The effects of changes in pH and PCO2 in blood and water on breathing in rainbow trout, Salmo gairdneri.

The effect of sustained hypercapnia on the acid-base balance and gill ventilation in rainbow trout, Salmo gairdneri, was studied. The response to an increase in PICO2 from 0.3 to 5.2 mm Hg was a five-fold increase in gill ventilation volume and a slight increase in breathing frequency. There was a concomitant rise in PACO2 and an immediate fall in pHa. If PICO2 was maintained at 5.2 mm Hg for several days, ventilation volume gradually returned to the initial, prehypercapnic level within three days. Arterial pH also returned to the initial level within 2-3 days. These results are consistent with the hypothesis that under these conditions fish regulate pH via HCO3/C1 exchange across the gills rather than by changes in ventilation and subsequent adjustment of PACO2. A reduction in environmental pH causes a reduction in pHa but only a slow gradual increase in VG. Injections of HC1 or NaHCO3 into the blood have opposite effects on pHa but both cause a marked increase in VG. It is concluded that a rise in PACO2 results in a rise in VG and that changes in pH in blood or water have little direct effect on VG in rainbow trout. Possible location for receptors involved in this reflex response are discussed.     

Arterial hydrogen ion versus CO2 on depth and rate of breathing in decerebrate cats.

Arterial blood hydrogen ion concentration (Ha+) was altered over the range of 25 to 110 nM (pH 7.60 to 6.96) by slow intravenous infusion of 1.0 N NaHCO3 or 0.5 N HC1 at controlled levels of Paco2in unanesthetized decerebrate cats. Respiratory f varied as a single function of Vt irrespective of a lterations in Paco2 and Ha+ even after interruption of the carotid sinus nerves. The dependence of f upon Vt was abolished by vagotomy. However, Vt continued to respond to changes in Ha+ over its entire range after combined section of the vagus and carotid sinus nerves. In all statxceeded by 5 to 10 times the delta Vt/delta Ha+ response to acid or bicarbonate infused under isocapnic control. Increases and decreases of ha+ caused downward and upward shifts, respectively, in the operating setpoint of the CO2 regulation system.     

Control of ventilation in the hypercapnic skate Raja ocellata: II. Cerebrospinal fluid and intracellular pH in the brain and other tissues

This study examined the possible role(s) of central acid-base stimuli in the increase in ventilation induced by hypercapnia in the skate, a response that is not due to an O2 signal (Graham et al., Respir. Physiol., 1990, 80: 251-270). Skate were sampled for cerebrospinal fluid (CSF) acid-base status, intracellular pH of the brain (14C-DMO method), and pHi in other tissues throughout 24 h of exposure to PICO2 = 7.5 Torr. CSF PCO2 rapidly equilibrated with the elevated PaCO2. Despite the much lower non-HCO3- buffer capacity in the CSF, CSF pH was not depressed to the same extent as blood pHa. CSF pH was also regulated rapidly, returning to control levels by 8-10 h, whereas pHa remained significantly depressed at 24 h. Similarly, the pHis of the weakly buffered brain and heart ventricle were initially compensated more rapidly than those of more strongly buffered white muscle and red blood cells. However, brain pHi adjustment slowed markedly after 4 h and stabilized at only 70% compensation by 20-24 h, suggesting that brain intracellular acidosis may play a role in the long-term increase in ventilation. CSF and brain were the only compartments which did not exhibit an apparent compounding metabolic acidosis during the initial stages of hypercapnic exposure. While these results illustrate the primacy of central acid-base regulation, they do not support a role for CSF pH in the long-term elevation of ventilation in response to hypercapnia. Depressions in pHa and brain pHi appear the two most likely candidates for proximate stimuli.     

