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

We tested the effect of certain newly synthesized allosteric modifiers of hemoglobin on the dilation induced by arterial hypoxia, arterial hypotension, and arterial hypercapnia in cerebral arterioles of anesthetized cats equipped with cranial windows for the observation of the cerebral microcirculation. The allosteric modifiers of hemoglobin are isomers of 2-(aryloxy)-2-methylpropionic acid. They shift the oxygen dissociation of hemoglobin to the right, thereby facilitating the local release of oxygen. When these compounds were applied topically by superfusion at a rate of 1 ml/min in a concentration of 0.1 mM, they had no significant effect on baseline arteriolar diameter but reduced significantly the vasodilation from arterial hypoxia and arterial hypotension. They did not influence the vasodilation from arterial hypercapnia. Spectrophotometric measurements of optical densities from pial veins 50-80 microns in diameter indicated that the superfusion with the allosteric compounds reduced hemoglobin oxygen saturation both during room air breathing and during hypoxia. We conclude that the vasodilations from arterial hypoxia and arterial hypotension are mediated by local oxygen-dependent mechanisms. The allosteric modifiers of hemoglobin may be useful as tools in investigating oxygen-dependent mechanisms.
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PMID:Effect of local change in O2 saturation of hemoglobin on cerebral vasodilation from hypoxia and hypotension. 823 31

It is well known that the incidence of cardiac arrhythmia is particularly high in patients with chronic respiratory insufficiency (CRI). This study examines the prevalence, incidence and prognostic clinical importance of arrhythmia occurring during the course of CRI on the basis of data taken from the literature and the authors' personal experience using dynamic electrocardiographic diagnosis (24-hour Holter monitoring). The majority of arrhythmias observed in these patients appeared to take the form of premature ventricular and/or supraventricular beats and less frequently of atrial fibrillation and/or attacks of supraventricular paroxysmal tachycardia. Cardiac rhythm alterations were observed using Holter monitoring in 70-90% of patients. No cardiac rhythm disorder is specific to this pathological condition. The aim of this study was to formulate, as far as was possible, a rational therapeutic approach which took account of the electrogenesis of arrhythmic phenomena, variations in the type of arrhythmia and the hemodynamic conditions under which they occur. The etiopathogenesis of arrhythmias within the framework of CRI is relatively complex and probably multifactorial since there are a number of concomitant pathological conditions able to trigger off arrhythmogenic processes both inducing the onset of reflux circuits and enhancing cardiac automatism centres. Many studies correlate the presence of arrhythmia with hypoxemia, hypercapnia and both respiratory and metabolic alkalosis. Even the combined effect of hypoxia with respiratory acidosis and the integrity or otherwise of cardiac function (chronic pulmonary heart, right ventricular hypertrophy, ischemic cardiopathy) have a notable pro-arrhythmic effect. Hypokalemia induced by both respiratory alkalosis and by drugs used during the course of CRI (eg diuretics and/or steroids) may induce a marked dispersion of refractory periods of the various fibrocells thus encouraging the onset of arrhythmia. With regard to drugs, it has been observed that both digitalis and theophylline and beta-2 stimulants if frequently used during the course of CRI may possibly induce arrhythmia. It is therefore important to underline that they should be used with particular caution. As far as concerns the use of beta-2 adrenergic compounds, it is advised that they be administered using an aerosol rather than systemic route. Digitalis has limited indications; the molecules of the methylxanthine classes require careful pharmacological dose monitoring. Arrhythmic therapy should also be seen in terms of prophylaxis and the correction of predisposing and decisive factors such as hypoxemia, hypercapnia, hemoglobin and electrolyte levels, and alterations in blood pH following the obstruction of small airways.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Respiratory insufficiency and cardiac arrhythmia: the rationale of treatment]. 833 38

