Adrenergic involvement in blood oxygen transport and acid-base balance during hypercapnic acidosis in the Rainbow Trout,Salmo gairdneri
Autor: | Steve F. Perry, M. G. Vermette |
---|---|
Rok vydání: | 1988 |
Předmět: |
medicine.medical_specialty
Physiology Chemistry Oxygen transport Root effect Biochemistry Red blood cell Endocrinology Phentolamine medicine.anatomical_structure Internal medicine medicine Arterial blood Animal Science and Zoology medicine.symptom Hypercapnia Ecology Evolution Behavior and Systematics medicine.drug Acidosis Whole blood |
Zdroj: | Journal of Comparative Physiology B. 158:107-115 |
ISSN: | 1432-136X 0174-1578 |
DOI: | 10.1007/bf00692734 |
Popis: | Rainbow trout (Salmo gairdneri) were subjected to 12 h of external hypercapnia (1% CO2 in air) during α- and/or β-adrenoceptor blockade in order to assess the importance of adrenergic responses in modulating blood oxygen transport and acid-base balance during an acute acidotic stress. External hypercapnia caused an elevation of blood carbon dioxide tension and a reciprocal decrease in whole blood pH. A gradual elevation of blood bicarbonate levels caused whole blood pH to increase toward pre-hypercapnic values throughout the hypercapnic period. Pre-treatment of fish with propranolol (a β-adrenoceptor antagonist) or phentolamine (an α-adrenoceptor antagonist) did not affect their ability to regulate extracellular acid-base status during hypercapnia. On the other hand, adrenergic responses were essential in the maintenance of arterial blood oxygen content during hypercapnia despite the severe extracellular acidosis and a marked Root effect in trout blood, in vitro. Important adrenergic responses included pronounced increases in haematocrit (an α-adrenergic effect) and arterial oxygen tension (α- and β-adrenergic effects) as well as partial regulation of red blood cell pH (a β-adrenergic effect). Although pre-treatment of fish with either propranolol or phentolamine caused a reduction in blood oxygen content during hypercapnia, fish died only during complete adrenoceptor blockade, presumably due to severe hypoxemia. |
Databáze: | OpenAIRE |
Externí odkaz: |