Alterations In PCO2 Research Articles

Choroid plexus aquaporin 1 and intracranial pressure are increased in obese rats: towards an idiopathic intracranial hypertension model?

Idiopathic intracranial hypertension (IIH) is a condition of increased intracranial pressure (ICP) without identifiable cause. The majority of IIH patients are obese, which suggests a connection between ICP and obesity. The aim of the study was to compare ICP in lean and obese rats. We also aimed to clarify if any ICP difference could be attributed to changes in some well-known ICP modulators; retinol and arterial partial pressure of CO2 (pCO2). Another potential explanation could be differences in water transport across the choroid plexus (CP) epithelia, and thus we furthermore investigated expression profiles of aquaporin 1 (AQP1) and Na/K ATPase. ICP was measured in obese and lean Zucker rats over a period of 28 days. Arterial pCO2 and serum retinol were measured in serum samples. The CPs were isolated, and target messenger RNA (mRNA) and protein were analyzed by quantitative PCR and western blot, respectively. Obese rats had elevated ICP compared to lean controls on all recording days except day 0 (P<0.001). Serum retinol (P=0.35) and arterial pCO2 (P=0.16) did not differ between the two groups. Both AQP1 mRNA and protein levels were increased in the CP of the obese rats compared to lean rats (P=0.0422 and P=0.0281). There was no difference in Na/K ATPase mRNA or protein levels (P=0.2688 and P=0.1304). Obese Zucker rats display intracranial hypertension and increased AQP1 expression in CP compared to lean controls. The mechanisms behind these changes are still unknown, but appear to be unrelated to altered pCO2 levels or retinol metabolism. This indicates that the increase in ICP might be related to increased AQP1 levels in CP. Although further studies are warranted, obese Zucker rats could potentially model some aspects of the IIH pathophysiology.

PCO2 effects on species composition and growth of an estuarine phytoplankton community

The effects of ongoing changes in ocean carbonate chemistry on plankton ecology have important implications for food webs and biogeochemical cycling. However, conflicting results have emerged regarding species-specific responses to pCO2 enrichment and thus community responses have been difficult to predict. To assess community level effects (e.g., production) of altered carbonate chemistry, studies are needed that capitalize on the benefits of controlled experiments but also retain features of intact ecosystems that may exacerbate or ameliorate the effects observed in single-species or single cohort experiments. We performed incubations of natural plankton communities from Narragansett Bay, RI, USA in winter at ambient bay temperatures (5–13 °C), light and nutrient concentrations. Three levels of controlled and constant CO2 concentrations were imposed, simulating past, present and future conditions at mean pCO2 levels of 224, 361, and 724 μatm respectively. Samples for carbonate analysis, chlorophyll a, plankton size-abundance, and plankton species composition were collected daily and phytoplankton growth rates in three different size fractions (<5, 5–20, and >20 μm) were measured at the end of the 7-day incubation period. Community composition changed during the incubation period with major increases in relative diatom abundance, which were similar across pCO2 treatments. At the end of the experiment, 24-hr growth responses to pCO2 levels varied as a function of cell size. The smallest size fraction (<5 μm) grew faster at the elevated pCO2 level. In contrast, the 5–20 μm size fraction grew fastest in the Present treatment and there were no significant differences in growth rate among treatments in the >20 μm size fraction. Cell size distribution shifted toward smaller cells in both the Past and Future treatments but remained unchanged in the Present treatment. Similarity in Past and Future treatments for cell size distribution and growth rate (5–20 μm size fraction) illustrate non-monotonic effects of altered pCO2 on ecological indicators and may be related to opposing physiological effects of high CO2 and low pH both within and among species. Interaction of these effects with other factors (e.g., nutrients, light, temperature, grazing, initial species composition) may explain variability among published studies. The absence of clear treatment-specific effects at the community level suggests that extrapolation of species-specific responses or experiments with only present day and future pCO2 treatments levels could produce misleading predictions of ocean acidification impacts on plankton production.

