Effects Of Carbon Dioxide Inhalation Research Articles

Behavioural and physiological effects of carbon dioxide inhalation in pigs

Behavioural and physiological effects of carbon dioxide inhalation in pigs

Effect of carbon dioxide inhalation on pulmonary hypertension induced by increased blood flow and hypoxia

There is now increasing evidence from the experimental and clinical setting that therapeutic hypercapnia from intentionally inspired carbon dioxide (CO 2) or lower tidal volume might be a beneficial adjunct to the strategies of mechanical ventilation in critical illness. Although previous reports indicate that CO 2 exerts a beneficial effect in the lungs, the pulmonary vascular response to hypercapnia under various conditions remains to be clarified. The purpose of the present study is to characterize the pulmonary vascular response to CO 2 under the different conditions of pulmonary hypertension secondary to increased pulmonary blood flow and secondary to hypoxic pulmonary vasoconstriction. Isolated rat lung ( n = 32) was used to study (1) the vasoactive action of 5% CO 2 in either N 2 (hypoxic-hypercapnia) or air (normoxic-hypercapnia) at different pulmonary arterial pressure levels induced by graded speed of perfusion flow and (2) the role of nitric oxide (NO) in mediating the pulmonary vascular response to hypercapnia, hypoxia, and flow-associated pulmonary hypertension. The results indicated that inhaled CO 2 reversed pulmonary hypertension induced by hypoxia but not by flow alteration. Endogenous NO attenuates hypoxic pulmonary vasoconstriction but does not augment the CO 2-induced vasodilatation. Acute change in blood flow does not alter the endogenous NO production.

Acute panicogenic, anxiogenic and dissociative effects of carbon dioxide inhalation in patients with post-traumatic stress disorder (PTSD)

Background Increased anxiety and panic to inhalation of carbon dioxide (CO 2) has been described in patients with anxiety disorders, especially panic disorder, compared to healthy subjects. Post-traumatic stress disorder (PTSD) has been hypothesised to resemble panic disorder and is currently classified as an anxiety disorder in DSM-IV. However, there are only very few data available about the sensitivity of patients with PTSD to CO 2. Methods In 10 patients with PTSD, 10 sex- and age-matched healthy subjects and 8 patients with panic disorder we assessed anxiety, panic, dissociative and PTSD symptoms before and after a single vital capacity inhalation of 35% CO 2. Results Patients with PTSD showed an increased anxiety, panic and dissociative reaction to the inhalation of 35% CO 2 compared to healthy participants. PTSD subjects’ responses were indistinguishable from those of panic patients. Additionally, PTSD-typical symptoms like post-traumatic flashbacks were provoked in patients with PTSD after the inhalation of CO 2. Conclusions In our sample, PTSD was associated with an increased CO 2 reactivity, pointing to an increased susceptibility of PTSD patients to CO 2 challenge.

P132 Carbon dioxide sensitivity in patients with hyperventilation syndrome

BackgroundMany body systems may be affected by chronic hyperventilation and symptoms may be wide-ranging. There is no obvious cause, no gold standard test and not all patients with Hyperventilation Syndrome...

Effects of Carbon Dioxide Inhalation on Psychomotor and Mental Performance During Exercise and Recovery

On separate days, 6 highly trained participants performed psychomotor tests while breathing for 60 mm 3 carbon dioxide (CO2) mixtures (room air, 3% CO2, or 4% CO2) prior to, between, and following two 15-mm treadmill exercise bouts (70% VO2max). Each individual was extensively practiced (at least 4 days) before testing began, and both gas conditions and order of tasks were counterbalanced. Results showed physiological reactions and work-related psychomotor effects, but no effects of gas concentration on addition, multiplication, grammatical reasoning, or dynamic postural balance. These findings help define behavioral toxicity levels and support a re-evaluation of existing standards for the maximum allowable concentrations (also emergency and continuous exposure guidance levels) of CO2. This research explored the selection of psychometric instruments of sufficient sensitivity and reliability to detect subtle changes in performance caused by exposure to low levels of environmental stress, in this case differential levels of CO2 in the inspired air.

Relationship between the effect of carbon dioxide inhalation or nilvadipine on orbital blood flow in normal-tension glaucoma.

