UMLS:C0020440 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

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

Anesthetized, paralyzed and mechanically ventilated pigs were hypoventilated to extreme hypercapnia (PaCO2 approximately 20 kPa) at FiO2 0.5, and allotted to receive hypothermia (approximately 31.5 degrees C) and buffer infusion, (HB-group, n = 6) or to a hypothermic control group (H-group, n = 6). The HB-group had higher arterial pH (7.34 vs 7.09, P < 0.01) and plasma bicarbonate (58.8 vs 35.4 mmol.l-1, P < 0.01) than the controls, but lower mean pulmonary arterial pressure (MPAP), (16 vs 23 mmHg (2.1 vs 3.1 kPa), P < 0.01) and pulmonary vascular resistance (PVR), (512 vs 699 dyn.s.cm-5 (5120 vs 6990 microN.s.cm-5), P < 0.05). Mixed venous PO2 (PVO2) was lower in the HB-group (5.1 vs 6.8 kPa, P < 0.01), as well as serum potassium (2.8 vs 3.7 mmol.l-1, P < 0.01) and ionized calcium (1.01 vs 1.29 mmol.l-1, P < 0.01). Subsequently, the inspired oxygen fraction (FiO2) was decreased stepwise (0.3, 0.25, 0.21, 0.15, 0.10) at 30 min intervals. At FiO2 0.3, the HB-group had lower PVO2 (6.6 vs 7.8 kPa, P < 0.01), O2 half saturation tension (3.6 vs 4.2 kPa, P < 0.01), MPAP (17 vs 25 mmHg (2.3 vs 3.3 kPa, P < 0.01) and PVR (598 vs 793 dyn.s.cm-5 (5980 vs 7930 microN.s.cm-5, P < 0.05) compared with the controls, but higher arterial O2 saturation (95.3 vs. 88.6%, P < 0.01) and O2 content (17.7 vs 15.7 ml.100 ml-1, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Effects of hypothermia with and without buffering in hypercapnia and hypercapnic hypoxemia. 802 72

We studied the effect of respiratory acidosis and respiratory alkalosis on acid-base composition and on microdissected renal adenosinetriphosphatase (ATPase) enzymes. Rats were subjected to hypercapnia or hypocapnia of 6, 24, and 72 h duration. After 6 h of hypercapnia, collecting tubule (CT) ATPases were not changed. At 24 h, plasma bicarbonate was 35 +/- 1 meq/l (P < 0.01) and CT H-ATPase and H-K-ATPase activities were 90% greater than controls (P < 0.01). By 72 h, plasma bicarbonate was 37 +/- 1 meq/l (P < 0.005 vs. control) and CT enzyme activity had increased even more, averaging approximately 130% of control (P < 0.05). Significant increases in enzyme activities were also observed in the proximal convoluted tubule and medullary thick ascending limb. Plasma aldosterone was three to four times that of control at all three time periods. In hormone-replete adrenalectomized rats, acid-base parameters and ATPase activities were the same as those seen in adrenal intact animals. After 6 h of hypocapnia, plasma bicarbonate was not significantly changed, but H-ATPase and Na-K-ATPase activities were decreased by 35% along the entire nephron (P < 0.05). H-K-ATPase activity in CT also decreased by 35%. At 24 h, plasma bicarbonate was 20.5 +/- 0.5 meq/l (P < 0.05 vs. control) and CT H-ATPase and H-K-ATPase activities were 60% less than control (P < 0.01). By 72 h, plasma bicarbonate was 18.5 +/- 0.5 meq/l (P < 0.05); however, only CT H-ATPase activity continued to fall, averaging 75% less than control (P < 0.005). Hypocapnia had no effect on plasma aldosterone or potassium. These results demonstrate that chronic, but not acute, respiratory acidosis stimulates activity of both renal proton ATPases. By contrast, both acute and chronic respiratory alkalosis decrease the two renal proton pumps. The stimulatory effect of hypercapnia and the inhibitory effect of hypocapnia on the renal ATPases appear to be potassium and aldosterone independent. Although the precise mechanisms for these results are not known, a direct effect of PCO2, pH, or changes in bicarbonate delivery may be involved.
...
PMID:Effect of respiratory acidosis and respiratory alkalosis on renal transport enzymes. 809 53

