Type 2 diabetes mellitus worsens neurological injury following cardiac arrest: an animal experimental study
Abstract Background Cardiac arrest carries a poor prognosis. The typical cardiac arrest patient is comorbid, and studies have shown that diabetes mellitus is an independent risk factor for increased mortality after cardiac arrest. Despite this, animal studies lack to investigate cardiac arrest in th...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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SpringerOpen
2018-08-01
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| Series: | Intensive Care Medicine Experimental |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s40635-018-0193-2 |
| _version_ | 1818249213999316992 |
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| author | Lauge Vammen Søren Rahbek Niels Secher Jonas Agerlund Povlsen Niels Jessen Bo Løfgren Asger Granfeldt |
| author_facet | Lauge Vammen Søren Rahbek Niels Secher Jonas Agerlund Povlsen Niels Jessen Bo Løfgren Asger Granfeldt |
| author_sort | Lauge Vammen |
| collection | DOAJ |
| description | Abstract Background Cardiac arrest carries a poor prognosis. The typical cardiac arrest patient is comorbid, and studies have shown that diabetes mellitus is an independent risk factor for increased mortality after cardiac arrest. Despite this, animal studies lack to investigate cardiac arrest in the setting of diabetes mellitus. We hypothesize that type 2 diabetes mellitus in a rat model of cardiac arrest is associated with increased organ dysfunction when compared with non-diabetic rats. Methods Zucker diabetic fatty (ZDF) rats (n = 13), non-diabetic Zucker lean control (ZLC) rats (n = 15), and non-diabetic Sprague Dawley (SprD) rats (n = 8), underwent asphyxia-induced cardiac arrest. Animals were resuscitated and monitored for 180 min after return of spontaneous circulation (ROSC). Blood levels of neuron-specific enolase were measured to assess neurological injury. Cardiac function was evaluated by echocardiography. Results No differences in cardiac output or neuron-specific enolase existed between the groups at baseline. Median levels of neuron-specific enolase 180 min after ROSC was 10.8 μg/L (Q25;Q75—7.6;11.3) in the ZDF group, which was significantly higher compared to the ZLC group at 2.0 μg/L (Q25;Q75—1.7;2.3, p < 0.05) and the SprD group at 2.8 μg/L (Q25;Q75—2.3;3.4, p < 0.05). At 180 min after ROSC, cardiac output was 129 mL/min/kg (SD 45) in the ZDF group, which was not different from 106 mL/min/kg (SD 31) in the ZLC group or 123 mL/min/kg (SD 26, p = 0.72) in the SprD group. Conclusions In a cardiac arrest model, neuronal injury is increased in type 2 diabetes mellitus animals compared with non-diabetic controls. Although this study lacks to uncover the specific mechanisms causing increased neuronal injury, the establishment of a cardiac arrest model of type 2 diabetes mellitus lays the important foundation for further experimental investigations within this field. |
| first_indexed | 2024-12-12T15:32:56Z |
| format | Article |
| id | doaj.art-1b0f8c94cdc14a28a1208ffc07424f4f |
| institution | Directory Open Access Journal |
| issn | 2197-425X |
| language | English |
| last_indexed | 2024-12-12T15:32:56Z |
| publishDate | 2018-08-01 |
| publisher | SpringerOpen |
| record_format | Article |
| series | Intensive Care Medicine Experimental |
| spelling | doaj.art-1b0f8c94cdc14a28a1208ffc07424f4f2022-12-22T00:20:05ZengSpringerOpenIntensive Care Medicine Experimental2197-425X2018-08-016111710.1186/s40635-018-0193-2Type 2 diabetes mellitus worsens neurological injury following cardiac arrest: an animal experimental studyLauge Vammen0Søren Rahbek1Niels Secher2Jonas Agerlund Povlsen3Niels Jessen4Bo Løfgren5Asger Granfeldt6Department of Intensive Care Medicine, Aarhus University HospitalResearch Center for Emergency Medicine, Aarhus University HospitalDepartment of Intensive Care Medicine, Aarhus University HospitalDepartment of Cardiology, Aarhus University HospitalDepartment of Clinical Pharmacology, Aarhus UniversityResearch Center for Emergency Medicine, Aarhus University HospitalDepartment of Intensive Care Medicine, Aarhus University HospitalAbstract Background Cardiac arrest carries a poor prognosis. The typical cardiac arrest patient is comorbid, and studies have shown that diabetes mellitus is an independent risk factor for increased mortality after cardiac arrest. Despite this, animal studies lack to investigate cardiac arrest in the setting of diabetes mellitus. We hypothesize that type 2 diabetes mellitus in a rat model of cardiac arrest is associated with increased organ dysfunction when compared with non-diabetic rats. Methods Zucker diabetic fatty (ZDF) rats (n = 13), non-diabetic Zucker lean control (ZLC) rats (n = 15), and non-diabetic Sprague Dawley (SprD) rats (n = 8), underwent asphyxia-induced cardiac arrest. Animals were resuscitated and monitored for 180 min after return of spontaneous circulation (ROSC). Blood levels of neuron-specific enolase were measured to assess neurological injury. Cardiac function was evaluated by echocardiography. Results No differences in cardiac output or neuron-specific enolase existed between the groups at baseline. Median levels of neuron-specific enolase 180 min after ROSC was 10.8 μg/L (Q25;Q75—7.6;11.3) in the ZDF group, which was significantly higher compared to the ZLC group at 2.0 μg/L (Q25;Q75—1.7;2.3, p < 0.05) and the SprD group at 2.8 μg/L (Q25;Q75—2.3;3.4, p < 0.05). At 180 min after ROSC, cardiac output was 129 mL/min/kg (SD 45) in the ZDF group, which was not different from 106 mL/min/kg (SD 31) in the ZLC group or 123 mL/min/kg (SD 26, p = 0.72) in the SprD group. Conclusions In a cardiac arrest model, neuronal injury is increased in type 2 diabetes mellitus animals compared with non-diabetic controls. Although this study lacks to uncover the specific mechanisms causing increased neuronal injury, the establishment of a cardiac arrest model of type 2 diabetes mellitus lays the important foundation for further experimental investigations within this field.http://link.springer.com/article/10.1186/s40635-018-0193-2Cardiac arrestResuscitationAnimal modelType 2 diabetes mellitusNeurological injuryEchocardiography |
| spellingShingle | Lauge Vammen Søren Rahbek Niels Secher Jonas Agerlund Povlsen Niels Jessen Bo Løfgren Asger Granfeldt Type 2 diabetes mellitus worsens neurological injury following cardiac arrest: an animal experimental study Intensive Care Medicine Experimental Cardiac arrest Resuscitation Animal model Type 2 diabetes mellitus Neurological injury Echocardiography |
| title | Type 2 diabetes mellitus worsens neurological injury following cardiac arrest: an animal experimental study |
| title_full | Type 2 diabetes mellitus worsens neurological injury following cardiac arrest: an animal experimental study |
| title_fullStr | Type 2 diabetes mellitus worsens neurological injury following cardiac arrest: an animal experimental study |
| title_full_unstemmed | Type 2 diabetes mellitus worsens neurological injury following cardiac arrest: an animal experimental study |
| title_short | Type 2 diabetes mellitus worsens neurological injury following cardiac arrest: an animal experimental study |
| title_sort | type 2 diabetes mellitus worsens neurological injury following cardiac arrest an animal experimental study |
| topic | Cardiac arrest Resuscitation Animal model Type 2 diabetes mellitus Neurological injury Echocardiography |
| url | http://link.springer.com/article/10.1186/s40635-018-0193-2 |
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