Arterial pH, airway caliber and response to acetylcholine and catecholamines in vivo

Direct assessment of tracheal circumference, which permits evaluation of constriction and dilatation in vivo, was made continuously in intact, pentobarbital-anesthetized, spontaneously breathing dogs. Immediate response to induction of hypercapnia included tracheal constriction and cessation of normal, vagus-dependent rhythmicity of airway tone. The characteristic constrictor response to acetylcholine was exaggerated significantly during hypercapnic acidosis and returned to normal when arterial pH, but not CSF pH, was corrected by NaHCO3 infusion. Epinephrine produced significant tracheal dilatation (infrequently followed by constriction) and isoproterenol produced only dilatation at normal pH. The catecholamine-induced dilatation was decreased significantly during hypercapnic acidosis, but improved after NaHCO3 infusion. Responses to acetylcholine and epinephrine were the the same as control during alkalemia, whereas the response to isoproterenol was unexplainedly diminished. Thus alkalemia may inhibit the action of isoproterenol; acidemia enhances parasympathomimetic constriction and reduces sympathomimetic dilatation; and correction of arterial pH returns these responses to normal, even if hypercapnia and CSF acidosis persist.     

Studies on the Mechanism of the Lower Esophageal Sphincter Pressure Response to Alkali Ingestion in Humans

To clarify the lower esophageal sphincter (LES) pressure response to alkali ingestion, normal subjects and postantrectomy patients with either a gastroduodenostomy or gastrojejunostomy were studied in a double-blind controlled fashion. LES pressure and serum gastrin concentrations were measured after ingestion of a 100 ml bolus of either 0.4 M NaHCO3 or 0.4 M NaCl. In addition, the effect of a therapeutic dose (30 ml) of a commercial antacid preparation was studied in a double-blind fashion in 14 patients with gastroesophageal reflux disease. Peak increases in LES pressure above basal were significantly higher (p less than 0.05) after NaHCO3 than after NaCl in normal subjects and in patients with vagotomy and Billroth I antrectomy, but not in patients with vagotomy and Billroth II antrectomy. Serum gastrin concentrations were unaffected by alkali. Thirty milliliters of liquid antacid containing aluminum and magnesium hydroxide resulted in a small sustained rise in LES pressure over the first 50 min after ingestion, but this was not statistically different than the placebo response. It is suggested that: 1) neither the antrum nor intact vagi nor gastrin were required for NaHCO3 ingestion to increase LES pressure; 2) the increase in LES pressure with NaHCO3 ingestion appears to rely upon an intact duodenum and may relate to volume and osmolarity of the alkali load; and 3) therapeutic doses of a liquid commercial antacid does not significantly increase LES pressure in the presence of an intact stomach.     

Dynamics of brain extracellular fluid pH and phrenic nerve activity in cats after end-tidal CO2 forcing

Ventilation is influenced by the interstitial [H+] of the brain. The pHecf, which in turn is determined largely by ventilation (via PaCO2) is sensed by the central chemoreceptors. In order to investigate the dynamics of both pHecf and neural tidal volume, we measured in cats with cut vagi and sinus nerves the dynamic medullary pHecf changes and the associated changes in integrated phrenic nerve activity after end-tidal CO2 forcing. The medullary surface ecf pH was measured with a glass electrode with a flat pH-sensitive surface. After CO2 up-steps, the pHecf changed with a time constant of about 43 sec, after down-steps 30 sec was found. The central time constant of the neural tidal volume response was 50 sec (mode) in both cases, whereas the overall response had a (modal) time constant of 80 sec. The results indicate that pHecf dynamics and the dynamic characteristics of the central neural respiratory organization are about equally important in determining the dynamic neural tidal volume response. It is argued that when PaCO2 changes, the dynamic pHecf change is perfusion limited and macroscopically homogeneous within the brainstem. Therefore, in our view it seems that the location of the central chemoreceptors within the brainstem is of minor importance in determining the dynamic neural tidal volume response to PaCO2 changes.     

