Does blood acid-base status modulate catecholamine secretion in the rainbow trout (Oncorhynchus mykiss)?

1998 ◽  
Vol 201 (22) ◽  
pp. 3085-3095 ◽  
Author(s):  
AE Julio ◽  
CJ Montpetit ◽  
SF Perry
Keyword(s):  
Rainbow Trout ◽  
Receptor Agonist ◽  
Catecholamine Release ◽  
Catecholamine Secretion ◽  
Acid Base ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Acid Base Status ◽  
Catecholamine Levels

The direct and modulating effects of acidosis on catecholamine secretion in rainbow trout (Oncorhynchus mykiss) were assessed in vivo using cannulated fish and in situ using a perfused cardinal vein preparation. In situ, acidosis (a reduction in perfusate pH from 7.9 to 7.4) did not elicit catecholamine release or modulate the secretion of catecholamines evoked by the non-specific cholinergic receptor agonist carbachol (3x10(-7) to 10(-5 )mol kg-1) or the muscarinic receptor agonist pilocarpine (10(-7 )mol kg-1). Acidosis, however, significantly increased the secretion rates of noradrenaline and adrenaline in response to nicotine (10(-8) to 10(-7 )mol kg-1). In vivo, intra-arterial injections of nicotine (300-600 nmol kg-1) into normocapnic or moderately hypercapnic fish (water PCO2=5 mmHg or 0.67 kPa) caused a dose-dependent elevation of circulating catecholamine levels. At the highest dose of nicotine, the rise in plasma catecholamine levels was significantly enhanced in the hypercapnic fish. Acute hypoxia in vivo caused an abrupt release of catecholamines when arterial haemoglobin O2-saturation was reduced to approximately 55-60 %; this catecholamine release threshold during hypoxia was unaltered in hypercapnic fish. However, the hypoxia-induced catecholamine release was significantly greater in hypercapnic fish than in normocapnic fish. The results of this study suggest that blood acid-base status, while not influencing catecholamine secretion directly or influencing the blood O2 content threshold for catecholamine release during hypoxia, may modulate the secretory process specifically in response to nicotinic receptor stimulation of chromaffin cells.

scholarly journals The effects of acute hypoxia on chemically or neuronally induced catecholamine secretion in rainbow trout (Oncorhynchus mykiss) in situ and in vivo

2000 ◽  
Vol 203 (9) ◽  
pp. 1487-1495 ◽  
Author(s):  
S.F. Perry ◽  
C.J. Montpetit ◽  
M. Borowska
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Muscarinic Receptor ◽  
Acute Hypoxia ◽  
Catecholamine Secretion ◽  
Cardinal Vein ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Catecholamine Levels

The potential direct and modulating effects of acute hypoxia on catecholamine secretion in rainbow trout (Oncorhynchus mykiss) were assessed in situ, using a perfused cardinal vein preparation, and in vivo, using chronically cannulated fish. Acute (10 min) perfusion with hypoxic (P(O2)<10 mmHg) saline or homologous hypoxic blood did not have a statistically significant effect on basal (non-stimulated) catecholamine secretion. A field stimulation technique was used to excite the sympathetic nerves innervating the chromaffin cells electrically in situ under conditions of high-P(O2) (saline P(O2)=152 mmHg; 1 mmHg=0.133 kPa) or low-P(O2) (saline P(O2)<10 mmHg) perfusion at constant P(CO2) (2.3 mmHg). The results demonstrated that neuronally evoked catecholamine secretion was significantly lowered by 50 % during perfusion with hypoxic saline. To assess whether the inhibitory effect of hypoxia during neuronal stimulation in situ resulted from modulation of nicotinic and/or muscarinic receptor-linked pathways, perfused posterior cardinal vein preparations were injected with selective nicotinic (10(−)(7) or 10(−)(6)mol kg(−)(1) nicotine) or muscarinic (10(−)(3)mol kg(−)(1) methacholine) receptor agonists. For both doses of nicotine, catecholamine secretion was significantly lowered during hypoxia by 55 %. During muscarinic receptor stimulation, perfusion with hypoxic saline caused a 42 % reduction in the rate of catecholamine secretion. In contrast, catecholamine secretion elicited by depolarising levels of KCl (60 mmol l(−)(1)) was unaffected by the oxygen status of the perfusate. In vivo, intra-arterial injections of nicotine (300–600 nmol kg(−)(1)) into normoxic (water P(O2)=155 mmHg) or moderately hypoxic fish (water P(O2)=80 mmHg) caused a dose-dependent elevation of circulating catecholamine levels. However, despite the inhibitory influence of localised hypoxia on chromaffin cell responsiveness previously demonstrated in situ, the increase in plasma catecholamine levels after intra-arterial injection of nicotine was significantly enhanced in the hypoxic fish. The differences between the results from the in vivo and in situ experiments may reflect the contribution of higher control centres and modulating factors in vivo that are absent in situ.

