Blood oxygen levels and acid-base status following air exposure in an air-breathing fish, Channa argus: The role of air ventilation

1983 ◽  
Vol 74 (4) ◽  
pp. 787-793 ◽  
Author(s):  
Ishimatsu Atsushi ◽  
Itazawa Yasuo
Keyword(s):  
Blood Oxygen ◽  
Acid Base ◽  
Air Exposure ◽  
Air Breathing ◽  
Oxygen Levels ◽  
Air Ventilation ◽  
Channa Argus ◽  
Acid Base Status

The Role of β-Adrenoreceptors in the Recovery from Exhaustive Exercise of Freshwater-Adapted Rainbow Trout

1989 ◽  
Vol 147 (1) ◽  
pp. 471-491 ◽  
Author(s):  
D. G. MCDONALD ◽  
Y. TANG ◽  
R. G. BOUTILIER
Keyword(s):  
Rainbow Trout ◽  
Exhaustive Exercise ◽  
Acid Base ◽  
Post Exercise ◽  
Nacl Concentration ◽  
Adrenergic Mechanism ◽  
Acid Base Status ◽  
Isoproterenol Infusion ◽  
Net Fluxes

Rainbow trout, fitted with arterial catheters, were exercised to exhaustion by manual chasing and then injected with either saline (controls), the β-agonist isoproterenol or the β-antagonist propranolol. Blood acid-base status, branchial unidirectional and net fluxes of Na+ and Cl−, and net fluxes of ammonia and acidic equivalents (JHnet) were monitored over the subsequent 4 h of recovery. These same parameters were also monitored in normoxic, resting fish following isoproterenol injection and in exercised fish following acute post-exercise elevation of external NaCl concentration. In addition to confirming an important role for β-adrenoreceptors in the regulation of branchial gas exchange and red cell oxygenation and acid-base status, we find a significant β-adrenergic involvement in the flux of lactic acid from muscle and in JHnet across the gills. Both isoproterenol infusion (into nonexercised fish) and exhaustive exercise were found to cause net acid excretion. The post-exercise JHnet was further augmented by elevating [NaCl] but was not affected, in this instance, either by β-stimulation or blockade, indicating that JHnet was not entirely regulated by a β-adrenergic mechanism. On the basis of a detailed analysis of unidirectional Na+ and Cl− fluxes, we conclude that the increase in JHnet following exercise arose mainly from increased Na+/H+(NH4+) exchange and that the upper limit on JHnet was set by the supply of external counterions and by the increase in branchial ionic permeability that invariably accompanies exhaustive exercise.

The Effects of Branchial Denervation and Pseudobranch Ablation on Cardioventilatory Control in an Air-Breathing Fish

1991 ◽  
Vol 161 (1) ◽  
pp. 347-365 ◽  
Author(s):  
DAVID J. McKENZIE ◽  
MARK L. BURLESON ◽  
DAVID J. RANDALL
Keyword(s):  
Cardiovascular Responses ◽  
Sodium Cyanide ◽  
Air Breathing ◽  
Ventilatory Responses ◽  
Reflex Bradycardia ◽  
Afferent Information ◽  
Gill Ventilation ◽  
Air Ventilation ◽  
Amia Calva

Present address and address for reprint requests: Istituto di Scienze Farmacologiche, via Balzaretti 9, Università di Milano, Milano 20133, Italy. The role of sensory afferent information from the gills of Amia calva in cardiovascular and ventilatory control was investigated by bilateral branchial denervation and pseudobranch ablation. Aquatic hypoxia or 1 mg of sodium cyanide (NaCN) in the water flowing over the gills stimulated bradycardia, and gill and air ventilation in sham-operated fish. Sodium cyanide, noradrenaline (NA) and adrenaline (A) infusion into the dorsal aorta increased gill ventilation, and NA and A infusion also stimulated tachycardia and an increase in blood pressure. Following denervation and pseudobranch ablation, O2 consumption (V·OO2), airbreathing frequency (fAB) and arterial O2 tension (PaOO2) declined, and circulating NA levels increased, as compared with sham-operated fish. Cardiovascular and air-breathing responses to hypoxia were abolished and gill ventilatory responses attenuated. All ventilatory and cardiovascular responses to NaCN were abolished and gill ventilatory responses to NA and A were attenuated in animals following denervation and pseudobranch ablation. These results demonstrate that O2-sensitive chemoreceptors in the gills and pseudobranch control reflex bradycardia and air-breathing responses in Amia, but that gill ventilatory responses to hypoxia, NA and A are partially mediated by extrabranchial mechanisms. Plasma NA levels increased during hypoxia in shamoperated and denervated animals, indicating that circulating NA may have mediated gill ventilatory responses in denervated animals.