Korean female unassisted divers (cachido ama) breath-hold dive > 100 times to depths of 3-7 m during a work day. We sought to determine the extent of arterial hypoxemia during normal working dives and reasonable time limits for breath-hold diving by measuring radial artery blood gas tensions and pH in five cachido ama who dove to a fixed depth of 4-5 m and then continued to breath hold for various times after their return to the surface. Eighty-two blood samples were withdrawn from indwelling radial artery catheters during 37 ocean dives. We measured compression hyperoxia [arterial PO2 = 141 +/- 24 (SD) Torr] and hypercapnia (arterial PCO2 = 46.6 +/- 2.4 Torr) at depth. Mean arterial PO2 near the end of breath-hold dives lasting 32-95 s (62 +/- 14 s) was decreased (62.6 +/- 13.5 Torr). Mean arterial PCO2 reached 49.9 +/- 5.4 Torr. Complete return of these values to their baseline did not occur until 15-20 s after breathing was resumed. In dives of usual working duration (< 30 s), blood gas tensions remained within normal ranges. Detailed analysis of hemoglobin components and intrinsic oxygenation properties revealed no evidence for adaptive changes that could increase the tolerance of the ama to hypoxic or hypothermic conditions associated with repetitive diving.
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PMID:Arterial blood gas tensions during breath-hold diving in the Korean ama. 837 76

The cardiopulmonary effects of eucapnia (arterial CO2 tension [PaCO2] 40.4 +/- 2.9 mm Hg, mean +/- SD), mild hypercapnia (PaCO2, 59.1 +/- 3.5 mm Hg), moderate hypercapnia (PaCO2, 82.6 +/- 4.9 mm Hg), and severe hypercapnia (PaCO2, 110.3 +/- 12.2 mm Hg) were studied in 8 horses during isoflurane anesthesia with volume controlled intermittent positive pressure ventilation (IPPV) and neuromuscular blockade. The sequence of changes in PaCO2 was randomized. Mild hypercapnia produced bradycardia resulting in a significant (P < 0.05) decrease in cardiac index (CI) and oxygen delivery (DO2), while hemoglobin concentration (Hb), the hematocrit (Hct), systolic blood pressure (SBP), mean blood pressure (MBP), systemic vascular resistance (SVR), and venous admixture (QS/QT) increased significantly. Moderate hypercapnia resulted in a significant rise in CI, stroke index (SI), SBP, MBP, mean pulmonary artery pressure (PAP), Hct, Hb, arterial oxygen content (CaO2), mixed venous oxygen content (CvO2), and DO2, with heart rate (HR) staying below eucapnic levels. Severe hypercapnia resulted in a marked rise in HR, CI, SI, SBP, PAP, Hct, Hb, CaO2, CvO2, and DO2. Systemic vascular resistance was significantly decreased, while MBP levels were not different from those during moderate hypercapnia. No cardiac arrhythmias were recorded with any of the ranges of PaCO2. Norepinephrine levels increased progressively with each increase in PaCO2, whereas plasma cortisol levels remained unchanged. It was concluded that hypercapnia in isoflurane-anesthetized horses elicits a biphasic cardiopulmonary response, with mild hypercapnia producing a fall in CI and DO2 despite an increase in MBP, while moderate and severe hypercapnia produce an augmentation of the cardiopulmonary performance and DO2.
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PMID:Cardiopulmonary effects of hypercapnia during controlled intermittent positive pressure ventilation in the horse. 852 55