To investigate the relationship between the effect of carbon dioxide (CO2) inhalation or oral nilvadipine, a calcium-channel blocker, on orbital blood flow in patients with normal-tension glaucoma, as determined by color Doppler imaging. Sixteen patients with normal-tension glaucoma (mean age, 55.6+/-9.8 years; male:female ratio, 3:13) underwent color Doppler imaging to measure the resistance index, and peak systolic and end-diastolic blood flow velocities of the ophthalmic artery, central retinal artery, and nasal and temporal short posterior ciliary arteries. Measurements were taken before and during CO2 supplementation sufficient to increase the end-tidal CO2 partial pressure by 10%. The color Doppler imaging measurements were repeated after 2 to 4 weeks of treatment with 2 mg oral nilvadipine, and comparisons were made between the effects of the two treatments. Both CO2 inhalation and nilvadipine treatment significantly reduced the resistance index in the central retinal artery, nasal short posterior ciliary artery, and temporal short posterior ciliary artery. There was a significant correlation between the effects of the two treatments on the difference in the resistance indexes of the ophthalmic artery and central retinal artery, but not on those of the nasal or temporal short posterior ciliary artery. Both CO2 inhalation and oral nilvadipine significantly reduce the resistance index measured by color Doppler imaging in orbital vessels. The effect of oral nilvadipine might be predicted by CO2 inhalation in patients with normal-tension glaucoma.

Comparison of vasodilatory effect of carbon dioxide inhalation and intravenous acetazolamide on brain vasculature using positron emission tomography

Carbon dioxide (C02) and acetazolamide are increasingly being used as vasodilators to detect cerebrovascular reserve capacity in patients of chronic cerebrovascular disease. The functional cerebrovascular reserve or ability of cerebral vessels to lower their resistance in response to decrease in cerebral perfusion pressure is expressed as change in cerebral blood flow from baseline under a vasodilatory stimuli. Theoretically a vasodilator causing maximum vasodilation, and thereby expressing complete reserve capacity would be more suitable for such a purpose. We quantitatively compared the vasodilating effect of 5% CO2 inhalation and 1 g of intravenous acetazolamide by positron emission tomography. Cerebrovascular reserve was quantified in six patients with chronic cerebrovascular disease in the same sitting, using oxygen-15 labeled water (H2 150) positron emission tomography at rest, during 5% CO2 inhalation and after 7 g intravenous acetazolamide. A significant linear correlation in both nonlesion hemisphere (r = 0.7071 p< 0.007) and in lesion hemisphere (r = 0.6261 p< 0.005) was found between CO2 and acetazolamide for cerebrovascular reserve capacity. This correlation improved by considering cerebrovascular reserve per unit change in arterial carbon dioxide (r = 0.7441 P<·0.007 in nonlesion hemisphere and r = 0.7271 P< 0.001 in lesion hemisphere). The quantitative value of global reserve capacity was different by CO2 stimuli (5.2%) and acetazolamide (49.7%). Though a similar vasodilatory response is elicited by both vasodilators, acetazolamide seems to be more potent and therefore should be preferred to detect patients with exhausted cerebrovascular reserve capacity. [Neural Res 1997; 19: 139–144]

Instructional set does not alter outcome of respiratory challenges in panic disorder

In an attempt to reproduce the findings of Rapee et al (1986) that instructional set could alter the anxiogenic effects of carbon dioxide inhalation, 45 patients with panic disorder received two sets of instructions and then underwent a series of respiratory challenges (room air hyperventilation, 5% and 7% CO2 inhalation). The instructions failed to alter the anxiogenic response to any of the interventions.

Proconflict effect of carbon dioxide inhalation in rats

The effect of brief inhalation of carbon dioxide (CO 2) was studied in a conflict situation (Vogel test) in the rat. This treatment, which inhibits γ-aminobutyric acid (GABA)-mediated transmission in rat brain and induces anxiety and panic attacks in humans, elicited a proconflict effect. Exposure of rats for l min to CO 2 decreased by ~ 40% the number of licking periods in the test. This effect was abolished by prior administration of alprazolam (0.5 mg per kilogram of body Mass, I.p.). Although these results may support a role for GABA-mediated transmission in the anxiogenic effect of CO 2 inhalation, the possibility that different neurotransmitters other than GABA are involved in the action of CO 2 can not be ruled out.

Effects of carbon dioxide inhalation on cerebral blood flow and oxygen tissue level in spontaneously hypertensive rabbits.

Because previous studies have yielded conflicting results, this study was designed to investigate the efficiency of cerebrovascular reactivity to carbon dioxide in hypertension associated with moderate diffuse cerebral ischemic lesions. The effects of carbon dioxide inhalation on mean arterial blood pressure, heart and respiration rates, cerebral cortical blood flow, polarographically detected oxygen currents (oxygen availability), and cerebral electrical activity were compared in 14 spontaneously hypertensive and 16 normotensive rabbits anesthetized with urethane and alpha-chloralose. Blood flow was measured with the hydrogen clearance and thermal clearance methods. In the resting state the frequency of electrical activity shifted to slower components, the levels of oxygen availability and cerebral blood flow were lower (p less than 0.01), and the ratio of the two latter parameters was greater (p less than 0.01) in hypertensive rabbits than in normotensive animals. Carbon dioxide inhalation induced more marked increases in cerebral blood flow, respiration rate, and oxygen availability in hypertensive (p less than 0.01) than in normotensive (p less than 0.05) rabbits. The ratio of oxygen availability to cerebral blood flow decreased (p less than 0.01) in the former and did not change significantly in the latter group. The carbon dioxide-induced rise in blood flow was also slower and more protracted in hypertensive rabbits (p less than 0.01). Histological investigation revealed groups of neurons with ischemic changes in the cortex of the hypertensive rabbits. We suggest that in hypertensive rabbits the mild multiple ischemic lesions are the basis of functional disturbances, including reduced resting cerebral blood flow, greater oxygen tissue level, slower response to carbon dioxide, and greater vasodilatory capacity.

