+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Continuous Hemodynamic Monitoring in an Intact Rat Model of Simulated Diving

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Cardiovascular risk is elevated in divers, but detailed information of cardiac function during diving is missing. The aim of this study was to apply an intact rat model with continuous monitoring of cardiac left ventricular (LV) function in a simulated diving experiment. Thirteen rats were inserted with a LV pressure–volume catheter and a pressure transducer in the femoral artery to measure hemodynamic variables, and randomly assigned to diving ( n = 9) and control ( n = 4) groups. The diving group was compressed to 600 kPa in air, maintained at pressure for 45 min (bottom phase), and decompressed to surface at 50 kPa/min. Data was collected before, during, and up to 60 min after exposure in the diving group, and at similar times in non-diving controls. During the bottom phase, stroke volume (SV) (−29%) and cardiac output (−30%) decreased, whereas LV end-systolic volume (+13%), mean arterial pressure (MAP) (+29%), and total peripheral resistance (TPR) (+72%) increased. There were no changes in LV contractility, stroke work, or diastolic function. All hemodynamic variables returned to baseline values within 60 min after diving. In conclusion, our simulated dive experiment to 600 kPa increased MAP and TPR to levels which caused a substantial reduction in SV and LV volume output. The increase in cardiac afterload demonstrated to take place during a dive is well tolerated by the healthy heart in our model, whereas in a failing heart this abrupt change in afterload may lead to acute cardiac decompensation.

          Related collections

          Most cited references 32

          • Record: found
          • Abstract: found
          • Article: not found

          Heat flow and distribution during induction of general anesthesia.

          Core hypothermia after induction of general anesthesia results from an internal core-to-peripheral redistribution of body heat and a net loss of heat to the environment. However, the relative contributions of each mechanism remain unknown. The authors evaluated regional body heat content and the extent to which core hypothermia after induction of anesthesia resulted from altered heat balance and internal heat redistribution. Six minimally clothed male volunteers in an approximately 22 degrees C environment were evaluated for 2.5 control hours before induction of general anesthesia and for 3 subsequent hours. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. To separate the effects of redistribution and net heat loss, we multiplied the change in overall heat balance by body weight and the specific heat of humans. The resulting change in mean body temperature was subtracted from the change in distal esophageal (core) temperature, leaving the core hypothermia specifically resulting from redistribution. Core temperature was nearly constant during the control period but decreased 1.6 +/- 0.3 degree C in the first hour of anesthesia. Redistribution contributed 81% to this initial decrease and required transfer of 46 kcal from the trunk to the extremities. During the subsequent 2 h of anesthesia, core temperature decreased an additional 1.1 +/- 0.3 degree C, with redistribution contributing only 43%. Thus, only 17 kcal was redistributed during the second and third hours of anesthesia. Redistribution therefore contributed 65% to the entire 2.8 +/- 0.5 degree C decrease in core temperature during the 3 h of anesthesia. Proximal extremity heat content decreased slightly after induction of anesthesia, but distal heat content increased markedly. The distal extremities thus contributed most to core cooling. Although the arms constituted only a fifth of extremity mass, redistribution increased arm heat content nearly as much as leg heat content. Distal extremity heat content increased approximately 40 kcal during the first hour of anesthesia and remained elevated for the duration of the study. The arms and legs are both important components of the peripheral thermal compartment, but distal segments contribute most. Core hypothermia during the first hour after induction resulted largely from redistribution of body heat, and redistribution remained the major cause even after 3 h of anesthesia.
            • Record: found
            • Abstract: found
            • Article: not found

            Effect of hyperoxia on left ventricular function and filling pressures in patients with and without congestive heart failure.

            To determine the effects of hyperoxia on left ventricular (LV) function in humans with and without congestive heart failure (CHF). An acute physiologic study of the effect of hyperoxia on right-heart hemodynamics, LV contractility (peak positive rate of rise of LV pressure [+dP/dt]), time constant of isovolumic left ventricular relaxation (tau), and LV filling pressures. Bayer Cardiovascular Clinical Research Laboratory at the Mount Sinai Hospital, Toronto, Ontario. Sixteen patients with stable CHF and 12 subjects with normal LV function received the hyperoxia intervention. Patients received 21% O(2) by a nonrebreather mask, followed by 100% O(2) for 20 min, and 21% O(2) for a 10-min recovery period. In response to hyperoxia, there was a 22 +/- 6% increase in LV end-diastolic pressure (LVEDP) in the CHF group and a similar 29 +/- 14% increase in LVEDP in the normal LV function group (p < 0.05 for both; mean +/- SEM). Hyperoxia was also associated with a prolongation in tau of 10 +/- 2% in the CHF group (p < 0.05) and 8 +/- 2% in the normal LV function group (p < 0.05). No changes in +dP/dt were observed in either group. Hyperoxia was associated with impairment of cardiac relaxation and increased LV filling pressures in patients with and without CHF. These observations indicate that caution should be used in the administration of high inspired O(2) fractions to normoxic patients, especially in the setting of CHF.
              • Record: found
              • Abstract: found
              • Article: not found

              Sex and the cardiovascular system: the intriguing tale of how women and men regulate cardiovascular function differently.

              The ability to recognize and appreciate from a reproductive standpoint that males and females possess different attributes has been long standing. Only more recently have we begun to look more deeply into both the similarities and differences between men and women, as well as between boys and girls, with respect to the structure and function of other organ systems. This article focuses on the cardiovascular system, with examples of sex differences in the control of coronary function, blood pressure, and volume. Recognizing the differences between the sexes with respect to cardiovascular function facilitates understanding of the mechanisms whereby homeostasis can be achieved using different contributions or components of the living system. Furthermore, recognition of the differences as well as the similarities permits the design of appropriate diagnostic instruments, recognition of sex-specific pathophysiology, and implementation of appropriate treatment of cardiovascular disease in men and women.

                Author and article information

                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                13 January 2020
                : 10
                1Møreforskning AS , Ålesund, Norway
                2Cardiovascular Research Group, Department of Medical Biology, UiT, The Arctic University of Norway , Tromsø, Norway
                3Department of Circulation and Medical Imaging, Norwegian University of Science and Technology , Trondheim, Norway
                4Anesthesia and Critical Care Research Group, Department of Clinical Medicine, UiT, The Arctic University of Norway , Tromsø, Norway
                5Division of Surgical Medicine and Intensive Care, University Hospital of North Norway , Tromsø, Norway
                Author notes

                Edited by: François Guerrero, Université de Bretagne Occidentale, France

                Reviewed by: Marko Ljubkovic, University of Split, Croatia; Danilo Cialoni, Dan Europe Foundation, Italy

                *Correspondence: Ingrid Eftedal, ingrid.eftedal@

                This article was submitted to Environmental, Aviation and Space Physiology, a section of the journal Frontiers in Physiology

                Copyright © 2020 Gaustad, Kondratiev, Eftedal and Tveita.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 3, Tables: 0, Equations: 0, References: 33, Pages: 8, Words: 0
                Funded by: Norges Forskningsråd 10.13039/501100005416
                Funded by: Utenriksdepartementet 10.13039/100007842
                Brief Research Report


                Comment on this article