myocardial function is well established but the mechanism for this effect has yet to be determined. To explore this area further, the studies described below were designed to determine the effect of different metabolic substrates, glucose or pyruvate, on myocardial response to hypercapnia. To assess this response, both the mechanical performance and the intracellular pH (pHi) were continuously measured. Intracellular pH was measured using the changes in absorbance of the vital staining dye, neutral red (NR). Although the presence of either substrate did not affect the response to hypercapnia, the addition of pyruvate was accompanied by a significant change in pHi. Specifically, there was a monotonic decrease in pHi comparable to that observed when PCO2 is increased from 5% to 10% (delta OD = -0.018 +/- 0.002 CO2; delta OD = -0.020 +/- 0.002 PYR, respectively). The mechanical response was similar for both; developed tension (tau) decreased initially (97 +/- 6% v. 93 +/- 8%) and then recovered (115 +/- 4% v. 101% +/- 5%). However, the changes in the maximum rate of relaxation, i.e. minimum time derivative: (tau mn) were dependent on the cause of the decrease in pHi. With hypercapnia, tau mn initially decreased and this was followed by a recovery phase which was 147 +/- 8% of the initial value. With pyruvate, tau mn decreased to 81 +/- 5% of control and was followed by no recovery. Because of the difference in the changes in tau mn, the effects of theophylline [3, 5] on these responses were determined. There was no effect on the response to an increase in PCO2. However, with theophylline present, the addition of pyruvate was accompanied by an increase in pHi (delta OD = + 0.005 +/- 0.001). The mechanical response was consistent with this increase and was similar to that seen when PCO2 is decreased from 10% to 5%. Specifically, there was an increase in tau (122 +/- 7%) followed by a small decrease (113 +/- 4%). Tissue assays for lactate showed a significant increase with the introduction of pyruvate. However, this increase was not affected by the presence of theophylline despite the opposite response of pHi. The data suggest that pyruvate affects myocardial function by altering pHi, and this effect is not due to an increase in lactate. In addition, the data are consistent with the model that the heart is capable of accommodating changes in pHi with only transient effects on contractile function.
J Mol Cell Cardiol 1986 Jul
PMID:A study of the effects of substrates on intracellular pH in toad ventricular strips. 309 40

Cardiopulmonary complications such as sudden death, congestive heart failure and hypercapnia are now recognized to punctuate the refeeding course of malnourished hospitalized patients; these effects in particular occur early in the recovery period. Data that indicate a time-dependent dose and composition effect of continuously infused formula on gas exchange, metabolic rate, ventilation and cardiac-related indexes are discussed. Unlike the interrupted feeding of regular meal ingestion, continuous feeding produces a sustained physiologic response. Delineation of continuous feeding effects on host metabolism provides a rational basis for managing the untoward cardiac and pulmonary complications of nutrition support.
Am J Cardiol 1987 Oct 30
PMID:Physiologic response and clinical implications of nutrition support. 311 92

Local brain tissue oxygen tension, temperature, and electrical potential were continuously and simultaneously measured at each of two different depths in anesthetized, paralyzed rat brain. Brain tissue temperature increases up to 1 degree C were recorded in response to direct electrical stimulation, spreading depression, PTZ-induced seizures, hypercapnia, and hypoxia. An increase in brain tissue temperature was also recorded during reoxygenation after hypoxia. Thus, we have shown that, in this preparation, increases in either blood flow or oxidative metabolism lead to transient warming of the brain.
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PMID:Brain tissue temperature: activation-induced changes determined with a new multisensor probe. 336 63

Myocardial contractility falls quickly during respiratory acidosis but if acidosis is maintained a slow gradual return towards control state is detected. In cat papillary muscle, changes in developed tension (DT) during isometric contractions (pacing rate 0.2 Hz) and intracellular pH (pHi) were continuously monitored before and during hypercapnia to study the contribution of pHi recovery to the recovery of contractility. On exposure to hypercapnia (extracellular pH [pHo] = 6.90) DT fell to 50.33 +/- 2.20% of control and pHi decreased from 7.21 +/- 0.05 to 6.90 +/- 0.02. After 30 mins of hypercapnia DT recovered to 64.66 +/- 4.05% of control, but no significant recovery in pHi was detected. Intracellular sodium concentration slowly rose to 61.05 +/- 23.79% over basal level 10 mins after the onset of hypercapnia and it remained elevated for 10 mins before gradually returning to control levels. When pHo was kept at 7.40 during hypercapnia by increasing sodium bicarbonate concentration, DT recovered to 79.11 +/- 6.94% of control after 30 mins of hypercapnia, while a significant recovery of pHi (0.12 +/- 0.02 pH units) was detected. Low extracellular sodium concentration diminished contractility recovery during hypercapnia without changing the initial decrease in DT. 5-[N-ethyl-N-isopropyl] amiloride (EIPA) (5 microM) increased the initial fall in DT to 34.33 +/- 8.68% of control and abolished the recovery. Sarcoplasmic reticulum (SR) inhibition by ryanodine (0.5 microM) markedly reduced the recovery of contractility without altering the recovery in pHi.(ABSTRACT TRUNCATED AT 250 WORDS)
Can J Cardiol
PMID:Myocardial contractility recovery during hypercapnic acidosis: its dissociation from recovery in pHi by ryanodine. 765 91