Cerebral blood flow and cerebral edema in rats with diabetic ketoacidosis.

OBJECTIVE— Cerebral edema (CE) is a potentially life-threatening complication of diabetic ketoacidosis (DKA) in children. Osmotic fluctuations during DKA treatment have been considered responsible, but recent data instead suggest that cerebral hypoperfusion may be involved and that activation of cerebral ion transporters may occur. Diminished cerebral blood flow (CBF) during DKA, however, has not been previously demonstrated. We investigated CBF and edema formation in a rat model of DKA and determined the effects of bumetanide, an inhibitor of Na-K-Cl cotransport.RESEARCH DESIGN AND METHODS— Juvenile rats with streptozotocin-induced DKA were treated with intravenous saline and insulin, similar to human treatment protocols. CBF was determined by magnetic resonance (MR) perfusion–weighted imaging before and during treatment, and CE was assessed by determining apparent diffusion coefficients (ADCs) using MR diffusion–weighted imaging.RESULTS— CBF was significantly reduced in DKA and was responsive to alterations in pCO2. ADC values were reduced, consistent with cell swelling. The reduction in ADCs correlated with dehydration, as reflected in blood urea nitrogen concentrations. Bumetanide caused a rapid rise in ADCs of DKA rats without significantly changing CBF, while saline/insulin caused a rapid rise in CBF and a gradual rise in ADCs. DKA rats treated with bumetanide plus saline/insulin showed a trend toward more rapid rise in cortical ADCs and a larger rise in striatal CBF than those observed with saline/insulin alone.CONCLUSIONS— These data demonstrate that CE in DKA is accompanied by cerebral hypoperfusion before treatment and suggest that blocking Na-K-Cl cotransport may reduce cerebral cell swelling.

Effects of increased atmospheric CO&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt; on small and intermediate sized osmotrophs during a nutrient induced phytoplankton bloom

Abstract. We report the transient population dynamic response of the osmotrophic community initiated by a nutrient pulse in mesocosms exposed to different pCO2 levels. Differences in phytoplankton and heterotrophic bacteria abundances associated with the CO2 treatment are also described. Coastal seawater was enclosed in floating mesocosms (27 m3) and nutrients were supplied initially in order to stimulate growth of microbial organisms, including the coccolitophorid Emiliania huxleyi. The mesocosms were modified to achieve 350 μatm (1×CO2), 700 μatm (2×CO2) and 1050 μatm (3×CO2) CO2 pressure. The temporal dynamics was related to nutrient conditions in the enclosures. Numerically small osmotrophs (picoeukaryotes and Synechoccocus sp.) dominated initially and towards the end of the experiment, whereas intermediate sized osmotrophs bloomed as the initial bloom of small sized osmotrophs ceased. Maximum concentrations of E. huxleyi were approximately 4.6×103 cells ml−1 whereas other intermediate sized osmotrophs reached approximately twice as high concentrations. The osmotrophic succession pattern did not change, and neither were we able to detect differences with regard to presence or absence of specific osmotrophic taxa as a consequence of altered pCO2. Towards the end of the experiment we did, however, record significantly higher picoeukaryotic- and lower Synechococcus-abundances in the higher CO2 treatments. Slightly increased cell concentrations of E. huxleyi and other nanoeukaryotes were also recorded at elevated pCO2 on certain days.