The effects of carbon dioxide inhalation of plasma MHPG, plasma hormones respiratory rate, and behavior in the Rhesus monkey

The effects of inhalation of air and 3 concentrations of carbon dioxide (CO2) on plasma levels of the norepinephrine metabolite, MHPG, plasma hormones, and behavioral activation were assessed in eight chair-adapted Rhesus monkeys (Macaca mulatta). In comparison to air, inhalation of 5%, 7.5% and 10% CO2 for 180 minutes produced significant dose-dependent increases in respiratory rate, plasma MHPG, cortisol, growth hormone and prolactin. CO2 at the 7.5% concentration produced peak changes in behavior at 15, growth hormone at 30, and cortisol and MHPG at 180 minutes without producing changes in prolactin. The lack of previously reported CO2 induced changes in MHPG, growth hormone and prolactin in humans exposed to 7.5% CO2 for only 15 minutes, may therefore relate to the relatively short duration of CO2 exposure.

Panic disorder, the ventilatory response to carbon dioxide and respiratory variables.

Increased sensitivity of the central carbon dioxide chemoreceptors to carbon dioxide has been hypothesized as a biologic determinant of panic attacks in panic disorder and on voluntary inhalation of carbon dioxide mixtures. The ventilatory response to carbon dioxide, a measure of sensitivity, was assessed in 12 patients with panic disorder and 12 matched normal controls. While mean sensitivity was similar for both groups, for the panic disorder patients, mean sensitivity due to the tidal volume component was significantly less than for the normal controls, and mean sensitivity due to the frequency component was significantly greater than for the normal controls. The interpretation of the effects of carbon dioxide inhalation as a neurobiologic and behavioral probe may be enhanced if the components of the ventilatory response are examined separately.

Effects of carbon dioxide inhalation on preoptic thermosensitive neurons.

The effects of inspired CO2 on preoptic thermosensitive neurons were studied in urethanized rats. Most of the neurons changed their activities diversely while the rat breathed 4%, 7%, and 10% CO2 gas mixtures. Half of the neurons increased activity during CO2 inhalation, but activity was not necessarily intensified by elevating CO2 concentration. Thermosensitive neurons tended to increase activity more than thermally insensitive neurons. The effect of CO2 on sensitivity of thermosensitive neurons was also examined by regression of neuronal activity on preoptic temperature. The slopes of the regression lines during CO2 inhalation did not differ significantly from those during air inhalation in either warm-sensitive or cold-sensitive neurons, but CO2 did elevate the intercepts in most instances (P less than 0.01). However, if P less than 0.05 is accepted as a significance level, the slopes of the regression lines for warm-sensitive neurons tended to decrease during CO2 inhalation (9/39 pairs). The present results indicate that preoptic thermosensitive neurons generally increase their activities and modify their thermosensitivities during CO2 inhalation.

Effects of carbon dioxide inhalation on psychomotor and mental performance during exercise and recovery.

Psychomotor and mental tests involving reaction time, rotor pursuit, short-term memory for digits and letters, and reasoning ability were administered to subjects inhaling up to 5% CO2 in air and in gas mixtures containing 50% O2, The psychomotor and mental tests were given during the 6 min of recovery following 10 min of treadmill running at 80% of aerobic capacity. Although the subjects inhaled the CO2 during the entire exercise and recovery period there was no difference in performance between the CO2 inhalation condition and the control condition for any of the performance measures.

