Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phenylethylamine can initiate migraine-type headaches in susceptible individuals. Migraine sufferers have a reduced ability to deaminate all monoamines, but particularly phenylethylamine. Phenylethylamine readily crosses the blood-brain barrier and thus could be a mediator of the cerebrovascular disturbances seen in migraine attacks. Cerebral blood flow was measured in 15 anesthetized baboons by the intracarotid 133Xe clearance technique. Phenylethylamine (4 x 10(-7) moles.kg-1min-1) produced significant increases in cerebral blood flow (36 percent) and cerebral oxygen consumption (45 percent) during the first 40 minutes of infusion. In contrast, an increased phenylethylamine concentration (2 X 10(-6) moles.kg-1min-1) constricted the cerebral bed (cerebral blood flow reduced by 28 percent). The response of the cerebral circulation to hypercapnia was preserved during the infusion. Phenylethylamine thus is capable of producing in an experimental animal a pattern of cerebrovascular events similar to those seen in migraine.
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PMID:Phenylethylamine and cerebral blood flow. Possible involvement of phenylethylamine in migraine. 40 34

The effects upon cerebral blood flow (CBF) and oxygen consumption (CMRO2) of the infusion into the internal carotid artery of tyramine and amphetamine were investigated in 24 anaesthetized baboons. The infusion of tyramine was without effect upon CBF and CMRO2 at normocapnia, even at concentrations which significantly raised arterial blood pressure. However, marked reductions in cerebral blood flow were noted at hypercapnia during the infusion of tyramine (2.5 X 10(-7) moles/kg/min). The infusion of amphetamine (7.5 X 10(-10) moles/kg/min) resulted in significant increases in CBF (32%) and CMRO2 (37%). However, an increased concentration of amphetamine (2.5 X 10(-7) moles/kg/min) significantly reduced CBF (22%) and CMRO2 (20%). It is suggested that amphetamine, by virtue of being able to cross the blood--brain barrier and interact with the cerebral monoamine systems, is able to influence cerebral blood flow by inducing changes in cerebral metabolism, and that the minimal reactivity of the cerebral circulation to the infusion of tyramine is the result of the inability of tyramine to cross the blood--brain barrier.
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PMID:Indirect sympathomimetic agents and cerebral blood flow and metabolism. 41 82

The effects of an acute cryogenic injury on cerebral flow (CBF) and cerebral vascular reactivity were studied in 12 anaesthetised, ventilated baboons. Autoregulation, defined in this study as intact with a greater than 20% change in cerebrovascular resistance in response to a change in cerebral perfusion pressure, was tested before the lesion by arterial hypotension. Intact autoregulation was found in half the animals, but all animals showed an increase in CBF with hypercarbia. The cryogenic lesion was followed by a marked rise in intracranial pressure, and a fall in CBF which was only partly related to the status of autoregulation beforehand. After injury, arterial hypertension caused an increase in cerebrovascular resistance of more than 20% in half the animals. This response was not related to the presence of autoregulation before the lesion, and was accompanied by a greater impairment of the cerebrovascular response to carbon dioxide, more severe brain oedema, and lower cerebral oxygen consumption, than in the remaining baboons which had a pressure passive response to arterial hypertension. This study confirms that the failure of CBF to increase with arterial hypertension may indicate severe brain damage rather than intact physiological autoregulation.
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PMID:Vascular reactivity in the primate brain after acute cryogenic injury. 41 85

