Comparative Biochemistry and Physiology Part A 120 (1998) 693 – 698 Changes in fibrinolytic activity in diving grey seals Susanna Lohman a, *, Lars P. Folkow a , Bjarne Østerud b , Georg Sager c a Department of Arctic Biology, Institute of Medical Biology, Medical Faculty, Uniersity of Tromsø, N-9037 Tromsø, Norway b Department of Biochemistry, Institute of Medical Biology, Medical Faculty, Uniersity of Tromsø, N-9037 Tromsø, Norway c Department of Pharmacology, Institute of Medical Biology, Medical Faculty, Uniersity of Tromsø, N-9037 Tromsø, Norway Received 5 January 1998; received in revised form 16 May 1998; accepted 1 June 1998 Abstract In order to test the hypothesis that enhanced fibrinolytic activity is a factor which prevents the blood of diving seals from clotting, we instrumented two female grey seals (Halichoerus grypus ) with subcutaneous electrodes for measurements of heart rate (HR) and an extradural intravertebral venous catheter for collection of blood samples before, during and after simulated dives of 10 min duration. Blood samples were used for in vitro determination of clot lysis time (CLT), which is a measure of the level of fibrinolytic activity, and for analyses of plasma levels of cortisol, noradrenaline and adrenaline (A). The seals displayed profound diving bradycardia indicative of a substantial reduction in blood flow rates (pre-dive HR: 78 (63–98) bpm; dive HR: 8 (7–10) bpm; (median (range); n =2)) and elevated catecholamine levels (pre-dive A: 121 (98 – 184) pg · ml -1 ; peak dive/post-dive A: 3510 (447 – 6181) pg · ml -1 ), both of which are factors which promote blood coagulation. Nevertheless, we found that CLT always increased in connection with diving (pre-dive CLT: 436 (356 – 568) min; peak CLT during diving: 1380 (640 – 1800) min), which implies a reduced, rather than enhanced, fibrinolytic activity in this situation. These results show that enhanced fibrinolytic activity is not part of the defence system which prevents fatal clotting from occurring in diving grey seals. © 1998 Published by Elsevier Science Inc. All rights reserved. Keywords: Diving physiology; Phocid seals; Blood; Clotting; Thrombosis; Catecholamines; Cortisol 1. Introduction Some pinnipeds are able to dive to depths in excess of 1500 m and to stay submerged for more than 1 h at a time [7,18]. This is possible because of their spectacu- lar morphological, physiological and biochemical adap- tations. First, most pinnipeds are able to store large quantities of oxygen in their myoglobin-rich muscles and in their large volume of hemoglobin-rich blood [19,27]. Second, they are able to economise with these O 2 -stores through dramatic cardiovascular adjustments, often referred to as the diving response. These adjust- ments involve profound sympaticus-mediated vasocon- striction, extreme bradycardia and extensive reduction of cardiac output (for review, see [2]). As a result, priority tissues such as the brain and to some extent the myocardium and adrenals receive most of the dramati- cally reduced cardiac output, whereas perfusion of low- priority tissues like skeletal muscles, liver and kidneys is reduced to very low levels, leaving such tissues to subsist on endogenous oxygen stores and anaerobic metabolism [3,28]. Many of the consequences of these cardiovascular adaptations and adjustments in diving mammals (e.g. the redistribution of blood which causes pooling of blood in almost stagnant venous reservoirs, high hematocrit levels, high levels of circulating cate- cholamines [12] and lactate) are known to favour blood coagulation [6,14]. Yet, diving seals do not seem to suffer from clotting problems. Though aspects of this question have been addressed previously [11,21], the question of how diving seals avoid clotting problems has not been resolved. * Corresponding author. Tel.: +47 77 644871; fax: +47 77 645770; e-mail: susannal@fagmed.uit.no 1095-6433/98/$19.00 © 1998 Published by Elsevier Science Inc. All rights reserved. PII S1095-6433(98)10088-0