Response of vertebral and carotid blood flow to isocapnic changes in end-tidal oxygen tension

The response of the vertebral and carotid blood flow to isocapnic hypoxia was measured in 9 cats anaesthetized with chloralose-urethane using perivascular electromagnetic flow probes. The carotid flow was already significantly increased when going from hyperoxia (PETO2 55 kPa) to normoxia. For the vertebral blood flow a significant increase compared to hyperoxia was observed at a moderate level of hypoxia (PETO2 9 kPa). The time course of the response of the blood flow to isocapnic step-like changes in PETO2 was fitted with a first order model. The mean time constant (+/- SD) for steps into hypoxia for the carotid flow was 35 +/- 38 sec(8 cats) and for the vertebral flow, 44 +/- 37 sec (5 cats). The mean time constant (+/- SD) for steps out of hypoxia was significantly smaller and found to be 23 +/- 22 sec (8 cats) and 19 +/- 18 sec (4 cats), respectively. We argue that a major part of the changes in vertebral and carotid blood flow to steps into hypoxia goes to brain tissue.     

Ventilatory responses to respiratory and metabolic acid-base disturbances in cats

To determine the relative importance of the peripheral and central chemoreceptors in the ventilatory response to acute metabolic acid-base disturbances we measured the normoxic ventilatory response to acute respiratory and metabolic acidosis and alkalosis in 10 chloralose-urethane anesthetized cats using a technique of vertebral artery perfusion that allows one to independently manipulate the PaCO2, PaO2 and the H+ concentration of the blood in the systemic circulation (peripheral) and the blood perfusing the brain stem (central) (Berkenbosch et al., 1979). The ventilation could be satisfactorily described by a linear function of the peripheral and central arterial H+ concentration and the central PaCO2. Mean values (+/- SEM) found for the peripheral arterial H+ sensitivity and the isocapnic central arterial H+ sensitivity were 26.0 +/- 3.2 and 12.7 +/- 1.8 ml X min-1 X nM-1, respectively; the isohydric central arterial CO2 sensitivity was 545.9 +/- 96.7 ml X min-1 X kPa-1. We conclude that in the ventilatory response to an acute metabolic acid-base disturbance both the peripheral and central chemoreceptors play a role. However, the sensitivity of the peripheral chemoreceptors to isocapnic changes in the arterial H+ concentration is twice as large as the sensitivity of the central chemoreceptors. It is argued that in the adaptation of the ventilation to an acute metabolic acidosis the stimulatory effect of the peripheral chemoreceptors is counteracted by a diminished stimulation of the central chemoreceptors.     

Effects of CO2 and H+ on the ventilatory response to peripheral chemoreceptor stimulation

To determine whether the stimulatory effect of CO2 on the peripheral chemoreceptors is due to molecular CO2, H+ or both we measured steady-state ventilation (Ve) during normoxia in 9 and during hypoxia in 5 chloralose-urethane anaesthetized cats using the artificial brain stem perfusion technique. This technique allows one to manipulate independently the PaCO2, PaO2 and the pHa of the blood in the systemic circulation (peripheral) and the blood perfusing the brain stem (central). Keeping the central conditions constant the H+ and CO2 concentrations in the systemic circulation were changed by i.v. infusion of 0.3 M HCl or 0.6 M NaHCO3 and by giving the animal different CO2 mixtures to inhale. The peripheral H+ concentration ([H+]p) range covered was from 27 to 103 nmol X 1(-1); the peripheral arterial CO2 tension (PaPCO2) ranged from 2.3 kPa to 8.4 kPa. Fitting the data with the function VE = a[H+]p + bPaPCO2 + c revealed that the coefficient b was not significantly different from zero at the 0.05 level during normoxia and hypoxia. The mean value (+/- SEM) found for the coefficient a was 33.0 +/- 3.6 at normoxia and 36.0 +/- 15.4 ml X min-1 X nM-1 at hypoxia. We conclude that the steady-state ventilatory response due to the stimulation of the peripheral chemoreceptors with CO2 is mediated by H+. The effects of molecular CO2 are negligible.     