Acid-base changes in the fetal lamb before and after lung expansion

1963 ◽  
Vol 18 (5) ◽  
pp. 877-880 ◽  
Author(s):  
N. S. Assali ◽  
W. A. Manson ◽  
L. W. Holm ◽  
M. Ross
Keyword(s):  
Blood Oxygen ◽  
Acid Base ◽  
Blood Ph ◽  
Lung Expansion ◽  
Fetal Lamb ◽  
Before And After ◽  
The Status ◽  
Acid Base Status ◽  
Near Term ◽  
Fetal Acidosis

The acid-base status of the fetal lamb was studied in near-term pregnant ewes subjected to spinal anesthesia. The status of the fetus was compared to its mother and the changes which occur after the fetal lungs were ventilated with oxygen or nitrogen were investigated. The results show that: 1) the fetus in utero is in a state of metabolic acidosis in relation to the mother, 2) the acidosis does not seem to be related to the fetal blood pCO2, and 3) the acidosis may be aggravated by hypoxia. fetal acidosis; blood pH; blood oxygen; blood carbon dioxide; hypoxia; hyperoxia; sheep Submitted on March 20, 1963

Gastric mucosal repair and release of HCO3- after damage by 2 M NaCl in cat: role of systemic acid base status

1994 ◽  
Vol 267 (4) ◽  
pp. G536-G545 ◽  
Author(s):  
K. Guttu ◽  
K. Grong ◽  
K. Svanes ◽  
J. E. Gronbech
Keyword(s):  
Mucosal Blood Flow ◽  
Mucosal Damage ◽  
Major Influence ◽  
Acid Base Balance ◽  
Acid Base ◽  
Mucosal Repair ◽  
Base Balance ◽  
Acid Base Status ◽  
Hyperemic Response

To study the influence of acid base balance on gastric mucosal repair, NH4Cl or NaHCO3 was given intravenously to anesthetized cats after mucosal damage induced by intraluminal 2 M NaCl. Saline at pH 5 or 1 was perfused via an oral tube through the stomach lumen and evacuated via a pyloric tube to a chamber with pH and PCO2 electrodes. Luminal bicarbonate (HCO3-) was markedly increased early after damage in both acidotic and alkalotic animals. In alkalotic animals mucosal blood flow increased about twofold in response to mucosal damage, whereas the early hyperemic response was either completely attenuated or blunted in acidotic animals. HCO3- release was correlated to availability of HCO3- by blood in alkalotic animals with luminal pH 5. Alkalotic animals showed improved repair compared with acidotic animals, and mucosal restitution was correlated to availability of HCO3- by blood. We conclude that luminal leakage of HCO3- or plasma after mucosal damage depends on availability by blood and consumption of HCO3- within the mucosa and that blood borne HCO3- has a major influence on gastric mucosal repair.

scholarly journals Analysis of Haemolymph and Muscle Acid-Base Status During Aerial Exposure in the Crayfish Austropotamobius Pallipes

1988 ◽  
Vol 134 (1) ◽  
pp. 409-422 ◽  
Author(s):  
R. TYLER-JONES ◽  
E. W. TAYLOR
Keyword(s):  
Base Excess ◽  
Abdominal Muscle ◽  
Internal Source ◽  
Intracellular Acidosis ◽  
Aerial Exposure ◽  
Acid Base ◽  
Bicarbonate Buffer ◽  
Air Exposure ◽  
Austropotamobius Pallipes ◽  
Acid Base Status

Exposure of the crayfish Austropotamobius pallipes to air resulted in an acidosis in the postbranchial haemolymph (pHa) and the abdominal muscle. The haemolymph acidosis was subsequently compensated and, after 24 h in air, pHa had returned to the settled, submerged value. The intracellular acidosis remained uncompensated throughout the period of aerial exposure. When crayfish were first removed into air, lactate concentrations in the haemolymph and abdominal muscle increased substantially. After 24 h in air lactate concentrations in both compartments had returned towards submerged levels. Possibilities for the fate of lactate are discussed. Re-analysis of haemolymph acid-base data for crayfish exposed to air (Taylor & Wheatly, 1981) revealed discrepancies between observed and expected base excess. Initially these may arise from exchanges of H+ or HCO3− with other compartments. During long-term air exposure, the removal of lactate from the haemolymph and an independent accumulation of base, probably from the mobilization of an internal source of bicarbonate buffer, result in the observed pH compensation. Determination of base excess for the changes in abdominal muscle acid-base status after 3 h of exposure to air corroborated the results of the haemolymph analysis, suggesting a retention of H+ despite the efflux of lactate.

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