Cerebrovascular response to CO 2 during hyperthermia

ARTICLESCerebrovascular response to CO 2 during hyperthermiaJS Colton, and HM FrankelJS Colton, and HM FrankelPublished Online:01 Nov 1972https://doi.org/10.1152/ajplegacy.1972.223.5.1041MoreSectionsPDF (798 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByEffect of short-term exercise-heat acclimation on ventilatory and cerebral blood flow responses to passive heating at rest in humansNaoto Fujii*, Bun Tsuji, Yasushi Honda, Narihiko Kondo, and Takeshi Nishiyasu1 September 2015 | Journal of Applied Physiology, Vol. 119, No. 5Last Word on Point:Counterpoint: Humans do/do not demonstrate selective brain cooling during hyperthermiaMatthew D. White, Jesse G. Greiner, and Patrick L. L. McDonald1 February 2011 | Journal of Applied Physiology, Vol. 110, No. 2Control of Cerebral Vascular Smooth Muscle During General Anaesthesia30 May 2008Cardiovascular Adjustments to Heat Stress1 January 2011Heat stress effects on capillary blood flow and its redistribution in the laying henPfl�gers Archiv European Journal of Physiology, Vol. 390, No. 1The Myogenic Response1 January 2011The redistribution of cardiac output in the dog during heat stressJournal of Thermal Biology, Vol. 1, No. 1The Effect of Carbon Dioxide Inhalation on Cerebral Blood Flow: A Two-Hour Duration Study in Dogs With MicrospheresStroke, Vol. 5, No. 3Effects of exposure to hot environments on the regional distribution of blood flow and on cardiorespiratory function in sheepPfl�gers Archiv European Journal of Physiology, Vol. 344, No. 2Effects of exposure to hot environments on total and regional blood flow in the brain and spinal cord of the sheepPfl�gers Archiv European Journal of Physiology, Vol. 344, No. 4 More from this issue > Volume 223Issue 5November 1972Pages 1041-1043 Copyright & PermissionsCopyright © 1972 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1972.223.5.1041PubMed4654338History Published online 1 November 1972 Published in print 1 November 1972 Metrics

Effect of carbon dioxide inhalation on the pattern of gaseous metabolism in ischaemic zones of the primate cortex. An experimental study of the 'intracerebral steal' phenomenon in baboons.

The cortical circulation of the baboon has been studied during ischaemia produced by middle cerebral occlusion. Evidence of reactive hyperaemia did not occur in hypercapnia. Metabolic studies as a whole present evidence of increased interference with gaseous metabolism during hypercarbic occlusion, despite raised venous pO(2) during hypercarbia. The significance of these findings is discussed.

Total and regional cerebral blood flow in unanesthetized dogs.

Total and regional cerebral blood flow in unanesthetized dogs.

The use of ultrasound to determine cerebral arterial reserve.

TEST to detect individuals likely to develop an ischemic cerebrovascular accident would have wide applicability. The majority of victims of cerebrovascular disease already have a neurological deficit when first seen by a physician. Such deficits are often permanent , the brain tolerating ischemia poorly. Some patients seek medical attention prior to a major stroke because of transient ischemic attacks. I f these patients have a correctable lesion, surgical results are favorable.4,13 Results of vascular surgery following a completed stroke have been discouraging. Consequently, some have considered such surgery primarily prophylactic. 8,~3 Also, medical therapy would likely have its best results when applied prophylactically. In order to apply appropriate preventive measures, the s troke-prone individual must first be identified. The patient with vascular disease such as a carotid occlusion may have a normal cerebral blood flow. 28 Such a patient, however, has been shown to have diminished cerebral arterial reserve. 2,7 For example, he is less able to maintain adequate cerebral blood flow in the face of hypotension, ~, 19 and to increase cerebral blood flow in response to stimulus such as carbon dioxide inhalation.2,24,27,a2 We suggest that a useful method for identifying the stroke-prone individual could be based on the concept of cerebrovaseular reserve. We have evaluated the effect of carbon dioxide inhalation on common carotid blood flow as an indication of cerebral arterial reserve.

The effect of hypercapnia on brain permeability to protein.

HYPERCAPNIA is known to influence the penetration of a variety of substances into the brain. Investigations have ranged from the effect of carbon dioxide inhalation on the regional uptake of trifluoroiododomethane labeled with radioactive iodine (131I),1a rapidly penetrating compound that essentially measures blood flow, to the entry of viruses and colloidal carbon,2particles that ordinarily have limited access to the central nervous system. In addition, the accumulation of various drugs3and ions4,5has been studied in the hypercapnic animal. An analysis of the results of these latter experiments has required consideration of enhanced blood flow, changes in ionization of drugs secondary to increased hydrogen ion activity, and alteration in the degree of metabolic incorporation or binding in brain and plasma. Other studies have implied a pathological increase in blood-brain permeability to plasma proteins. Clemedson et al6exposed rabbits, guinea pigs, and cats

EFFECTS OF CARBON DIOXIDE INHALATION UPON CEREBRAL BLOOD FLOW.

A method of coupling indirect brachial artery injection with high‐speed film changing in order to investigate the effects of inhaled CO2 on cerebral blood flow is described. Inhalation of 95 per cent oxygen and 5 per cent carbon dioxide results in increased arterial flow and increased numbers of visible vessels. The site of this effect is thought to be the arteriole‐capillary network.