1. Mongrel dogs were anaesthetized with chloralose, paralysed, ventilated and vagotomized and given a beta-blocking drug, sotalol, in sufficient doses to block the effects of 5 microgram of adrenaline. 2. Changes in inspired CO2 concentration were produced, causing increases of arterial PCO2 up to 120 mmHg. The effects on myocardial blood flow were measured with radioactive microspheres. Coronary sinus and arterial blood was sampled. 3. In the absence of beta-blockade, an increase in arterial PCO2 produced variable effects. In some dogs coronary blood flow increased, while in others there was no change. There was a mean increase in coronary blood flow at arterial PCO2 values above 85 mmHg which was abolished by beta-blockade. 4. In the presence of beta-blockade, an increase of arterial PCO2 produced depression of left ventricular performance, i.e. a fall of maximum rate of rise of left ventricular pressure and a rise of left ventricular end-diastolic pressure. 5. In the presence of beta-blockade, there were no consistent changes in myocardial blood flow, left ventricular pressure or cardiac output. 6. In the absence of beta-blockade, coronary arterial minus venous ocygen content was reduced by hypercapnia. In the presence of beta-blockade, the changes were small and not statistically significant. The direct coronary vasodilator effect was therfore negligible. 7. It is concluded that the previously reported hypercapnic vasodilatation was mainly an effect of sympatho-adrenergic stimulation by hypercapnia. 8. In the presence of beta-blockade, coronary sinus PO2 increased markedly, with little change in coronary sinus oxygen content; this was consistent with a shift to the right of the oxy-haemoglobin dissociation curve. Under circumstances of hypercapnia, a rise in coronary sinus (and presumably tissue) PO2 failed to produce vasoconstriction. 9. It is argued that the vasodilator effect of hydrogen ions and the vasoconstrictor effect of oxygen probably cancel one another when the arterial PCO2 is raised.
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PMID:The effect of carbon dioxide upon myocardial contractile performance, blood flow and oxygen consumption. 43 Mar 87

Six patients with chronic obstructive pulmonary disease (COPD) (forced expiratory volume in one second, 1.01 +/- 0.08 L [mean +/- SEM] ) were given either 1 mL of 100% alcohol per kilogram of body weight in an aqueous solution or a similar volume of water in a crossover design on consecutive days. All subjects became intoxicated and the peak alcohol concentration was 137 +/- 11 mg/dL, 40 minutes after ingestion. No significant difference was found in either PaO2 or PaCO2 between the alcohol and control period. A significant decrease in arterial pH occurred following alcohol (P less than .05), and represented a mild metabolic acidosis. Alcohol ingestion resulted in an increase in oxygen consumption (P less than .05) and carbon dioxide production (P less than .05) but no change in respiratory rate. It appears that small to moderate amounts of alcohol will not cause marked changes in oxygen tension or alveolar hypoventilation in patients with severe COPD who do not have marked hypercapnia. Nevertheless, other effects of alcohol on the cardiopulmonary system and the concomitant use of sedatives have to be considered before condoning the use of alcohol.
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PMID:Moderate alcohol dose and chronic obstructive pulmonary disease: not a cause of hypoventilation. 43 97

The effect of carbon dioxide on oxygen dioxide tension in the endolymph was determined by the micropolarographic technique. Different concentrations (5% and 10% CO2) and different exposure times (3, 5, and 20 minutes) were investigated. The highest levels of PO2 in the endolymph (101.7, 93.9 and 69.5 mm Hg) were accomplished by respiration of 10% CO2, 90% O2, for 20, 5 and 3 minutes consecutively. The lowest PO2 increase, 50.7 mm Hg was observed after breathing 5% CO2, 90% O2 for 20 minutes. Extreme hypercapnia caused an increase of endocochlear potentials (EP) in all groups. In the second group EP increased from +79.3 to +84.9 and in all groups they had returned to the pretreatment level after CO2 discontinuation. These results support the theory that carbonic anhydrase participates in the generation of EP. At the same time that EP increased, cochlear microphonics declined and opposite after the breathing mixture was discontinued. The results permit the conclusion that high levels of PO2 in endolymph is achievable even with short periods of respiration with high CO2 mixture, and suggest the role of carbonic anhydrase during EP generation.
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PMID:Variation of endocochlear PO2 and cochlear potentials by breathing carbon dioxide. 44 16