Near-infrared spectroscopy may allow continuous and noninvasive monitoring of regional brain hemoglobin oxygen saturation by measuring the differential absorption of infrared light by oxyhemoglobin and deoxyhemoglobin. We have previously examined the correlation between the spectroscopic signal generated by a prototype cerebral oximeter (Invos 3100; Somanetics, Troy, MI), and global brain hemoglobin oxygen saturation calculated from arterial and jugular venous bulb oxygen saturations. Because the technology does not distinguish between arterial and venous hemoglobin saturation, changes in the proportion of cerebral arterial and venous blood volume, which may result from changes in blood flow or venous distending pressure, may confound measurements. In eight conscious volunteers breathing hypoxic oxygen mixtures, we examined the influence of supine, 20 degrees Trendelenburg, and 20 degrees reverse Trendelenburg positions on the correlation of the spectroscopic measurement of cerebral oxygen saturation in the field assessed by the probe (CSfO2) and the calculated brain hemoglobin oxygen saturation (CScombO2), estimated as 0.25 x arterial saturation plus 0.75 x jugular venous bulb oxygen saturation. We found that changes in position did not influence the association between CSfO2 and CScombO2 (r2 = 0.69-0.885) during hypoxic challenge. In a second set of eight volunteers, we studied the influence of hypercapnia and hypocapnia and body position on the association between CSfO2 and CScombO2, and found that they were less well correlated (r2 = 0.366-0.976) in individual patients. Because changes in body position and Paco2 confound the relationship between CSfO2 and CScombO2, changes in CSfO2 can best be assessed if position and Paco2 are constant.
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PMID:The influence of carbon dioxide and body position on near-infrared spectroscopic assessment of cerebral hemoglobin oxygen saturation. 856 27

With the use of isolated perfused rabbit lungs (n = 152), roles of endothelium-derived relaxing factor (EDRF) in pulmonary vascular responses to hypocapnia and hypercapnia were studied. Lungs were ventilated with a gas mixture containing 1, 5, or 10% CO2 and 21% O2, adjusting the perfusate pH to 7.8, 7.4, or 7.1, respectively. Methemoglobin (MetHb), hemoglobin (Hb), methylene blue (MB), and L-argininosuccinic acid (L-ASA) were used as modulators of EDRF. To eliminate augmented shear stress, we used papaverine during hypercapnia. As a measure of EDRF, we spectrophotometrically examined nitric oxide (NO) metabolites in the perfusate. Hypocapnia and hypercapnia evoked, respectively, unsustainable vasodilatation and vasoconstriction. Hb, MB, and L-ASA, but not MetHb, produced an increase in baseline pulmonary arterial pressure (Ppa). These agents also exacerbated vasoconstriction during hypercapnia. Hypercapnia and hypocapnia caused an increase and decrease, respectively, in EDRF production. L-ASA suppressed EDRF production in hypercapnic lungs. Papaverine did not suppress EDRF production under hypercapnia. In conclusion, 1) the effects of pH on pulmonary circulation are transient, 2) the increase in Ppa caused by hypercapnia is modulated by EDRF, and 3) the pulmonary EDRF genesis is activated by hypercapnic acidosis but suppressed by hypocapnic alkalosis.
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PMID:Endothelial modulation of pH-dependent pressor response in isolated perfused rabbit lungs. 876 59

The ventilatory and metabolic responses of lesser spear-nosed bats to hypoxia and hypercapnia were measured to determine whether these corresponded to preliminary allometries and a positive relationship between hypoxic ventilatory threshold and P50. Ventilatory responses of lesser spear-nosed bats to 3, 5 and 7% CO2 differed significantly from ventilation on air and each other. The magnitude of their ventilatory response to CO2 is consistent with the prediction of a smaller ventilatory response to hypercapnia in small compared to large mammals [% delta V varies MB0.130; Williams et al. (1994)]. Among 12, 10 and 8% O2 treatments only the ventilatory response to 8% O2 differed significantly from ventilation on air or the other treatments. Metabolic rate was significantly reduced at both 10 and 8% O2. The hypoxic ventilatory response of these bats does not support the prediction of a greater response in small compared to large mammals [% delta V veries MB0.273; Boggs and Tenney (1984)]. Their metabolic response is consistent with the hypoxic hypometabolism typical of small mammals, though not of comparable magnitude. The response, expressed as percent change in convection requirement (V/VO2), is also less than that observed in other small mammals. This relative insensitivity to hypoxia may be associated with this bat's unusually high affinity hemoglobin (P50 = 27.5 torr).
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PMID:Ventilatory and metabolic responses of a bat, Phyllostomus discolor, to hypoxia and CO2: implications for the allometry of respiratory control. 892 44