A 17-month-old boy developed grand mal seizures secondary to lidocaine toxicity during balloon dilatation of a congenital pulmonary valve stenosis. Lidocaine at 38 mg/kg (nine times the recommended maximum dose of 4.5 mg/kg) was administered during a 90-min period in order to optimize local anesthesia. This resulted in toxic serum lidocaine levels (8.7 mg/L; therapeutic range, 1.5-5 mg/L) at the time of seizures. Caution should be exercised with local anesthetics during invasive cardiac catheterizations. Hypercarbia (which lowers the seizure threshold to local anesthetics) should be avoided and the temptation to exceed the maximum recommended dose resisted.
Pediatr Cardiol 1993 Mar
PMID:Seizures due to lidocaine toxicity in a child during cardiac catheterization. 846 28

The purpose of the present study was to determine the effect of various types of acidosis on vessel diameter, intracellular pH (pHi), and calcium concentration ([Ca2+]i) in a cannulated preparation of the mesenteric arteriole of the rabbit. The effect of acidosis on vessel contraction was also studied in the wire-mounted preparation. In the cannulated preparation, pre-contracted by noradrenaline, hypercapnia caused vasoconstriction and increases in [Ca2+]i. In the wire-mounted preparation pre-contracted by either noradrenaline or high KCl, hypercapnia caused a transient vasoconstriction. In contrast, in the cannulated preparation pre-contracted by high KCl, hypercapnia caused a transient vasorelaxation and decreases in [Ca2+]i. Intracellular acidosis, induced by a NH4Cl prepulse, caused vasoconstriction and increases in [Ca2+]i even in the cannulated preparation pre-contracted by high KCl. The decrease in pHi during hypercapnia was similar to that observed after NH4Cl withdrawal. These data suggest that: (1) the effect of acidosis on vascular tone and [Ca2+]i is different depending upon the type of preparation and the mode of pre-activation, and (2) [Ca2+]i may, at least partly, regulate vascular contraction and relaxation during acidosis.
J Mol Cell Cardiol 1996 Aug
PMID:Effect of acidosis on contraction, intracellular pH and calcium in the rabbit mesenteric small artery. 887 81

Patients with heart failure have, compared with normal subjects, an increased minute ventilation (VE) at matched workloads. This heightened ventilatory drive may contribute to their limitation of functional capacity through an increase in the work of breathing and further worsening in the lung ventilation-perfusion mismatch. To measure the ventilatory response to exercise, VE should not be assessed in absolute units but be related to one of its main determinants, e.g., carbon dioxide production (VCO2). Particularly, as VE is closely related to VCO2 during exercise, the ventilatory response to exercise has been assessed using the slope of the relation of VE versus VCO2. This slope is significantly increased in heart failure patients compared with normal subjects and is inversely related to other parameters of maximal exercise capacity, namely peak VO2. The mechanisms of exercise hyperpnea in heart failure patients are still unsettled. A first possibility is that it is a compensatory response to the abnormal exercise hemodynamics with secondary increase of the pulmonary dead space to tidal volume ratio. This mechanism should be aimed to maintain constancy of the arterial gas composition and acid-base balance. However, exercise-induced hypoxemia and/or hypercapnia do not generally develop in heart failure patients. This might imply that other mechanisms, such as an increased sensitivity of the arterial chemoreceptors and/or the activation of reflexes by the abnormal skeletal muscles, stimulate the ventilatory response in heart failure patients. Regardless of its mechanisms, exercise hyperpnea may be clinically relevant in the assessment of patients with chronic heart failure. In fact, it is inversely related with peak exercise capacity, and interventions known to improve peak functional capacity such as therapy with ACE inhibitors, physical training and heart transplantation, also tend to normalize exercise hyperpnea.
Basic Res Cardiol 1996
PMID:Role of exercise ventilation in the limitation of functional capacity in patients with congestive heart failure. 889 41

Cardiac arrhythmias are common in patients with respiratory failure from chronic obstructive pulmonary disease (COPD). Several factors may be potentially arrhythmogenic in these patients, including hypoxemia and hypercapnia, acid-base disturbances, cor pulmonale and the use of digitalis, methylxanthines, and sympathomimetic drugs. The aim of this study was to examine the effect of hypoxemia and hypercapnia on QTc dispersion (QTcD) in COPD patients, and to evaluate the effect of a partial correction of one of these pro-arrhythmic factors, the hypoxemia, on Qtc dispersion, as QTcD has been proposed as a marker of heterogeneous repolarization and, hence of ventricular electrical instability. We showed that in 15 hypoxemic/hypercapnic COPD patients, compared to 20 controls, the QTcD was significantly higher (49.7 +/- 10.6 vs. 22.9 +/- 9.8 ms; P = 0.0001); furthermore, after only 24 h of oxygen therapy, and hence after a partial correction of hypoxemia, there was a significant reduction in QTcD in COPD patients (49.7 +/- 10.6 vs. 36.3 +/- 10.1 ms; P = 0.018). The data of the present study suggest that the increase in QTcD may be an early marker of a blood gas mediated electropathy in COPD patients.
Int J Cardiol 1997 Feb
PMID:Effect of blood gas derangement on QTc dispersion in severe chronic obstructive pulmonary disease: evidence of an electropathy? 907 57


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