Abstract

Electrolyte and fluid imbalances are common in stranded or otherwise compromised phocid seals. Hyponatremia has been associated with long-term stress in both captive and free ranging seals, whereas hyponatremia has been associated with starvation, dehydration, and possible ingestion of sea water (mariposia). Therapeutic intervention requires not only the administration of balanced fluids, but also an understanding of the metabolic and endocrine systems involved in salt and water homeostasis. At present, therapy to correct such imbalances is undertaken without specific knowledge of many of the physiologic factors contributing to these conditions.

The high prevalence of hyponatremia in stranded phocid seals cared for at and the therapeutic challenge that these cases often present suggests the possibility of an underlying defect in hormonal regulation, leading to active sodium retention or impaired excretion. Atrial natriuretic peptide (ANP), released in response to atrial stretch, has been reported to inhibit the renin-angiotensin-aldosterone system, and to be associated with natriuresis and vasodilation of the renal vascular bed. We used adult harbor seals (Phoca vitulina) as models in an investigation of endocrine regulation of fluids and electrolytes in phocids.

We monitored circulating levels of atrial natriuretic peptide (ANP), and arginine vasopressin (AVP) following intravenous administration of 0.9% NaCl in five (3K 2F) adult harbor seals. Saline solutions were infused over a one hour period, and serial blood samples drawn via an indwelling catheter placed in the extradural vein. Initially, we infused two harbor seals with 500 mL of saline. The remaining three animals received 1250 mL one day and 2000 mL the following day. Blood was collected immediately before each infusion began and at thirty minute intervals thereafter for two hours. As a control, blood samples were collected at the same intervals without infusion. Samples were analyzed to determine PCV, plasma ANP and AVP, and serum BUN, creatinine and Na levels.

During the 1250 mL and the 2000 mL infusions, PCV declined significantly relative to the controls, reaching a maximum mean decline of 6.5 + 1.8 units at the end of the 2000 mL infusion. At 90 and 120 minutes post infusion, PCV values showed a slight increase toward baseline but remained significantly lower than in controls. No significant changes or trends were noted in creatinine, BUN or electrolytes in any of the trials. AVP values for all sample times (n=55) averaged 7.9±3.0 pg/mL (range 2.1-13.8 pg/mL) with no apparent or significant trends in any of the treatment or control groups.

Baseline values for ANP ranged from 8.8-66.8 pg/mL (mean ± SD - 26.2 ± 16.9 pg/mL, n=1 1). During the first hour of the three control trials, ANP levels decreased steadily from starting values and remained low in the 90 and 120 min samples. In six of the eight infusions, ANP levels peaked at an average of 89.7 ± 96. 1% (range - 29-277%) above pre-infusion values in either or both of the 30 and 60 min samples. In the other two infusion trials, ANP levels decreased at a rate comparable to the controls for those individuals. One of the trials in which ANP did not increase was a 1250 mL infusion in an animal that did show an ANP response to 2000 mL, suggesting that the smaller volume was inadequate in producing a response. ANP also declined in one of the 2000 mL infusions, in an animal that inexplicably showed an ANP response to the smaller volume. Taken together, these findings demonstrate that volumetric expansion in a phocid seal can stimulate ANP release. The reduced response in seals compared with that in humans and other animals could relate to cardiovascular adaptations related to diving in the phocids.