Comparison of central venous and arterial pH and PCO2 during open-chest CPR in the canine model

Arterial blood gases are difficult to obtain during cardiopulmonary resuscitation (CPR) in human beings, and the possibility of venous sampling is raised frequently. The reliability of central venous gases as a substitute for arterial blood gases in assessing acid base status, however, has not been investigated adequately under conditions of CPR. Therefore, femoral arterial and central venous catheters were placed in 24 mongrel dogs, and ventricular fibrillation was electrically induced. After varying predetermined downtimes from five to 60 minutes, open-chest CPR was begun, and arterial and central venous blood gases were simultaneously drawn every five minutes during a 30-minute period. Arterial pH (pHa) was consistently higher than central venous pH (pHcv) by an average of .048 units. A significant correlation existed between the pHa and pHcv at all times during CPR, with an overall r = .9771 (P less than .0001). The difference between central venous PCO2 (PcvCO2) and arterial PCO2 (PaCO2) was 5.17 mm Hg prior to cardiac arrest, but it increased 300% to a mean of 15.51 mm Hg during CPR. Correction of pHcv using conventional methods to account for this respiratory component decreased the correlation between pHa and pHcv to r = .6905. The ability of pHcv to substitute for pHa was assessed, and showed a sensitivity of 100% when pHa of 7.2 was used as a criterion for treatment. In this model, pHcv is a sensitive indicator of pHa and it may be used to guide bicarbonate therapy. The increased PcvCO2 during CPR probably results from the marked tissue lactic acid production and subsequent shift of the bicarbonate buffer into free carbon dioxide.     

Response of intrapulmonary chemoreceptors in the duck to changes in PCO2 and pH.

We have estimated the relative importance of changes in blood PCO2 and pH in determining activity of intrapulmonary chemoreceptors (IPC) in the unidirectionally ventilated duck. The response of single unit vagal afferents from IPC to changing lung gas PCO2 was tested before and after changing blood pH by intravenous infusion of NaHCO3. Using multiple linear regression analysis, we calculated how much of the change in IPC activity for a given change in PCO2 was due to the changing PCO2 at constant pH (CO2 sensitivity) or to the change in pH concomitant with the change in PCO2 (H+ sensitivity). For 10 IPC, the CO2 sensitivity was on the average 2.3 times larger than the H+ sensitivity. Changes in pH as well as PCO2 of lung blood should be considered in assessing the role of IPC in control of breathing.     

Continuous monitoring of tissue pH with a fiberoptic conjunctival sensor

To assess the relationship between conjunctival pH (pHcj), arterial pH (pHa), and cardiorespiratory variables during normal and low-flow conditions, hemorrhagic hypotension was induced in eight dogs. Conjunctival pH became significantly less than control values after a hemorrhage volume of 15 mL/kg (P less than .05); mean arterial pressure (MAP) did not fall until blood loss was 20 mL/kg. There was poor correlation between pHcj and pHa, cardiac index (CI), or MAP. There was a high degree of correlation, however, between pHcj-pHa difference (delta pH) and MAP (r = -0.886), CI (r = -0.846), and tissue oxygen extraction ratio (r = .896). The results of these experiments indicate that pHcj is a sensitive monitor of peripheral tissue perfusion, and that the degree of physiologic compromise associated with hemorrhage can be determined by analysis of the difference between arterial and conjunctival pH.     

