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Effects of circulating catecholamines on diving in ducks (Anas platyrhynchos) Lacombe, A. M. A.,


Plasma catecholamines have been measured in chronically adrenalectomised (ADX) ducks, in chronically adrenal denervated ducks (DNX), in their respective sham-operated controls (SH-adx, SH-dnx) as well as in intact ducks after 3 minutes forced submergence. The results showed that 100% of the plasma Epinephrine (EP) and 40 to 80% of plasma Norepinephrine (NE) released during the dive came from the adrenal glands. 20 to 60% of plasma NE came from endings of the autonomic vascular sympathetic nerves which are strongly stimulated during diving. Adrenal catecholamines were released by nerve activation only; non neural mechanisms did not play any role in their release. Maximum dive times (MDT) in chronically adrenalectomised ducks (ADX: 5 min. 19 ± 20 sec.) and in chronically adrenal denervated ducks (DNX: 7 min. 10 ± 13 sec.) were significantly lower than in sham-operated controls (respectively SH-adx: 9 min. 58 ± 45 sec., SH-dnx: 12 min. 10 ± 28 sec). Venous infusion of catecholamines in ADX and DNX during the dive increased MDT: MDT of DNX ducks perfused with catecholamines (9 min. 46 ± 20 sec.) were significantly higher than in DNX perfused with saline (7 min. 21 ± 17 sec.), but did not reach the MDT observed in the SH-dnx: other adrenal products must be involved. Diving heart rates of ADX and DNX (at 4 min. dive respectively: 62 ± 16 and 31 ± 2 beats/min.) were significantly higher than in their sham-operated controls (23 ± 3 and 17 ± 2 beats/min.) . Blood pressure during the dive was signifi- cantly lower in ADX and DNX (at 4 min. dive respectively: 93 ± 8 and 98 ± 4 mmHg) compared with their sham-operated controls (131 ± 12 and 118 ± 6 mmHg). Infusion of catecholamines in DNX raised blood pressure towards SH-dnx values, but there was no change in heart rate. PaO₂, CaO₂, pHa and lactate levels in DNX (respectively: 42 ± 2 mmHg, 4.5 ± 0.8 ml 02 /100ml blood, 7.233 ± 0.016, 3.1 + 0.3 mM) were significantly lower than in SH-dnx after 5 minutes submergence (53 ± 1 mmHg, 6.8 ± 0.4 ml 02 /100 ml blood, 7.301 ± 0.007, 4.8 + 0.4 mM). There was also a significant increase of plasma N⁺ (+ 5.4 ± 1.7 mEq/L) in SH-dnx after 5 minutes submergence, but this was not the case in DNX where it was K⁺ (+ 1.1 ± 0.4 mEq/L) which increased. This suggested that adrenal catecholamines increase tolerance to underwater submersion by enhancing peripheral vasoconstriction, thus preserving the O₂ stores for the heart and brain. Moreover, they may affect the acid-base equilibrium during diving by increasing the activity of the Na⁺K⁺ pump and may also have a direct effect on the rate of glycogenolysis. Preventing the actions of catecholamines on the heart by injecting beta-blocker during forced submersion did not decrease MDT; however the cardiovascular response was markedly affected. During beta-blockade, diving heart rate rose steadily from 24 ± 6 beats/minute after 2 minutes to 52 ± 8 beats/minute after 6 minutes diving. In contrast, heart rates remained close to the levels reached at 2 minutes (17 ± 3 and 19 ± 4 beats/minute) throughout the control dives. Perfusion pressure and blood flow have been recorded simultaneously in both hind limbs of ducks. One leg was perfused with different blood mixtures devoid of catecholamines (Test leg) and compared with the other, perfused with the ducks'own blood (autoperfused leg). This showed that hyper-capnia has a depressant effect on the neural component of the peripheral vasoconstriction. Perfusion of test legs with hypoxic-hypercapnic blood to which catecholamines were added, showed that circulating catecholamines are needed to increase peripheral vasoconstriction during diving. In summary, during forced submergence circulating catecholamines, released mainly by the adrenal glands, compensate for the depressant action of hypercapnia on the neural component of peripheral vasoconstriction. Maintenance of this peripheral vasoconstriction during forced diving ensures that O₂ stores are not wasted on peripheral tissues, and this explains how MDT is prolonged.

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