Optimized stomatal conductance and the climate sensitivity to carbon dioxide

Stomatal conductance shapes the exchange of water and carbon of vegetated land surfaces. Previous studies have demonstrated that optimized stomatal functioning that maximizes productivity provides a realistic description of how stomata operate. Here I investigate the role of optimum stomatal functioning for the sensitivity of terrestrial productivity and land surface climate to concentrations of atmospheric carbon dioxide (pCO2). I conduct sensitivity simulations with a coupled vegetation‐climate system model with different values of maximum stomatal conductance at different prescribed levels of pCO2. The optimum in stomatal conductance shifts to lower values with increasing pCO2, which is consistent with observed sensitivities of stomatal density of leaves. If this change in optimum conditions is not taken into account, the climate sensitivity shows (1) a general underestimation of terrestrial productivity under altered pCO2, and (2) different sensitivities of key climatic variables to pCO2. The climate sensitivity of land temperature for a doubling of pCO2 ranges from ΔT = 2.7 K to ΔT = 3.2 K, depending on whether stomata adapt optimally or not at all. These results demonstrate that the assumed ability of vegetation to adapt to its environment can have important consequences for the simulated climate system sensitivity to pCO2.

Development of diffuse correlation techniques for non-invasive measurement of cerebral blood flow and oxygen metabolism in rats

Our group has pioneered the development of diffuse correlation tomography (DCT) for measurement of cerebral blood flow (CBF) through the intact skull in animal models and finally in adult human brain. By combining DCT with simultaneous diffuse optical tomography(DOT) which images changes in oxyhemoglobin (rHbO2), deoxyhemoglobin (rHb) and total hemoglobin (rTHC) concentrations, and blood oxygen saturation (dYt), we can derive an image of the relative cerebral metabolic rate of oxygen (rCMRO2). Previously, we have obtained images in rat brain during hypercapnia 1 and focal transient ischemia 2, and now present data in cortical spreading depression (CSD). The development of this technique enables us to carry out longitudinal studies in small animals relatively noninvasively. After validating the combined DOT/DCT technique using a well characterized system (hypercapnia) 1, we then obtained data in a middle cerebral artery occlusion model in the rat 2. In the penumbra, rCBF decreased to 424%, dYt decreased by 114% and rCMRO2 decreased to 594%. These data are in reasonable agreement with values reported in the literature and were the first images of rCMRO2 obtained by diffuse optical methods. Recently, we have induced cortical spreading depression (CSD) in twenty-six rats by applying KCl through a burr hole over the parietal cortex under hypocapnia, normocapnia, and hypercapnia. Figure 1a shows images of rCBF at selected time points and at different depths. A region of increased CBF progressed from the point where the KCl was applied, spreading throughout the cortex. The observed response was mainly constrained to the upper cortex, illustrating the depth selectivity of the imaging technique (Figure 1b). We observed significant correlations of the peak amplitude of rCBF and frequency of the CSD waves with alterations in pCO2 (Figure 1c). Similar results were obtained in the oxygenation and CMRO2 images. By imaging multiple parameters simultaneously we are able to characterize the CSD physiology more thoroughly than usual DOT. Overall these results have validated and demonstrated the utility of DCT methods in obtaining 3D dimensional, dynamic images of blood flow and hence enabling measurement of CMRO2. We discuss the extension of this technique to measurements in the adult human in an accompanying abstract.

Differential responses to CO2 and sympathetic stimulation in the cerebral and femoral circulations in humans