Relationship between blood O2 content and catecholamine levels during hypoxia in rainbow trout and American eel

1992 ◽  
Vol 263 (2) ◽  
pp. R240-R249 ◽  
Author(s):  
S. F. Perry ◽  
S. D. Reid
Keyword(s):  
Rainbow Trout ◽  
Catecholamine Release ◽  
Plasma Catecholamine ◽  
American Eel ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Interspecific Differences ◽  
Arterial Blood ◽  
Order Of Magnitude ◽  
Catecholamine Levels

Plasma catecholamine levels and arterial blood respiratory variables were monitored in rainbow trout (Oncorhynchus mykiss) and American eel (Anguilla rostrata) acutely exposed (30 min) to graded levels of external hypoxia [water PO2 (PWO2) 20-90 Torr]. The experiments were designed to evaluate the factors controlling catecholamine mobilization in hypoxic fish and to elucidate the basis of marked interspecific differences. In trout, plasma catecholamine levels were unchanged when PWO2 remained above 50 Torr but increased markedly when PWO2 was lowered below this value; the predominant catecholamine released into the circulation was epinephrine. In eel, there was no such obvious PWO2 threshold for catecholamine release although plasma levels were consistently elevated above baseline only at PWO2 less than 35 Torr. The magnitude of the catecholamine release in eel was approximately an order of magnitude less than in trout. Unlike in trout, there was no increase in the plasma epinephrine-to-norepinephrine concentration ratio. During hypoxia, the relationship between arterial blood PO2 (PaO2) and PWO2 was similar in both species and thus could not explain the differences in the PWO2 thresholds for catecholamine release. In trout, the calculated PaO2 thresholds for catecholamine release were 25.3 (epinephrine) and 20.5 Torr (norepinephrine) whereas in eel the corresponding values were 12.5 and 11.6 Torr, respectively. These PaO2 thresholds were in good agreement with the in vivo values for PaO2 at half-maximal hemoglobin (Hb)-O2 saturation (P50) for trout and eel blood of 22.9 and 11.1 Torr, respectively. Thus both species displayed essentially equivalent catecholamine release thresholds when expressed in terms of arterial blood O2 content corresponding to approximately 45-60% Hb-O2 saturation.

scholarly journals SEROTONIN-MEDIATED RELEASE OF CATECHOLAMINES IN THE RAINBOW TROUT ONCORHYNCHUS MYKISS

1993 ◽  
Vol 178 (1) ◽  
pp. 191-204 ◽  
Author(s):  
R. Fritsche ◽  
S. G. Reid ◽  
S. Thomas ◽  
S. F. Perry
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Chromaffin Cells ◽  
Head Kidney ◽  
Catecholamine Release ◽  
Perfusion Fluid ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Dose Dependent

The effects of serotonin (5-hydroxytryptamine; 5-HT) on catecholamine release from chromaffin tissue were investigated in the rainbow trout (Oncorhynchus mykiss) in vivo and in situ. Intra-arterial injections of serotonin in vivo caused dose-dependent (50–250 nmol kg-1) increases in both plasma noradrenaline and adrenaline levels. Pre-treatment of fish with the serotonergic receptor antagonist methysergide did not abolish these increases. An in situ saline-perfused head kidney preparation was developed and validated to study the potential direct effect of serotonin on catecholamine release. The chromaffin cells in the preparation showed a dose-dependent release of catecholamines in response to bolus injections of the cholinergic receptor agonist carbachol (10–7-10-4 mol kg-1). The carbachol-induced release of noradrenaline, but not of adrenaline, was reduced significantly when the nicotinic receptor antagonist hexamethonium (10–4 mol l-1) was present in the perfusion fluid. The removal of calcium from the perfusion fluid prevented the usual release of catecholamines evoked by carbachol. Bolus injections of serotonin (250 nmol kg-1) into the inflowing perfusion fluid resulted in significantly increased levels of adrenaline and noradrenaline in the outflowing perfusate. Addition of hexamethonium to the perfusion fluid did not abolish this serotonin-induced release of catecholamines. The serotonin-induced release of adrenaline, however, was abolished totally by the addition of methysergide. Serotonin is present in high concentrations (44.61+/−5.96 microgram g-1 tissue) in the anterior region of the posterior cardinal vein within the head kidney. Carbachol (10–5 mol kg-1) did not elicit release of the stored serotonin from the perfused head kidney preparation. We conclude that the chromaffin cells in the perfused trout head kidney preparation display characteristics similar to those of other vertebrates and that this preparation is a useful tool for studying the control of catecholamine release in fish. The results demonstrate that serotonin has a direct impact on the chromaffin cells by interacting with methysergide-sensitive receptors to initiate the release of adrenaline. The potential physiological role of serotonin on catecholamine release in trout is discussed.