Ventilatory response to carbonic anhydrase inhibition in cats: effects of acetazolamide in intact vs peripherally chemodenervated animals

Hyperventilation induced by red cell carbonic anhydrase inhibition (CAI) has been observed frequently; its mechanism, however, is still obscure. In the present study in anaesthetized cats, we have investigated the effect of 50 mg/kg acetazolamide, a carbonic anhydrase inhibitor, on ventilation. In order to determine the role of the peripheral chemoreceptors, we compared the response in peripherally chemodenervated and intact cats. Furthermore, in cats with intact peripheral chemoreceptors, we determined hypoxic sensitivity before and 2 h after i.v. infusion of the drug. In all animals, acetazolamide caused a large increase in ventilation. However, the peripherally chemodenervated animals developed a significantly larger response than the intact animals (respectively about 200 and 100% increases in ventilation). The first group also showed a significantly larger fall in PACO2. In the intact animals studied, acetazolamide virtually abolished the hypoxic sensitivity which existed before infusion of the drug. We conclude that acetazolamide, at the dose studied, causes a decrease in activity of the peripheral chemoreceptors, and also a decrease (c.q. removal) of their sensitivity to PaO2 changes. The increase in ventilation by acetazolamide is probably caused by an action of the drug on the central nervous system, possibly on the central chemoreceptors.     

Carotid body chemoreceptor and ventilatory responses to sustained hypoxia and hypercapnia in the cat

To understand the role of carotid chemoreceptor activity in the ventilatory responses to sustained hypoxia (30 min) the following measurements were made in cats anesthetized with alpha-chloralose: (1) carotid chemoreceptor and ventilatory responses to isocapnic hypoxia and to hypercapnia during hyperoxia; (2) carotid chemoreceptor responses to isocapnic hypoxia after dopamine receptor blockade; and (3) ventilatory responses to hypoxia after bilateral section of carotid sinus nerves (CSN). Transition to hypoxia (PaO2 approximately equal to 52 Torr) from hyperoxia gradually increased carotid chemoreceptor activity by ten fold and ventilation by two fold without any detectable overshoot. Termination of isocapnic hypoxia with hyperoxia (PaO2 greater than 300 Torr) at 30 min promptly restored the carotid chemoreceptor activity to prehypoxic level. Ventilation also decreased promptly, but remained above the control value. Induction of hypercapnia (from 31.8 Torr to 43.9 Torr) during hyperoxia was followed by a prompt increase in the chemoreceptor activity by four fold which subsequently diminished, and by a gradual four fold increase in ventilation. Termination of hypercapnia after 30 min was followed by a prompt return of chemoreceptor activity and by a slow return of ventilation to near control levels. Dopamine receptor blockade increased carotid chemoreceptor responsiveness to acute hypoxia but did not alter the response pattern during sustained hypoxia. After bilateral CSN section, ventilation decreased during maintained hypoxia. Thus, a stimulatory peripheral and inhibitory central effects of hypoxia could produce a biphasic ventilatory response to short-term hypoxia in the anesthetized cat with intact CSN but did not manifest it. The results suggest that the chemosensory input not only promptly stimulates ventilation but also prevents the subsequent depressant effect of hypoxia on the brain-stem respiratory mechanisms and hence presumably a biphasic ventilatory response in the anesthetized cat.     

Use of automatic computerised pump to maintain constant intragastric pH.

We used continuous variable rate infusions of famotidine in eight normal volunteers under fasting conditions to raise intragastric pH to 5.0. An intragastric glass electrode continuously monitored acidity and this information was automatically computed to regulate an intravenous infusion system (GastroJet). The computer was programmed to aim for pH 6.0, increasing and lowering infusion rates accordingly. Two regimens were compared with placebo (10 mg bolus followed by infusion or infusion of famotidine alone). Volunteers were admitted to an investigation ward and each study was preceded by a standard normal meal. Hydration was maintained with intravenous fluids. During placebo treatment the median pH was 1.5 and the pH was less than 5.0 for 98% of the time. All volunteers responded to famotidine but dosage requirements varied (range 41 mg to 126 mg). The median pH rose to 6.5 when infusions of famotidine followed boluses and to 6.6 when infusions alone were used - the pH was less than 5.0 for 20% and 16% of the time respectively (p less than 0.05 Wilcoxon compared with placebo). Mean drug use was greater with boluses (98 mg v 87 mg p = 0.03: paired Student's t test) and onset was not apparently faster. Blood famotidine concentrations followed infusion rate changes. Famotidine infused by GastroJet maintains a high fasting intragastric pH and priming boluses are probably unnecessary.     