The relative importance of CO2 and sympathetic stimulation in the regulation of cerebral and peripheral vasculatures has not been previously studied in humans. We investigated the effect of sympathetic activation, produced by isometric handgrip (HG) exercise, on cerebral and femoral vasculatures during periods of isocapnia and hypercapnia. In 14 healthy males (28.1 +/- 3.7 (mean +/- S.D.) years), we measured flow velocity (VP; transcranial Doppler ultrasound) in the middle cerebral artery during euoxic isocapnia (ISO, +1 mmHg above rest) and two levels of euoxic hypercapnia (HC5, end-tidal P(CO(2)), P(ET,CO2), = +5 mmHg above ISO; HC10, P(ET,CO2) = +10 above ISO). Each P(ET,CO2) level was maintained for 10 min using the dynamic end-tidal forcing technique, during which increases in sympathetic activity were elicited by a 2-min HG at 30% of maximal voluntary contraction. Femoral blood flow (FBF; Doppler ultrasound), muscle sympathetic nerve activity (MSNA; microneurography) and mean arterial pressure (MAP; Portapres) were also measured. Hypercapnia increased VP and FBF by 5.0 and 0.6% mmHg-1, respectively, and MSNA by 20-220%. Isometric HG increased MSNA by 50% and MAP by 20%, with no differences between ISO, HC5 and HC10. During the ISO HG there was an increase in cerebral vascular resistance (CVR; 20 +/- 11%), while VP remained unchanged. During HC5 and HC10 HG, VP increased (13% and 14%, respectively), but CVR was unchanged. In contrast, HG-induced sympathetic stimulation increased femoral vascular resistance (FVR) during ISO, HC5 and HC10 (17-41%), while there was a general decrease in FBF below ISO. The HG-induced increases in MSNA were associated with increases in FVR in all conditions (r = 0.76-0.87), whereas increases in MSNA were associated with increases in CVR only during ISO (r = 0.91). In summary, in the absence of hypercapnia, HG exercise caused cerebral vasoconstriction, myogenically and/or neurally, which was reflected by increases in CVR and a maintained VP. In contrast, HG increased FVR during conditions of ISO, HC5 and HC10. Therefore, the cerebral circulation is more responsive to alterations in PCO2, and less responsive to sympathetic stimulation than the femoral circulation.

Cerebrovascular carbon dioxide reactivity assessed by intracranial pressure dynamics in severely head injured patients.

Appropriate management of intracranial pressure (ICP) in severely head injured patients depends in part on the cerebral vessel reactivity to PCO2; loss of CO2 reactivity has been associated with poor outcome. This study describes a new method for evaluating vascular reactivity in head-injured patients by determining the sensitivity of ICP change to alterations in PCO2. This method was combined with measurements of the pressure volume index (PVI), which allowed calculation of blood volume change necessary to alter ICP. The objective of this study was to investigate the ICP response and the blood volume change corresponding to alterations in PCO2 and to examine the correlation of responsivity and outcome as measured on the Glasgow Outcome Scale. The PVI and ICP at different end-tidal PCO2 levels produced by mild hypo- and hyperventilation were obtained in 49 patients with Glasgow Coma Scale scores of less than 8 and over a wide range of PCO2 (25 to 40 mm Hg) in eight patients. Given the assumption that the PVI remained constant during alteration of PaCO2, the estimated blood volume change per torr change of PCO2 was calculated by the following equation: BVR = PVI x delta log(ICP)/delta PCO2, where BVR = blood volume reactivity. The data in this study showed that PVI remained stable with changes in PCO2, thus validating the assumption used in the blood volume estimates. Moreover, the response of ICP to PCO2 alterations followed an exponential curve that could be described in terms of the responsivity indices to capnic stimuli. It was found that responsivity to hypocapnia was reduced by 50% compared to responsivity to hypercapnia measured within 24 hours of injury (p < 0.01). The sensitivity of ICP to estimated blood volume changes in patients with a PVI of less than 15 ml was extremely high with only 4 ml of blood required to raise ICP by 10 mm Hg. The authors conclude from these data that, following traumatic injury, the resistance vessels are in a state of persistent vasoconstriction, possibly due to vasospasm or compression. Furthermore, BVR correlates with outcome on the Glasgow Coma Scale, indicating that assessment of cerebrovascular response within the first 24 hours of injury may be of prognostic value.

Complications of Intrahospital Transport in Critically Ill Patients

To determine the frequency of hemodynamic and respiratory complications during movement within the hospital, we conducted a prospective study involving 36 critically ill, ventilator-dependent patients who needed procedures done outside the intensive care unit. During the first 20 transports, patients received ventilation through a manual resuscitation bag. Arterial blood gas measurements showed frequent changes from baseline with alterations in PCO2 (greater than 10 torr) or pH (greater than 0.05) occurring on 14 occasions. In a subsequent study, 16 patients received ventilation during transit with the aid of a portable mechanical ventilator. Although 6 patients showed changes in arterial blood gas values, mean changes in PCO2 and pH were significantly less than in the group that received manual ventilatory support. (p less than 0.01). Hemodynamic complications of hypotension and cardiac arrhythmia showed a significant correlation with disturbances in arterial blood gases (p less than 0.05). Although limited by the lack of a control period, this study shows that the transport of critically ill patients may result in severe hemodynamic complications; it also suggests that these complications might be prevented by more careful monitoring of ventilation.