THE EFFECTS OF ACCLIMATION TEMPERATURE ON THE DYNAMICS OF CATECHOLAMINE RELEASE DURING ACUTE HYPOXIA IN THE RAINBOW TROUT ONCORHYNCHUS MYKISS

1994 ◽  
Vol 186 (1) ◽  
pp. 289-307 ◽  
Author(s):  
S. Perry ◽  
S. Reid
Keyword(s):  
Rainbow Trout ◽  
Acute Hypoxia ◽  
Catecholamine Release ◽  
Acclimation Temperature ◽  
Plasma Catecholamine ◽  
Blood Oxygen ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Arterial Blood ◽  
The Difference ◽  
Catecholamine Levels

The response of cannulated rainbow trout (Oncorhynchus mykiss) to acute hypoxia was studied in fish acclimated to two temperatures (5 and 15 °C). Blood/water respiratory variables and plasma catecholamine levels were measured before and 15 min after exposure to hypoxic water varying between 4.0 and 10.7 kPa (30–80 mmHg) oxygen partial pressure (PwO2). Arterial blood PO2 (PaO2) and oxygen content (CaO2) fell during hypoxia in a similar manner at both temperatures, although the changes in CaO2 were often more pronounced in the fish acclimated to 15 °C. Regardless of acclimation temperature, plasma catecholamine levels were consistently elevated at PwO2 values below 8.0 kPa (60 mmHg); the largest increases in plasma catecholamine levels occurred below PwO2=5.3 kPa (40 mmHg). Adrenaline was the predominant catecholamine released into the circulation. Adrenaline was released at PwO2 values of 8.0 kPa or below, whereas noradrenaline was released at PwO2 values of 6.7 kPa or below. The construction of in vivo oxygen dissociation curves demonstrated an obvious effect of acclimation temperature on haemoglobin (Hb) oxygen-affinity; the P50 values at 15 °C and 5 °C were 3.6 kPa (26.7 mmHg) and 1.9 kPa (14.0 mmHg), respectively. At 15 °C, catecholamines were released into the circulation abruptly at a PaO2 threshold of 4.6 kPa (34.5 mmHg) while at 5 °C the catecholamine release threshold was lowered to 3.3 kPa (24.5 mmHg). The difference in the PaO2 catecholamine release thresholds was roughly equivalent to the difference in the P50 values at the two distinct temperatures. Catecholamine release thresholds, calculated on the basis of arterial blood oxygen-saturation (expressed as CaO2/[Hb]), were similar at both temperatures and were approximately equal to 53–55 % Hb O2-saturation. The results support the contention that the lowering of blood oxygen content/saturation rather than PO2 per se is the proximate stimulus/signal causing catecholamine release in rainbow trout during acute hypoxia.

Physiological and morphological regulation of acid–base status during hypercapnia in rainbow trout (Oncorhynchus mykiss)

1993 ◽  
Vol 71 (8) ◽  
pp. 1673-1680 ◽  
Author(s):  
Greg G. Goss ◽  
Steve F. Perry
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Chloride Cell ◽  
Morphological Alteration ◽  
Acid Base ◽  
Rapid Reduction ◽  
Fractional Area ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Positive Formula ◽  
Acid Base Status