The sickle-cell gene is most concentrated in West Central Africa, the northeast corner of Saudi Arabia and East Central India. Sickle cell trait is the heterozygous condition for Hb S gene. Thirty to fifty per cent of their hemoglobin is Hb S and the remainder is Hb A. The sickle-cell crisis is induced by hypoxia, hypercarbia, acidosis, low flow condition, and hypothermia, which leads to vasoocclusion. A 39-year-old black man from Burkina Faso located in West Africa with left ventricular rupture was admitted for operation using cardiopulmonary bypass (CPB). He had been diagnosed as sickle-cell trait. The Hb S concentration was 36.2 per cent before operation with hemoglobin electrophoresis. During CPB, the minimum blood temperature was 31 degrees C and an aortic cross-clamp was not done. Total CPB time was 1 hour 31 minutes. Use of vasodilator and hyperventilation was effective. No neurological sequelae were observed.
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PMID:[Cardiac surgery using cardiopulmonary bypass in a patient with sickle-cell trait]. 893 27

To evaluate the effect of prostagrandin E1 (PGE1)-induced hypotension on cerebral blood flow (CBF) and carbon dioxide (CO2) reactivity of CBF, regional cerebral hemoglobin oxygen saturation (rSo2) was measured in non-neurosurgical patients (n = 10) under sevoflurane-anesthesia using near infrared spectroscopy. PGE1 was infused intravenously to maintain arterial pressure at a level of about 75% of the MAP (hypotensive group) under sevoflurane-anesthesia alone (normotensive group). Ventilation was controlled to adjust PaCO2 to hypocapnia (25-30 mmHg), normocapnia (35-40 mmHg) and hypercapnia (45-50 mmHg) in both normotensive and hypotensive groups. rSo2 during hypotension did not change by hypocapnia and normocapnia, but significantly increased by hypercapnia, compared with rSo2 during normotension. Significant correlations between rSo2 and PaCO2 during both normotensive and hypotensive groups were observed. Slope of the regression line of rSo2 and PaCO2 did not differ between the normotensive and hypotensive groups. When arterial oxygen content and cerebral metabolic rate of oxygen are constant, changes in rSo2 correlate with those of CBF. Therefore, CBF and CO2 reactivity of CBF that indicates autoregulation in response to changes in CO2 during hypotension were maintained as those during normotension. The results show that PGE2-induced hypotension maintains CBF and CO2 reactivity well in non-neurosurgical patients under sevoflurane anesthesia.
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PMID:[Prostagrandin E1-induced hypotension well maintains cerebral circulation and carbon dioxide reactivity in non-neurosurgical patients under sevoflurane-anesthesia]. 907 Nov 2

Previous studies from our group have indicated a heterogeneity of plasma transit times in brain capillaries. The heterogeneity was decreased with increasing cerebral blood flow during hypercapnia. In the present study, the hypothesis was tested that these apparent changes in microvascular plasma perfusion heterogeneity depend on the existence of red blood cells (RBC). To this end, the blood of anesthetized and paralyzed rats was replaced by a shear rate-independent oxygen-carrying substitute, ultrapurified polymerized bovine hemoglobin (UPBHB). Cerebral blood flow ([14C]iodoantipyrine technique) or microvascular perfusion pattern (intravenous bolus injection of Evans blue and decapitation 3-4 s later) was measured. After exchange transfusion with UPBHB, cerebral blood flow still varied with arterial PCO2, whereas in contrast to the unexchanged condition, the heterogeneity of the intracapillary Evans blue concentration remained unchanged. Compared with the unexchanged normocapnic condition, the heterogeneity of intracapillary dye concentration was decreased by one-quarter. It is concluded that RBC contribute to the microvascular perfusion heterogeneity in the brain.
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PMID:Flow-independent heterogeneity of brain capillary plasma perfusion after blood exchange with a Newtonian fluid. 913 70


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