The response of nasal airway resistance (Rn) to various degrees of hypoxia and hypercapnia was measured in six subjects using active posterior mask rhinomanometry. All resistances were computed during expiration at the flow rate of 0.5 liter/sec. Hypercapnia, induced by breathing gas mixtures of various contents of carbon dioxide, significantly decreased Rn (P less than 0.05, Wilcoxon signed rank test). The reduction in Rn was proportional to the inspired partial pressure of carbon dioxide over a range of 0 to 50 torr. Breathing gas mixtures of high and low contents of oxygen produced no significant change in Rn (P less than 0.05, Wilcoxon signed rank test). These results indicate that the nasal airway is actively involved in the respiratory response to hypercapnia but not to moderate hypoxia.
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PMID:Response of nasal airway resistance to hypercapnia and hypoxia in man. 44 19

As a result of the studies, carried out upon 30 patients following lung operations, it has been found that an optimal hyperventilation of a single lung with an increased oxygen level in the respiratory mixture prevents the occurrence of hypoxemia and hypercapnia.
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PMID:[Effect of the type of anesthesia and the parameters of single-lung ventilation on the extent of venous shunt in lung surgery]. 45 58

Pyrenebutyric acid (PBA), the intracellular fluorescent indicator, was used to measure the partial pressure of oxygen (PO2) in the exposed cerebral cortex of anesthetized cats at hyperbaric pressures up to 4 ATA. The validity of the PBA method for determining cortical PO2 was confirmed by demonstrating a precise linear relationship between Pao2 and the reciprocal of the fluorescence of PBA in the brain as the cat was ventilated with sequentially greater oxygen pressures while holding the Paco2 nearly constant. Increments in the Paco2 while the Pao2 was maintained at a high (about 2,000 Torr) level resulted in stepwise greater oxygen tensions in the brain until an oxygenation end point was reached with a Paco2 averaging near 122 Torr. Greater amounts of CO2 did not bring the mean PO2 of the brain, 1,017 Torr, closer to 2,000 Torr. During normocapnia the cortical PO2 was greater than the PO2 of cerebral venous blood collected from the superior sagittal sinus; however, in hypercapnia (PaCO greater than 45 Torr), the PO2 of the sinus blood exceeded the value determined in the cortex. This latter observation is taken as evidence for convective shunting of cerebral arterial blood to venous circulation when hypercapnia is present.
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PMID:Oxygen tensions measured in cat cerebral cortex under hyperbaric conditions. 45 30

A statistical analysis of the case material at the Intensive Care Unit, Freiburg, for the years 1975 and 1976 established that 40% and 39% respectively of patients with multiple injuries had also suffered a chest trauma and that the latter was the direct cause of respiratory insufficiency in 61% (1975) and 57% (1976) of patients in need of controlled respiration, i.e. respiratory insufficiency dominated the clinical and pathophysiological picture. The causes were: restricted respiratory movements due to pain, compression of the lungs or pathological changes in the injured lung, and they affected the normal gaseous exchange in a variety of ways. Alveolar hypoventilation with disturbance of ventilation-perfusion, increase in the functional shunt volume, rise in the functional dead space combined with reduced functional residual capacity and compliance result, if left uncorrected, in a drastic increase of resistance on the part of the pulmonary vessels and finally in, often fatal, hyoxaemia and hypercapnia. Regular estimations of the arterial blood gases in air and pure oxygen, of the arterio-alveolar difference in oxygen pressure, shunt volume, dead space and effective compliance of the chest wall and lungs are, therefore, essential. Treatment in an intensive care unit comprises the relief of any acute condition, such as tension pneumothorax, haemothorax, and general measures. Means to relieve pain in patients whose chest injuries are not sufficiently severe to require artificial ventilation are: intercostal blocking, acupuncture or peridural analgesia; efficient breathing exercises are important. The indications for artificial ventilation should be interpreted generously and the decision to perform it should be made at an early stage. The technique is determined by the type of pathological changes in the gaseous exchange and should aim at restoring normal conditions as far as possible.
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PMID:[Intensive care in chest trauma (author's transl)]. 46 37


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