A kinetic analysis (Michaelis constant (Km) and maximal flux (Jmax)) of the branchial Na+ and Cl− influx mechanisms, along with measurements of blood total CO2 content [Formula: see text], net acidic–basic equivalent fluxes, and gill chloride cell morphology, was performed using rainbow trout (Oncorhynchus mykiss) before, during, and after 96 h exposure to environmental hypercapnia (water [Formula: see text]; 1 torr = 133.3 kPa). Exposure to hypercapnia caused (i) a net acidic equivalent loss (negative [Formula: see text]) that was accounted for entirely by reductions in titratable alkalinity flux (JTA), (ii) an increase in [Formula: see text] from 8.4 ± 0.5 to 20.7 ± 0.4 mmol/L, and (iii) no alteration either in [Formula: see text], [Formula: see text], or [Formula: see text]; [Formula: see text] increased (affinity was reduced). Chloride cell fractional area was reduced by 40% from 174 250 ± 15 650 μm2/mm2 under control conditions to 104 329 ± 17 991 μm2/mm2 after 96 h of hypercapnia. In the posthypercapnic period, there was (i) a net acidic equivalent gain (positive [Formula: see text]) that was accounted for entirely by an elevation in JTA, (ii) a rapid reduction of blood [Formula: see text], (iii) an increase of chloride cell fractional area to control values (179 105 ± 35 233μm2/mm2), and (iv) increases and decreases in [Formula: see text] (564 ± 50 versus 224 ± 21 μmol∙kg−1∙h−1 in the prehypercapnic period) and [Formula: see text] (381 ± 85 versus 585 ± 92 μmol∙kg−1∙h−1), respectively. The results suggest that morphological alteration of the gill chloride cell fractional area is an important response to acid–base disturbances. The results are discussed with respect to the relative roles of morphological alteration of gill chloride cell fractional area and variation in internal substrate (HCO3−) in modifying branchial Cl−/HCO3− exchange for acid–base regulation.

Renal expression and localization of SLC9A3 sodium/hydrogen exchanger and its possible role in acid-base regulation in freshwater rainbow trout (Oncorhynchus mykiss)

2008 ◽  
Vol 295 (3) ◽  
pp. R971-R978 ◽  
Author(s):  
Goran Ivanis ◽  
Marvin Braun ◽  
Steve F. Perry
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Transcriptional Activation ◽  
Plasma Cortisol ◽  
Renal Tubules ◽  
Acid Base ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Sodium Hydrogen Exchanger ◽  
Renal Expression

Experiments were performed to assess the possible involvement of the Na+/H+ exchanger isoform 3 (NHE3; SLC9A3) in renal acid-base regulation in adult rainbow trout ( Oncorhynchus mykiss). NHE3 mRNA was expressed at high levels in the kidney relative to its paralog, NHE2. The results of in situ hybridization demonstrated an abundance of NHE3 mRNA in renal tubules. The combination of immunocytochemistry and histological staining revealed that NHE3 was confined to the apical membrane of proximal tubules, where it was colocalized with the vacuolar-type H+-ATPase. Levels of NHE3 protein (assessed by Western blotting) were increased during hypercapnia, likely as a result of increased transcription, as indicated by increasing levels of NHE3 mRNA (as determined by real-time PCR). Plasma cortisol concentration was increased during hypercapnia, and administration of exogenous cortisol caused a marked increase in NHE3 mRNA and protein. Thus we speculate that the elevation of plasma cortisol during hypercapnia contributes to transcriptional activation of NHE3 that ultimately promotes acid-base regulation by stimulating H+ secretion and HCO3− reabsorption.

scholarly journals Vasoactive intestinal polypeptide- and pituitary adenylate cyclase activating polypeptide-mediated control of catecholamine release from chromaffin tissue in the rainbow trout, Oncorhynchus mykiss

2000 ◽  
Vol 166 (3) ◽  
pp. 705-714 ◽  
Author(s):  
CJ Montpetit ◽  
SF Perry
Keyword(s):  
Rainbow Trout ◽  
Chromaffin Cells ◽  
Catecholamine Secretion ◽  
Cardinal Vein ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Neuronal Control ◽  
Pituitary Adenylate Cyclase ◽  
Posterior Cardinal Vein ◽  
Chromaffin Tissue