The increase in blood flow in the cerebral cortex of the anaesthetized rat during hypoxia and hypercapnia was investigated. Cerebral blood flow (CBF) was measured using the hydrogen clearance method with acutely implanted platinum electrodes. Hypoxia (PaO2 35.3 +/- 2.4 Torr) and hypercapnia (PaCO2 68.1 +/- 5.1 Torr) increased basal CBF from 76.3 +/- 9.0 ml/100g/min to 168.1 +/- 20.1 ml/100g/min and 162.4 +/- 31.9 ml/100g/min respectively. The sulphonylurea tolbutamide (1mM in 1%DMSO) had no significant effect on CBF in hyperoxia or in hypercapnia. However, it attenuated the increase of CBF during hypoxia by 66 +/- 11% (p < 0.01). This suggests that opening of tolbutamide-sensitive potassium channels may be involved in the process of hypoxic vasodilation in the rat cerebral cortex.
...
PMID:The effect of tolbutamide on cerebral blood flow during hypoxia and hypercapnia in the anaesthetized rat. 830 97

Plasma potassium concentrations during anesthesia with N2O and enflurane in O2 were measured in 12 patients on chronic hemodialysis (HD) who underwent HD for about 2 hours just before anesthesia. Pre-HD and pre-anesthetic plasma potassium concentrations were 5.0 +/- 0.2 and 4.3 +/- 0.2 mEq.l-1, respectively. The potassium levels decreased slightly following induction of anesthesia, but increased significantly during and after surgery; and at the end of anesthesia the levels were similar to those measured just before HD. None of the patients developed acidosis, hypoxia or hypercapnia. Based on our results, we consider that plasma potassium levels should be measured frequently during surgery in patients who have high potassium levels just before HD and are subjected to HD just before anesthesia, because hyperkalemia may occur.
...
PMID:[Plasma potassium concentrations during N2O-enflurane anesthesia in patients on chronic hemodialysis]. 846 84

Previous studies found that regular confinement of dogs in an experimental environment preceding onset of an avoidance task was associated with increases in blood pressure and decreases in heart rate and respiration rate that were not prevented by adrenergic antagonists. The present study investigated a) whether divergent changes in blood pressure and heart rate also occur in micropigs preceding onset of an avoidance task, and b) the nature of changes in blood gases, plasma pH, plasma bicarbonate, hematocrit, and plasma electrolytes observed under these conditions. Blood pressure increased and heart rate decreased during 2-h preavoidance periods, whereas both blood pressure and heart rate were elevated during 20-min avoidance periods. During preavoidance periods, pO2, plasma pH, and plasma potassium pCO2 were decreased below home kennel levels during early preavoidance, whereas pCO2 and plasma bicarbonate were persistently increased and hematocrit was persistently decreased for the duration of the preavoidance periods. Each of these changes was reversed during the avoidance sessions. These findings suggest that behaviorally induced hypercapnia might participate in blood pressure regulation via increased renal sodium/hydrogen exchange and renal sodium retention.
...
PMID:Preavoidance hypercapnia and decreased hematocrit in micropigs. 877 77

1. The effects of raising extracellular potassium concentration ([K+]o) from 3.0 to 5.3, 9.5 or 16.8 mM on chemoreceptor responses to hypoxia, hypercapnia and asphyxia were examined in a superfused in vitro rat carotid body preparation. 2. Single-exponential functions with offset were fitted to the chemoreceptor discharge responses to ramp decreases in Po2. Increasing [K+]o was without effect upon the rate constants of the fitted exponential functions (P > 0.20). Increasing [K+]o, significantly increased the horizontal asymptote (chemoreceptor discharge in hyperoxia) in a non-linear fashion when all levels of [K+]o were included in the analysis (P < 0.001) but not when a comparison was made only between 3.0 and 5.3 mM Ko+ (P > 0.40). The rightward position of the response curves, as quantified by the Po2 at 50% maximum discharge, was linearly related to [K+]o but only when all levels of [K+]o were included in the analysis (P < 0.03). Chemoreceptor sensitivity to [K+]o increased non-linearly as [K+]o was increased but this effect was not dependent upon the Po2 (P > 0.90). 4. Increasing PCO2 in hyperoxia increased chemoreceptor discharge linearly at all levels of [K+]o. Whilst discharge at any level of PCO2 was elevated by increased levels of [K+]o, raising [K+]o did not increase CO2 sensitivity (P > 0.20). Similarly, increasing PCO2 did not increase chemosensitivity to [K+]o. The lack of effect of [K+]o upon CO2 chemosensitivity was also observed as Po2 was decreased to hypoxic levels (P > 0.10). 5. Our data demonstrate that an elevation of [K+]o can increase chemoreceptor discharge in the in vitro carotid body in a PO2- and PCO2-independent manner, suggesting that the PO2-dependent effects of [K+]o, previously reported in vivo may be due to other indirect effects of [K+]o or hypoxia.
...
PMID:Extracellular potassium and chemosensitivity in the rat carotid body, in vitro. 879 3