Interactive effects of CO2 and upper airway negative pressure on breathing pattern.

The interactive effects of upper airway negative pressure and hypercapnia on the pattern of breathing were assessed in pentobarbital-anesthetized cats. At any given level of pressure in the upper airway, hypercapnia increased respiratory rate, reduced inspiratory time, and augmented tidal volume, inspiratory airflow, and the peak and rate of rise of diaphragm electrical activity. Conversely, at any given level of CO2, upper airway negative pressure decreased respiratory rate, prolonged inspiratory time, and depressed inspiratory airflow and diaphragm electromyogram (EMG) rate of rise. Application of negative pressure to the upper airway shifted the relationship between tidal volume and inspiratory time upward and rightward. The relationship between inspiratory and expiratory times, however, was linearly correlated over a wide range of chemical drives and levels of upper airway pressure. These results suggest that in the anesthetized cat upper airway negative pressure afferent inputs 1) interact in an additive fashion with hypercapnia to alter the pattern of breathing, 2) interact multiplicatively with CO2 to influence mean inspiratory airflow and diaphragm EMG rate of rise, 3) depress the generation of central inspiratory activity, 4) increase the time-dependent volume threshold for inspiratory termination, and 5) affect the ratio between inspiratory and expiratory times in a similar manner as alterations in PCO2.

Contribution of the Bohr effect to the fall in fetal PO2 caused by maternal alkalosis.

A decrease in the PO2 of fetal arterial blood is observed in maternal alkalosis caused by hyperventilation in labour or exercise. The contribution of altered blood oxygen affinity to this effect was studied experimentally and by computer simulation of placental gas exchange. Thirteen guinea pigs near term of pregnancy were anesthetized and the right atrium of the fetus was catheterized to enable continuous and simultaneous measurement of PO2 and PCO2 by mass spectrometry. An infusion of base was given through a catheter in the descending aorta of the dam and the effect on fetal respiratory gas tensions observed. The mean change in maternal arterial pH measured in blood taken from a femoral artery was 0.07 +/- 0.04 (mean +/- S. D.). There was an immediate decrease in PO2 in the right atrium of the fetus, but no consistent alteration in PCO2. Two minutes after the start of the infusion, PO2 had fallen by 3.2 +/- 1.6 Torr (p less than 0.001) and PCO2 had risen by 1.7 +/- 1.8 Torr (not significant). The experiments were simulated using a mathematical model of placental gas exchange in the guinea pig. The model was able to predict the change in fetal arterial PO2, given numerical values for the pH, PO2 and PCO2 of fetal and maternal arterial blood prior to infusion of base and for maternal blood during the infusion of base. These values were obtained from the experimental data. Other input variables of the model were maternal and fetal hematocrit and DPG concentration, and the rates of blood flow on the two sides of the placenta.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of a calcium antagonist (nimodipine) on basal cerebral blood flow and reactivity to various agonists.

In vitro studies suggest that cerebrovascular contraction is more dependent on the influx of calcium to smooth muscle than general systemic arteries. The present study tested the in vivo effects of a calcium influx blocker (nimodipine) on cerebral blood flow and metabolism in 16 baboons. The 133xenon clearance technique was used together with careful control of EEG and blood gases. With normal blood gases intravenous nimodipine infusion (1 microgram/kg/min) produced an 18% increase in cerebral blood flow with no alteration in cerebral oxidative metabolism or blood pressure. Higher doses (above 10 micrograms/kg/min) resulted in a decreased arterial blood pressure and a return to control cerebral flow. Infusion of the dose producing maximal increase in flow, decreased the cerebral reactivity to altered PCO2 (n = 5). These results suggest that nimodipine may be a relatively selective cerebrovascular dilator.

