Delphine Boërio1, Thiago D Corrêa2,3, Stephan M Jakob3, Karin A Ackermann1, Hugh Bostock4, Werner J Z'Graggen1,5. 1. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. 2. Intensive Care Unit, Hospital Israelita Albert Einstein, São Paulo, Brazil. 3. Department of Intensive Care Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. 4. Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, United Kingdom. 5. Department of Neurosurgery, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
Abstract
INTRODUCTION: Sepsis-induced myopathy and critical illness myopathy are common causes of muscle weakness in intensive care patients. This study investigated the effect of different mean arterial blood pressure (MAP) levels on muscle membrane properties following experimental sepsis. METHODS: Sepsis was induced with fecal peritonitis in 12 of 18 anesthetized and mechanically ventilated pigs. Seven were treated with a high (75-85 mmHg) and 5 were treated with a low (≥60 mmHg) MAP target for resuscitation. In septic animals, resuscitation was started 12 h after peritonitis induction, and muscle velocity recovery cycles were recorded 30 h later. RESULTS: Muscles in the sepsis/high MAP group showed an increased relative refractory period and reduced early supernormality compared with the remaining septic animals and the control group, indicating membrane depolarization and/or sodium channel inactivation. The membrane abnormalities correlated positively with norepinephrine dose. DISCUSSION: Norepinephrine may contribute to sepsis-induced abnormalities in muscle by impairing microcirculation. Muscle Nerve 57: 808-813, 2018.
INTRODUCTION:Sepsis-induced myopathy and critical illness myopathy are common causes of muscle weakness in intensive care patients. This study investigated the effect of different mean arterial blood pressure (MAP) levels on muscle membrane properties following experimental sepsis. METHODS:Sepsis was induced with fecal peritonitis in 12 of 18 anesthetized and mechanically ventilated pigs. Seven were treated with a high (75-85 mmHg) and 5 were treated with a low (≥60 mmHg) MAP target for resuscitation. In septic animals, resuscitation was started 12 h after peritonitis induction, and muscle velocity recovery cycles were recorded 30 h later. RESULTS: Muscles in the sepsis/high MAP group showed an increased relative refractory period and reduced early supernormality compared with the remaining septic animals and the control group, indicating membrane depolarization and/or sodium channel inactivation. The membrane abnormalities correlated positively with norepinephrine dose. DISCUSSION: Norepinephrine may contribute to sepsis-induced abnormalities in muscle by impairing microcirculation. Muscle Nerve 57: 808-813, 2018.
Authors: Mohamad Hakam Tiba; Brendan M McCracken; Robert P Dickson; Jean A Nemzek; Carmen I Colmenero; Danielle C Leander; Thomas L Flott; Rodney C Daniels; Kristine E Konopka; J Scott VanEpps; Kathleen A Stringer; Kevin R Ward Journal: PLoS One Date: 2020-12-11 Impact factor: 3.240
Authors: Karen J Suetterlin; S Veronica Tan; Roope Mannikko; Rahul Phadke; Michael Orford; Simon Eaton; Avan A Sayer; Miranda D Grounds; Emma Matthews; Linda Greensmith; Michael G Hanna Journal: JCSM Rapid Commun Date: 2021-05-05
Authors: Heta Lad; Tyler M Saumur; Margaret S Herridge; Claudia C Dos Santos; Sunita Mathur; Jane Batt; Penney M Gilbert Journal: Int J Mol Sci Date: 2020-10-22 Impact factor: 5.923