Brage Håheim1, Timofey Kondratiev2, Erik Sveberg Dietrichs3, Torkjel Tveita4. 1. Anesthesia and Critical Care Research Group, Department of Clinical Medicine, UiT, The Arctic University of Norway, 9037 Tromsø, Norway. Electronic address: bha035@post.uit.no. 2. Anesthesia and Critical Care Research Group, Department of Clinical Medicine, UiT, The Arctic University of Norway, 9037 Tromsø, Norway. Electronic address: timofey.kondratiev@uit.no. 3. Anesthesia and Critical Care Research Group, Department of Clinical Medicine, UiT, The Arctic University of Norway, 9037 Tromsø, Norway; Department of Research and Education, Norwegian Air Ambulance Foundation, 1441 Drøbak, Norway. Electronic address: erik.sveberg.dietrichs@uit.no. 4. Anesthesia and Critical Care Research Group, Department of Clinical Medicine, UiT, The Arctic University of Norway, 9037 Tromsø, Norway; Division of Surgical Medicine and Intensive Care, University Hospital of North Norway, 9038 Tromsø, Norway. Electronic address: torkjel.tveita@uit.no.
Abstract
BACKGROUND: Rewarming from hypothermia is associated with depressed cardiac function, known as hypothermia-induced cardiac dysfunction (HCD), and increased systemic vascular resistance (SVR). Previous studies on pharmacological treatment of HCD have demonstrated beneficial effects when using drugs with the combined effects; cardiac inotropic support and peripheral vasodilation. The presented study aims to investigate the isolated effects of arterial dilatation on cardiac functional variables during rewarming from hypothermia using sodium nitroprusside (SNP). METHODS: We utilized a rat model designed to induce HCD following 4 h at 15 °C and rewarming. To study effects on left ventricular (LV) functional variables in response to afterload reduction by SNP during rewarming a conductance catheter was used. Index of LV contractility, preload recruitable stroke work (PRSW), was obtained with inferior vena cava occlusions at 37 °C before and after hypothermia. Pressure signals from a catheter in the left femoral artery was used to pharmacologically adjust SVR. RESULTS: After rewarming both animal groups showed significant reduction in both SV and CO as a manifestation of HCD. However, compared to saline controls, SV and CO in SNP-treated animals increased significantly during rewarming in response to afterload reduction displayed as reduced SVR, mean arterial- and end-systolic pressures. The cardiac contractility variable PRSW was equally reduced after rewarming in both groups. CONCLUSION: When rewarming the present model of HCD a significant increase in SVR takes place. In this context, pharmacologic intervention aimed at reducing SVR show clear positive results on CO and SV. However, a reduction in SVR alone is not sufficient to fully alleviate CO during HCD, and indicate the need of additional inotropic support.
BACKGROUND: Rewarming from hypothermia is associated with depressed cardiac function, known as hypothermia-induced cardiac dysfunction (HCD), and increased systemic vascular resistance (SVR). Previous studies on pharmacological treatment of HCD have demonstrated beneficial effects when using drugs with the combined effects; cardiac inotropic support and peripheral vasodilation. The presented study aims to investigate the isolated effects of arterial dilatation on cardiac functional variables during rewarming from hypothermia using sodium nitroprusside (SNP). METHODS: We utilized a rat model designed to induce HCD following 4 h at 15 °C and rewarming. To study effects on left ventricular (LV) functional variables in response to afterload reduction by SNP during rewarming a conductance catheter was used. Index of LV contractility, preload recruitable stroke work (PRSW), was obtained with inferior vena cava occlusions at 37 °C before and after hypothermia. Pressure signals from a catheter in the left femoral artery was used to pharmacologically adjust SVR. RESULTS: After rewarming both animal groups showed significant reduction in both SV and CO as a manifestation of HCD. However, compared to saline controls, SV and CO in SNP-treated animals increased significantly during rewarming in response to afterload reduction displayed as reduced SVR, mean arterial- and end-systolic pressures. The cardiac contractility variable PRSW was equally reduced after rewarming in both groups. CONCLUSION: When rewarming the present model of HCD a significant increase in SVR takes place. In this context, pharmacologic intervention aimed at reducing SVR show clear positive results on CO and SV. However, a reduction in SVR alone is not sufficient to fully alleviate CO during HCD, and indicate the need of additional inotropic support.
Authors: Anders L Selli; Adrina K Kuzmiszyn; Natalia Smaglyukova; Timofei V Kondratiev; Ole-Martin Fuskevåg; Roy A Lyså; Aina W Ravna; Torkjel Tveita; Georg Sager; Erik S Dietrichs Journal: Front Physiol Date: 2021-07-30 Impact factor: 4.566
Authors: Adrina Kalasho Kuzmiszyn; Anders Lund Selli; Natalia Smaglyukova; Timofei Kondratiev; Ole-Martin Fuskevåg; Roy Andre Lyså; Aina Westrheim Ravna; Torkjel Tveita; Georg Sager; Erik Sveberg Dietrichs Journal: Front Physiol Date: 2022-07-13 Impact factor: 4.755