Effects of acute alterations in PCO2 on proximal HCO-3, Cl-, and H2O reabsorption

The effect of acute changes in arterial PCO2 on absolute proximal reabsorption of bicarbonate, chloride, and water has not been systematically studied. In the present free-flow micropuncture studies in Munich-Wistar rats, arterial PCO2 was increased or decreased by 20 mmHg. Under conditions of stable SNGFR, proximal and whole kidney electrolyte reabsorption was measured. Acute hypocapnia decreased absolute proximal bicarbonate reabsorption by 23% (from 1,008 +/- 38 to 773 +/- 36 pmol/min). Proximal volume reabsorption also decreased. Although bicarbonate delivery out of the superficial proximal convoluted tubule did not exceed normal levels, bicarbonaturia developed, suggesting an additional suppression of acidification by distal and/or juxtamedullary nephron segments. Acute hypercapnia increased absolute proximal bicarbonate reabsorption by only 10% in chronically alkalotic animals (from 1,050 +/- 68 to 1,176 +/- 77 pmol/min). In acutely alkalotic animals, hypercapnia caused no significant increment in the higher basal level of absolute proximal bicarbonate reabsorption (from 1,158 +/- 120 to 1,234 +/- 97 pmol/min). Whole kidney bicarbonate reabsorption rose, again suggesting a distal and/or juxtamedullary effect. Hypercapnia inhibited proximal chloride reabsorption and caused a chloruresis. In conclusion, acute hypo- and hypercapnia caused alterations in proximal bicarbonate, chloride, and sodium transport that may participate, at least in part, in the changes in whole kidney electrolyte reabsorption observed in these conditions. Distal and/or juxtamedullary nephrons also appeared to contribute to the changes in renal acidification induced by alterations in systemic PCO2.

Temperature-induced changes in blood acid-base status: Donnan rCl and red cell volume.

The Donnan ratio for chloride ion (rCl) was determined for human red cells in plasma utilizing 36Cl. The effect of altered PCO2 and pH on rCl was followed in two ways. CO2 partial pressure was varied (1-1.5% CO2 in O2; pH range 7.1-7.9) at 37.5 degrees C (isothermal); PCO2 and pH were also changed by altering temperature (range 5-45 degrees C) at constant CO2 content (temperature induced). At pH 7.4 and 37.5 degrees C, rCl was 0.631 +/- 0.0269 (SE, N = 5); isothermal drcl/dpH = -0.306 +/- 0.0234. When measured under conditions of variable temperature at constant CO2 content (pH range 7.3-7.9), drcl/dpH = .018 +/- 0.0232, significantly different from isothermal response (P less than 0.001). Hematocrit (H) changes with pH for conditions of initial H(7.4) of 0.45, under these conditions were also determined: isothermal dH/dpH = -0.031 +/- 0.0019; temperature induced, -0.004 +/- 0.0009. Temperature change alone at constant carbon dioxide content produces no significant change in distribution of chloride ions or water between erythrocyte and plasma compartments.

Method for measuring brain tissue pressure. Response to alteration in pCO-2 systemic blood pressure, and middle cerebral artery occlusion.

The authors report a method for measuring total local brain tissue pressure (BTP) using a miniature catheter transducer stereotaxically introduced into the white matter of the cat's cerebrum. Quantitative rapid phasic pressure changes were satisfactorily demonstrated. Due to some drift of baseline of the transducers and inability to perform in vivo calibration, reliable long-term quantitative pressure measurements sometimes could not be studied. The BTP from each cerebral hemisphere and the cisternal pressure (CP) were monitored during alterations of pCO-2 and systemic blood pressure, and distilled H20 injection prior to and after right middle cerebral artery (MCA) ligation. The catheter transducers functioned well on chronic implantation for up to 6 weeks. Compared to the chronically implanted catheters, acutely implanted catheters responded identically except for drift. The response of intracranial pressure and CP to MCA occlusion, alterations in pCO2, and systemic blood pressure were similar. No BTP gradients appeared in response to MCA ligation, hypercapnia, hypertension, or progressive swelling of the resulting infarction.