The aim of the present investigation was to assess the relative contributions of cholinergic (acetylcholine) and non-cholinergic vasoactive intestinal polypeptide (VIP), and pituitary adenylate cyclase activating polypeptide (PACAP) neurotransmitters in the neuronal control of catecholamine secretion from the chromaffin tissue lining the posterior cardinal vein of the rainbow trout (Oncorhynchus mykiss). Using an in situ saline-perfused posterior cardinal vein preparation, it was demonstrated that exogenous administration of chicken VIP or human PACAP-27 caused a dose-dependent increase in adrenaline secretion; noradrenaline secretion was unaffected. Analysis of dose-response curves indicated that VIP and PACAP stimulated the secretion of adrenaline with a similar degree of potency (ED(50) for VIP=1.90x10(-11) mol/kg; ED(50) for PACAP=1.03x10(-11) mol/kg). The VIP/PACAP-elicited secretion was diminished in the presence of the VIP receptor antagonist, VIP 6-28, but was unaffected by the PACAP receptor antagonist, PACAP 6-27, or the cholinergic antagonists, hexamethonium and atropine. Thus, this is the first study to demonstrate a direct stimulatory role for VIP or PACAP in catecholamine secretion from piscine chromaffin cells. The relative contribution of cholinergic and non-cholinergic neurotransmitters in the neuronal control of catecholamine secretion from the chromaffin tissue was evaluated using an in situ nerve-stimulating technique previously validated by us in the rainbow trout. This was accomplished by comparing catecholamine secretion in the presence or absence of cholinergic and the VIP and PACAP receptor antagonists during different levels of electrical stimulation. The results demonstrated that cholinergic stimulation predominated during high frequency of electrical stimulation (20 Hz) while the non-cholinergic component prevailed at low frequency (1 Hz). Overall, the results of the present investigation demonstrate that VIP and/or PACAP may directly stimulate adrenaline secretion from trout chromaffin cells at low levels of neuronal activity. Therefore, the neuronal control of catecholamine secretion in teleosts may not be confined to cholinergic-evoked events.

scholarly journals Transbranchial ammonia gradients and acid-base responses to high external ammonia concentration in rainbow trout (Oncorhynchus mykiss) acclimated to different salinities

1992 ◽  
Vol 166 (1) ◽  
pp. 95-112 ◽  
Author(s):  
R. W. Wilson ◽  
E. W. Taylor
Keyword(s):  
Rainbow Trout ◽  
Sea Water ◽  
Ammonia Excretion ◽  
Ammonia Concentration ◽  
Acid Base ◽  
Experimental Conditions ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Total Ammonia ◽  
Acid Base Status ◽  
The Difference

Transbranchial ammonia gradients and blood acid-base status have been examined in rainbow trout acclimated to fresh water (FW), 33% sea water (33% SW) and sea water (SW) and exposed to 1.0 mmol l-1 total ammonia (TAmm) at pH 7.9 for 24 h. At all three salinities trout maintained large negative (inwardly directed) NH3 and NH4+ gradients throughout the exposure, presumably by active excretion of NH4+ to counteract the passive inward diffusion of ammonia. Analysis of blood non-respiratory acid-base status (delta H+m) revealed an acid load in FW trout and a base load in SW trout following 24 h of exposure. This indicates that active NH4+/H+ exchange predominates in FW whereas NH4+/Na+ is the principal exchange utilised in SW under these experimental conditions. The plasma TAmm load incurred during ammonia exposure increased with salinity. Compared to FW trout, plasma TAmm values were 34 and 73% higher in the 33% SW and SW trout, respectively, after 24 h. This cannot be explained by differences in the prevailing transbranchial PNH3 gradient because ambient PNH3 was substantially lower at the higher salinities (due to higher pK' and solubility values). We interpret the difference between FW and SW trout as an increased permeability to NH4+ in fish acclimated to the higher-salinity environments. Transbranchial diffusion of NH4+ is, therefore, probably more important as a route for ammonia excretion in SW than in FW trout, especially considering the favourable transepithelial potentials normally found in SW teleosts. In addition, increased NH4+ permeability implies that the toxicity of ammonia will be greater in seawater than in freshwater teleosts and should not simply be measured as a function of the unionised ammonia concentration when considering seawater-adapted species.