1. Mechanisms that regulate the cerebral circulation have been intensively investigated in recent years. The role of several vasodilator mechanisms has been examined in the cerebral circulation, including nitric oxide (NO), trigeminal peptides and potassium channels, as well as the potent vasoconstrictor endothelin. These mediators appear to play a role in physiological and pathophysiological responses of the cerebral circulation. In the present review, we will focus on some recent developments in each of these areas. 2. Nitric oxide is an important regulator of cerebral vascular tone. Tonic production of NO maintains the cerebral vasculature in a dilated state. NO appears to be an important vasodilator during activation of neurons by excitatory amino acids, somatosensory stimulation and cortical spreading depression. Tonic production of NO appears to be critical in vasodilatation during hypercapnia, although NO may not directly mediate vasodilatation. NO produced by immunological NO-synthase appears to be important in dilatation following exposure to bacterial endotoxin. 3. Calcitonin gene-related peptide (CGRP), released from trigeminal perivascular sensory nerves in the brain, is an extremely potent dilator of brain vessels. CGRP may limit noradrenaline-induced constriction of cerebral vessels and contribute to dilatation during hypotension (autoregulation), reactive hyperaemia, seizures and cortical spreading depression. 4. Activation of potassium channels leads to hyperpolarization of cerebral vascular smooth muscle and appears to be a major mechanism for dilatation of cerebral arteries. Agents that increase the intracellular concentration of cyclic 3' 5'-adenosine monophosphate (cAMP) produce vasodilatation in part by activation of large conductance calcium-activated potassium channels (BKCa) and ATP-sensitive potassium channels (KATP). Activation of both KATP and BKCa channels also appears to contribute to vasodilatation during hypoxia. In contrast to KATP channels, BKCa channels appears to be active under basal conditions, contributing to tonic dilatation of cerebral blood vessels. 5. Endothelin is produced in the brain, but its role in the physiological regulation of cerebral blood flow is not known. Endothelin may contribute to the spasm of cerebral arteries following subarachnoid haemorrhage.
...
PMID:Recent insights into the regulation of cerebral circulation. 880 May 65

We compare and contrast the putative mechanisms underlying CO2 chemoreceptor function in air breathing vertebrates and terrestrial pulmonate snails. We discuss the role of intracellular pH (pHi) in central respiratory responses to CO2 and describe a variety of patterns of pHi regulation in chemosensory areas. One pattern, in which pHi retains a fixed relationship to the CO2 stimulus over time, seems well suited to chemoreceptor cells. Alphastat regulation of ventilation is apparent in both air breathing vertebrates and terrestrial pulmonate snails. Diethyl pyrocarbonate inhibits respiratory responses to hypercapnia in both groups of animals. The neuronal basis of chemosensitivity is similar, in that putative chemoreceptor cells depolarize during hypercapnic stimulation, but the ionic basis of excitability appears to be a potassium conductance in the vertebrates studied to date and a calcium conductance in the snails. Despite divergent evolutionary histories, chemosensory responses and mechanisms are remarkably similar in air breathing vertebrates and terrestrial pulmonate snails.
...
PMID:Comparative aspects of central CO2 chemoreception. 940 10