An implantable glass electrode used for pH measurement in working skeletal muscle.

ArticleAn implantable glass electrode used for pH measurement in working skeletal muscle.G Gebert, and S M FriedmanG Gebert, and S M FriedmanPublished Online:01 Jan 1973https://doi.org/10.1152/jappl.1973.34.1.122MoreSectionsPDF (470 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAnaerobic MetabolismCauses of differences in exercise-induced changes of base excess and blood lactate7 November 2006 | European Journal of Applied Physiology, Vol. 99, No. 2Effects of changes in pH on the afferent impulse activity of isolated cat muscle spindlesBrain Research, Vol. 1043, No. 1-2Regulation and Modulation of pH in the BrainMITCHELL CHESLER1 October 2003 | Physiological Reviews, Vol. 83, No. 4Control of skeletal muscle perfusion at the onset of dynamic exerciseMedicine & Science in Sports & Exercise, Vol. 31, No. 7Relationship of peak exercise capacity with indexes of peripheral muscle vasodilationMedicine &amp Science in Sports &amp Exercise, Vol. 28, No. 1031P-Nuclear magnetic resonance spectroscopy study of the time course of energy metabolism during exercise and recoveryEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 66, No. 6Changes in intracellular pH during repeated exerciseEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 67, No. 3The regulation and modulation of pH in the nervous systemProgress in Neurobiology, Vol. 34, No. 5Changes in extracellular pH during electrical stimulation of isolated rat vagus nerveNeuroscience Letters, Vol. 64, No. 2Continuous monitoring of tissue pH with a fiberoptic conjunctival sensorAnnals of Emergency Medicine, Vol. 14, No. 9The relevance of tumour pH to the treatment of malignant diseaseRadiotherapy and Oncology, Vol. 2, No. 4Differential serotonin responses in the skeletal muscle microcirculationLife Sciences, Vol. 34, No. 12Effects of pH onin vitro gallbladder responses to cholecystokinin octapeptideDigestive Diseases and Sciences, Vol. 27, No. 7Tumour pH in human mammary carcinomaEuropean Journal of Cancer and Clinical Oncology, Vol. 18, No. 5Alkalinization of phosphorylase kinase-deficient muscle during tetanic contractionBioscience Reports, Vol. 1, No. 2The Use of ISMs in Working Skeletal Muscles and Venous Effluent BloodExtracellular K+ concentration and K+ Balance of the gastrocnemius muscle of the dog during exercisePfl�gers Archiv European Journal of Physiology, Vol. 387, No. 3Modification of α-adrenergic responses of small arteries by altered PCO2 and pHEuropean Journal of Pharmacology, Vol. 57, No. 4On-line, computer-controlled potentiometric analysis system1 May 2002 | Analytical Chemistry, Vol. 48, No. 2Glass microelectrode probes for routine pH measurements1 May 2002 | Analytical Chemistry, Vol. 48, No. 2The interstitial pH of the working gastrocnemius muscle of the dogPfl�gers Archiv European Journal of Physiology, Vol. 367, No. 2Reversible metal/salt interfaces and the relation of second kind and all-solid-state membrane electrodes1 May 2002 | Analytical Chemistry, Vol. 46, No. 14Ion selective electrodes, potentiometry, and potentiometric titrations1 May 2002 | Analytical Chemistry, Vol. 46, No. 5 More from this issue > Volume 34Issue 1January 1973Pages 122-4 https://doi.org/10.1152/jappl.1973.34.1.122PubMed4697369History Published online 1 January 1973 Published in print 1 January 1973 Metrics

Vasodilator effect of hypercapnic acidosis on human forearm blood vessels.