Effect of systemic pH, PCO2 and bicarbonate concentration on biliary bicarbonate secretion in the rat

The effect of acute metabolic or respiratory acid-base disturbances on biliary bicarbonate secretion was examined in bile fistula rats. Animals were infused with ursodeoxycholate at a rate that stimulates bicarbonate secretion (1 mumole . min-1 X 100 gm-1), in control conditions and during acute acid-base disturbances. Metabolic acidosis or alkalosis were induced by HCl or NaHCO3 infusions, and respiratory acidosis or alkalosis were created respectively by adding CO2 to the inspired gas or by hyperventilation in artificially ventilated animals. Biliary bicarbonate concentration was always higher than plasma bicarbonate concentration. During metabolic disturbances, changing the plasma bicarbonate concentration from 9.2 to 30.2 mM stimulated biliary bicarbonate secretion by 113%. During respiratory disturbances, changing the plasma PCO2 from 25.5 to 59.8 mm Hg also increased biliary bicarbonate secretion by 89%. Biliary bicarbonate output was thus independent of plasma pH. When all animals were considered, bile flow was positively correlated with biliary bicarbonate concentration (r = 0.71, p less than 0.001). Acetazolamide significantly decreased ursodeoxycholate-induced bile flow and bicarbonate secretion by 20 and 22%, respectively. These results support the hypothesis that there is a relationship between ursodeoxycholate-induced bicarbonate secretion and bile flow. They are also consistent with the view that ursodeoxycholate-stimulated biliary bicarbonate secretion in the rat is strongly affected by plasma bicarbonate and PCO2, but not by plasma pH, and involves carbonic anhydrase.     

Oral buffered esomeprazole is superior to i.v. pantoprazole for rapid rise of intragastric pH: A wireless pH metry analysis

Background and Aims:  A pH of more than 6 is required for clot stability and hemostasis. Intravenous proton pump inhibitors have a rapid onset of action compared to oral and have been preferred for management of non-variceal bleeding. Intravenous pantoprazole has been used extensively. Buffered esomeprazole (BE) is an oral preparation consisting of an inner core of non-enteric-coated esomeprazole with a shell of sodium bicarbonate. The buffer protects against acid degradation of esomeprazole in addition to immediate antacid action. The aim of this study was to assess the efficacy of BE for raising and maintaining an intragastric pH of more than 6 in comparison to i.v. pantoprazole in equivalent dosing.
Methods:  A randomized two-way cross-over study was conducted. Ten healthy volunteers were randomized to twice daily BE 40 mg or pantoprazole 40 mg i.v. bolus. Intragastric pH was measured with a wireless pH radiotelemetry capsule (Bravo, Medtronic). A 2-week washout period was given between doses.
Results:  BE achieved a steady pH of more than 6 in a median time of 2 min (range 1–5 min) after the first dose. The mean % time that intragastric pH was more than 6.0 for BE was 96%, and 90% of the 24-h period compared to pantoprazole (47% and 18%), P  = 0.000. A median pH (interquartile range) for the BE group was 6.2 (6.175–6.2) which was higher than i.v. pantoprazole 4.60 (4.5–5.0) ( P  = 0.005).
Conclusion:  BE achieves and maintains a pH of more than 6 within minutes of administration. It was significantly superior to i.v. pantoprazole in equivalent dosing. This finding could have implications in the management of non-variceal bleed where a rapid and sustained pH of more than 6 is desirable.     