The conclusion that cyclic 3'-5 guanosine monophosphate (cGMP) functions in a 'permissive' manner in promoting cerebrovasodilation during hypercapnia was based on findings showing that the nitric oxide synthase (NOS) inhibitor-induced repression of the CO2 response could be reversed upon addition of exogenous cGMP. We hypothesized that the action of cGMP revealed in those studies does not define its normal role in hypercapnic cerebral vasodilation, but rather is a unique function of the artificial situation of NOS inhibition coupled with cGMP repletion. Thus, although CO2 reactivity may be the same in normal versus cGMP-repleted animals, the factors contributing to that response may differ. To test that possibility, the effects of calcium-dependent (KCa) or ATP-sensitive (KATP) potassium channel blockers on pial arteriolar CO2 reactivity, in vivo, were evaluated in the presence and absence of NOS inhibition plus administration of a cGMP analogue. Pial arteriolar diameter changes in hypercapnia were measured in three principal groups of anesthetized rats: (I) KCa channel-inhibited (via iberiotoxin); (II) KATP channel-inhibited (via glibenclamide); and (III) controls. Group I and II rats were further divided into: (a) those treated with the neuronal NOS (nNOS) inhibitor, 7-nitroindazole (7-NI), followed by successive suffusions of the cGMP analogue, 8-bromo-cGMP (8Br-cGMP) and 8Br-cGMP+K-channel blocker; and (b) rats where 7-NI and 8Br-cGMP applications were omitted. Group III rats were divided into time and 8Br-cGMP controls. Hypercapnia (PCO2 congruent with60 mmHg, 3 min)-induced dilations were reduced by 70-80% following 7-NI and restored by 8Br-cGMP. That restoration was reversed by both K-channel blockers. In the absence of 7-NI and exogenous cGMP, CO2 reactivity was unaffected by K-channel inhibition. These findings confirmed that nNOS-derived NO is critically important to the hypercapnic reactivity of cerebral arterioles, and that cGMP repletion, following NOS inhibition, could restore CO2 reactivity. The observation that KCa and KATP channel blockade did not alter CO2 reactivity under baseline conditions, but attenuated CO2 reactivity only in the presence nNOS inhibition (and cGMP repletion), suggests that multiple, redundant, and interactive mechanisms participate in CO2-induced vasodilation. These results also imply that current strategies for revealing permissive actions of cGMP (or NO) may need to be re-evaluated.
...
PMID:Calcium-dependent and ATP-sensitive potassium channels and the 'permissive' function of cyclic GMP in hypercapnia-induced pial arteriolar relaxation. 963 Jun 23

Hypercapnic respiratory failure due to chronic obstructive pulmonary disease (COPD) is an indicator of poor prognosis compared to that for normocapnic patients. On the other hand, there exist particular patients who are hypercapnic during an acute exacerbation of COPD but revert to normocapnia after adequate therapy. The aims of this study were: 1) to document the admission characteristics of such patients in terms of clinical and laboratory findings; and 2) to analyse the long-term course and survival of chronic and reversible hypercapnic and normocapnic patients. Fifty-six consecutive patients, admitted with an acute exacerbation of COPD, were enrolled and divided into three groups according to arterial carbon dioxide tension (Pa,CO2) at first admission: 22 chronic hypercapnic (group 1), 15 reversible hypercapnic (group 2) and 19 normocapnic (group 3) patients. Age, sex, smoking history, white blood cell count, serum sodium, potassium, urea and albumin levels and pulmonary function tests at first admission were similar in the three groups. The haematocrit level was significantly higher in group 1 compared with the other groups. Groups 1 and 2 had lower pH, arterial oxygen tension (Pa,O2) and arterial oxygen saturation (Sa,O2) and a higher Pa,CO2 than group 3. The Pa,CO2 was also higher in group 1 than in group 2. The presence of cor pulmonale was significantly higher in group 1 compared with groups 2 and 3 (81.8 versus 60 and 10.5%, respectively). During the follow-up period, a significant increase was observed in airway obstruction associated with progressive hypercapnia and hypoxaemia in chronic hypercapnic patients, and 12 of 15 (80%) reversible hypercapnic patients progressed to a chronic hypercapnic status. The survival analyses after 10 yrs of follow-up revealed comparable survival durations in chronic and reversible hypercapnic patients (median of 8.86 versus 9.52 yrs, p > 0.05). In conclusion, despite careful monitoring of particular characteristics in chronic and reversible hypercapnic patients at the time of admission, no long-term predictivity of these features for either the course of the disease or survival could be found.
...
PMID:Distinctive features and long-term survival of reversible and chronic hypercapnic patients with COPD. 1044 72

<< Previous 1 2 3 4 5 6 7 8 Next >>