ARTICLESVasodilator effect of hypercapnic acidosis on human forearm blood vesselsHA Kontos, DW Richardson, and Patterson JL JrHA Kontos, DW Richardson, and Patterson JL JrPublished Online:01 Dec 1968https://doi.org/10.1152/ajplegacy.1968.215.6.1403MoreSectionsPDF (615 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByHypercapnia elicits differential vascular and blood flow responses in the cerebral circulation and active skeletal muscles in exercising humans24 April 2022 | Physiological Reports, Vol. 10, No. 8Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humansStephane Delliaux, Masashi Ichinose, Kazuhito Watanabe, Naoto Fujii, and Takeshi Nishiyasu1 July 2015 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 309, No. 1Local Analgesia18 July 2014α 1 -Adrenergic responsiveness in human skeletal muscle feed arteries: the impact of reducing extracellular pH15 August 2012 | Experimental Physiology, Vol. 98, No. 1Surgery of the Thoracic Wall18 July 2014The effects of breathing 5% CO 2 on human cardiovascular responses and tolerance to orthostatic stress23 June 2004 | Experimental Physiology, Vol. 89, No. 4Effect of Carbon Dioxide on Cochlear Blood Flow in Guinea Pigs8 July 2009 | Acta Oto-Laryngologica, Vol. 120, No. 1Effect of Carbon Dioxide-Enriched Water and Fresh Water on the Cutaneous Microcirculation and Oxygen Tension in the Skin of the Foot2 July 2016 | Angiology, Vol. 48, No. 4Alkalinizing Agents for the Treatment of Cardiac ArrestAlkali therapy of diabetic ketoacidosis: Biochemical, physiologic, and clinical perspectivesDiabetes / Metabolism Reviews, Vol. 5, No. 8Gas Exchange in Acid‐Base Disturbances1 January 2011Effects of Acid Base Disturbance, Septic Shock, and Calcium and Phosphorous Abnormalities on Cardiovascular FunctionCritical Care Clinics, Vol. 3, No. 4Near Infrared Optical Monitoring of Cat Skeletal Muscle during HypercapniaModification of α-adrenergic responses of small arteries by altered PCO2 and pHEuropean Journal of Pharmacology, Vol. 57, No. 4Effects of altered carbon dioxide tension on hemoglobin oxygenation in hamster cheek pouch microvesselsMicrovascular Research, Vol. 13, No. 2Changes in Microvascular Diameter and Oxygen Tension Induced by Carbon DioxideCirculation Research, Vol. 32, No. 3The effects of acid-base disturbances on cardiovascular and pulmonary functionKidney International, Vol. 1, No. 5Plasma-Renin-Aktivität der Ratte bei systemischer Alkalose und AcidoseZeitschrift für die gesamte experimentelle Medizin einschließlich experimentelle Chirurgie, Vol. 153, No. 3The Influence of Blood pH on Peripheral Vascular Tone: Possible Role of Proteases and Vaso-Active Polypeptides More from this issue > Volume 215Issue 6December 1968Pages 1403-1405 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.215.6.1403PubMed5723001History Published online 1 December 1968 Published in print 1 December 1968 Metrics

Intrcellular hydrogen ion changes and potassium movement.

Intracellular hydrogen ion concentration was determined on skeletal muscle by the DMO technique in dogs subjected to various acid-base alterations. The data verified the fact that a given alteration in Pco2 produces a larger hydrogen ion change in intracellular fluid than in extracellular fluid. In spite of this, however, the ratio (See PDF) decreased. On the basis of this change in ratio, the Donnan equilibrium would predict that potassium would move from intracellular to extracellular compartment and not in the reverse direction as had been assumed previously. Using the change in plasma potassium as the criterion of direction of movement of potassium between intracellular and extracellular fluids, the movement of potassium produced by any of the acid-base alterations which were studied was usually that which would be predicted by the Donnan equilibrium.