Electrophysiological effects of low pH in human atrial fibres

In the studies of the electrophysiological properties of human atrial fibres obtained at cardiac surgery, it has often been reported that the diastolic potential, the maximum upstroke velocity of the phase 0 depolarization (Vmax) and the amplitude of action potential are relatively low. The same findings were also obtained in our previous study when the tissue preparations were perfused with a Tyrode solution which, as usually described in literatures on cardiac cell studies had a NaHCO3 concentration of 12 mM and was aerated with a gas mixture of 95% O2-5% CO2 at 37 degrees C. Recently we found that the relatively poor electrical activities of the human atrial fibres were related to the low pH value (around 7.06) of the perfusate used. Raising the pH value of the perfusate either by increasing the NaHCO3 concentration or by reducing the CO2 in the bubbling gas mixture significantly improved the electrical activities of the fibres. There is evidence that the suppressive effect of low pH on the electrical activities is due to the hindering action of H+ on the transportation of other cations across the plasma membrane.     

Renal nerve and blood pressure responses to stimulation of cardiac receptors in dogs and cats by bradykinin

Summary It has been recently demonstrated in anesthetized, sinoaortic denervated-vagotomized (SAD+V_x) cats that epicardial or intracoronary (IC) bradykinin (BK) evokes an increase in efferent renal nerve activity (RNA) and a pressor response which is mediated by the cardiac sympathetic afferent nerves. The purpose of this study was to compare the effect of epicardial, IC, and left atrial (LA) administration of BK on arterial blood pressure (ABP) and RNA in intact and SAD+V_x cats and dogs. A total of seven cats and eight dogs anesthetized with chloralose were prepared with a left circumflex coronary arterial catheter (dogs) or a LA catheter (cats). Changes in ABP and RNA were determined in both dogs and cats when 1 to 100 g/ml of BK was applied to the anterior surface of the left ventricle or injected IC or LA (0.3 and 3.0 g/kg BK) in the intact and SAD+V_x state. In both the intact and SAD +V_x cat, a pressor response was consistently elicited with epicardial BK. In the SAD+V_x state, epicardial BK increased ABP by 33.4±4.7 mm Hg (p<.001). RNA followed this same trend showing a consistent and significant increase with both LA and epicardial BK (+24.8±8.4% in the SAD+V_x state; P<.05). Changes in RNA in dogs were highly variable with epicardial and IC BK in intact and in SAD V_x dogs, resulting in insignificant changes in this parameter. The results of this study demonstrate that the reflex effects of stimulation of cardiac sympathetic afferents by BK are species specific and need not evoke an increase in peripheral sympathetic outflow.Supported by National Institutes of Health Gran #HL-22594 and American Heart Association Grant # 81672.     

Changes in ventilation and breathing pattern produced by changing body temperature and inspired CO2 concentration in turtles

Respiratory minute ventilation (VE), breathing pattern, oxygen consumption (VO2) and arterial blood gases and pH were measured in freshwater turtles (Chrysemys picta) at 10, 20 and 30 degrees C while the animals breathed gases of varying CO2 concentration (FICO2 = 0, 2, 4, 6 and 8%). Increasing body temperature produced unequal increases in VE and VO2 such that VE/VO2 decreased. This relative hypoventilation led to a rise in PaCO2 and fall in pHa. Increasing FICO2 at all temperatures greatly elevated VE. The magnitude of this response increased with increasing temperature. Thus, paradoxically, there was an increase in both PaCO2 and CO2 sensitivity with increasing temperature. Increases in VE due to increases in temperature were primarily due to a shortening of the periods of breath holding. Although changes in VT contributed to changes in VE with increasing FICO2, the changes in f, due to shortening the periods of breath holding, contributed twice as much. In relative terms, increasing temperature had no effect on the CO2 response of any respiratory variable. Analysis of the data indicates that all changes which occurred in VE, PaCO2 and pHa with changes in body temperature can be explained by equal Q10 effects of roughly two on both metabolic rate and ventilatory sensitivity to changes in PaCO2.