Cardiovascular effects of hypercarbia in rainbow trout (Oncorhynchus mykiss): a role for externally oriented chemoreceptors

2001 ◽  
Vol 204 (1) ◽  
pp. 115-125 ◽  
Author(s):  
J.E. McKendry ◽  
S.F. Perry
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Systemic Resistance ◽  
Rainbow Trout Oncorhynchus Mykiss

In situ and in vivo experiments were performed on rainbow trout (Oncorhynchus mykiss) to examine (i) the direct effect of CO(2) on the systemic vasculature and (ii) the influence of internal versus external hypercapnic acidosis on cardiovascular variables including blood pressure, cardiac output and systemic vascular resistance. Results from in situ saline-perfused trunk preparations indicated that CO(2) (0.6, 1.0 or 2.0% CO(2)) elicited a significant vasodilation, but only in the presence of pre-existing humoral adrenergic tone. In the absence of pre-existing vascular tone, CO(2) was without effect on systemic resistance. In contrast, hypercarbia in vivo triggered a statistically significant increase in systemic resistance (approximately 70 %) that was associated with elevated ventral aortic (approximately 42 %) and dorsal aortic (approximately 43 %) blood pressures and with a significant bradycardia (approximately 12 %); cardiac output was not significantly affected. To determine the potential roles of internal versus external chemoreceptors in mediating the cardiovascular responses to hypercarbia, experiments were performed to elevate the endogenous arterial partial pressure of CO(2) (Pa(CO2)) without an accompanying increase in external P(CO2) (Pw(CO2)). In one series, trout were given a bolus injection of the carbonic anhydrase inhibitor acetazolamide (30 mg kg(−1)) to inhibit CO(2) excretion, and thus raise Pa(CO2), 5–7 h prior to being exposed to an acute increase in Pw(CO2) (maximum Pw(CO2)=6.3+/−0.4 mmHg; 1 mmHg=0.133 kPa). Despite a marked increase in Pa(CO2) (approximately 7 mmHg) after injection of acetazolamide, there was no increase in dorsal aortic blood pressure (P(DA)) or systemic resistance (R(S)). The ensuing exposure to hypercarbia, however, significantly increased P(DA) (by approximately 20 %) and R(S) (by approximately 35 %). A second series of experiments used a 5–7 h period of exposure to hyperoxia (Pw(O2)=643+/−16 mmHg) to establish a new, elevated baseline Pa(CO2) (7.8+/−1.1 mmHg) without any change in Pw(CO2). Despite a steadily increasing Pa(CO2) during the 5–7 h of hyperoxia, there was no associated increase in P(DA) or R(S). Ensuing exposure to hypercarbia, however, significantly increased P(DA) (by approximately 20 %) and R(S) (by approximately 150 %). Plasma adrenaline levels were increased significantly during exposure to hypercarbia and, therefore, probably contributed to the accompanying cardiovascular effects. These findings demonstrate that the cardiovascular effects associated with hypercarbia in rainbow trout are unrelated to any direct constrictory effects of CO(2) on the systemic vasculature and are unlikely to be triggered by activation of internally oriented receptors. Instead, the data suggest that the cardiovascular responses associated with hypercarbia are mediated exclusively by externally oriented chemoreceptors.

scholarly journals Tissue intracellular acid-base status and the fate of lactate after exhaustive exercise in the rainbow trout

1986 ◽  
Vol 123 (1) ◽  
pp. 123-144 ◽  
Author(s):  
C. L. Milligan ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
White Muscle ◽  
Atp Hydrolysis ◽  
Early Period ◽  
Extracellular Fluid ◽  
Acid Base ◽  
Extracellular Acidosis ◽  
Acid Base Status ◽  
Lactate And Pyruvate

Exhaustive ‘burst-type’ exercise in the rainbow trout resulted in a severe acidosis in the white muscle, with pHi dropping from 7.21 to a low of 6.62, as measured by DMO distribution. An accumulation of lactate and pyruvate, depletions of glycogen, ATP and CP stores, and a fluid shift from the extracellular fluid to the intracellular fluid of white muscle were associated with the acidosis. The proton load was in excess of the lactate load by an amount equivalent to the drop in ATP, suggesting that there was an uncoupling of ATP hydrolysis and glycolysis. Initially, lactate was cleared more quickly than protons from the muscle, a difference that was reflected in the blood. It is suggested that during the early period of recovery (0–4 h), the bulk of the lactate was oxidized in situ, restoring pHi to a point compatible with glyconeogenesis. At that time, lactate and H+ were used as substrates for in situ glyconeogenesis, which was complete by 24 h. During this time, lactate and H+ disappearance could account for about 75% of the glycogen resynthesized. The liver and heart showed an accumulation of lactate, and it is postulated that this occurred as a result of uptake from the blood. Associated with the lactate load in these tissues was a metabolic alkalosis. Except for an apparent acidosis immediately after exercise, the acid-base status of the brain was not appreciably affected. Despite the extracellular acidosis, red cell pHi remained nearly constant.

Sign in / Sign up

Export Citation Format

Share Document