Novel Modification of Potassium Chloride Induced Cardiac Arrest Model for Aged Mice

Liu, Huaqin; Zhang, Yu; Li, Ying; Xu, Bin; Yan, Baihui; Paschen, Wulf; Warner, David S.; Yang, Wei; Sheng, Huaxin

doi:10.14336/ad.2017.0221

Cited by 17 publications

(24 citation statements)

References 39 publications

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“…Following extubation, body temperature was maintained with active heating in a recovery cage for 2 hours. However, body temperatures fell significantly after active heating was stopped, which is consistent with post-arrest changes in humans [28] as well as previous mouse models of SCA [15,29]. The SCA mice continued to show significant temperature dysregulation and depressed HR at one day (Fig 1, Table 1).…”

Section: Plos Onesupporting

confidence: 85%

A novel ultrasound-guided mouse model of sudden cardiac arrest

et al. 2020

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Aim Mouse models of sudden cardiac arrest are limited by challenges with surgical technique and obtaining reliable venous access. To overcome this limitation, we sought to develop a simplified method in the mouse that uses ultrasound-guided injection of potassium chloride directly into the heart. Methods Potassium chloride was delivered directly into the left ventricular cavity under ultrasound guidance in intubated mice, resulting in immediate asystole. Mice were resuscitated with injection of epinephrine and manual chest compressions and evaluated for survival, body temperature, cardiac function, kidney damage, and diffuse tissue injury. Results The direct injection sudden cardiac arrest model causes rapid asystole with high surgical survival rates and short surgical duration. Sudden cardiac arrest mice with 8-min of asystole have significant cardiac dysfunction at 24 hours and high lethality within the first seven days, where after cardiac function begins to improve. Sudden cardiac arrest mice have secondary organ damage, including significant kidney injury but no significant change to neurologic function. Conclusions Ultrasound-guided direct injection of potassium chloride allows for rapid and reliable cardiac arrest in the mouse that mirrors human pathology without the need for intravenous access. This technique will improve investigators’ ability to study the mechanisms underlying post-arrest changes in a mouse model.

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Section: Plos Onesupporting

confidence: 85%

A novel ultrasound-guided mouse model of sudden cardiac arrest

et al. 2020

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“…We compared CA outcome in young (24.10±0.43 g) versus aged (31.69±1.03 g) mice using our recently established CA/CPR model 13. After 8.5 minutes CA, 3 mice (1 in 8 young and 2 in 9 aged mice) were not successfully resuscitated and, therefore, excluded.…”

Section: Resultsmentioning

confidence: 99%

“…CA/cardiopulmonary resuscitation (CPR) surgery was performed as described previously, with minor modifications 13. Briefly, anesthesia was induced with 5% isoflurane.…”

Section: Methodsmentioning

confidence: 99%

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Aging Is Associated With Impaired Activation of Protein Homeostasis‐Related Pathways After Cardiac Arrest in Mice

Shen

Yan

Zhao

et al. 2018

JAHA

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BackgroundThe mechanisms underlying worse outcome at advanced age after cardiac arrest (CA) and resuscitation are not well understood. Because protein homeostasis (proteostasis) is essential for cellular and organismal health, but is impaired after CA, we investigated the effects of age on proteostasis‐related prosurvival pathways activated after CA.Methods and ResultsYoung (2–3 months old) and aged (21–22 months old) male C57Bl/6 mice were subjected to CA and cardiopulmonary resuscitation (CPR). Functional outcome and organ damage were evaluated by assessing neurologic deficits, histological features, and creatinine level. CA/CPR‐related changes in small ubiquitin‐like modifier conjugation, ubiquitination, and the unfolded protein response were analyzed by measuring mRNA and protein levels in the brain, kidney, and spinal cord. Thiamet‐G was used to increase O‐linked β‐N‐acetylglucosamine modification. After CA/CPR, aged mice had trended lower survival rates, more severe tissue damage in the brain and kidney, and poorer recovery of neurologic function compared with young mice. Furthermore, small ubiquitin‐like modifier conjugation, ubiquitination, unfolded protein response, and O‐linked β‐N‐acetylglucosamine modification were activated after CA/CPR in young mice, but their activation was impaired in aged mice. Finally, pharmacologically increasing O‐linked β‐N‐acetylglucosamine modification after CA improved outcome.ConclusionsResults suggest that impaired activation of prosurvival pathways contributes to worse outcome after CA/CPR in aged mice because restoration of proteostasis is critical to the survival of cells stressed by ischemia. Therefore, a pharmacologic intervention that targets aging‐related impairment of proteostasis‐related pathways after CA/CPR may represent a promising therapeutic strategy.

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“…Once OHCA occurred, several factors including hypoxic injury, ischemia/reperfusion injury, cell injury, and renal failure contribute to the rise in the potassium level [ 16 , 17 , 33 ]. Some previous studies have demonstrated that high level potassium might induce cardiac arrest and decrease the chance of successful CPR [ 34 , 35 ]. However, only few studies have focused on OHCA patients.…”

Section: Discussionmentioning

confidence: 99%

Impact of Different Serum Potassium Levels on Postresuscitation Heart Function and Hemodynamics in Patients with Nontraumatic Out-of-Hospital Cardiac Arrest

Lin

Syue

Lee

et al. 2018

Bioinorganic Chemistry and Applications

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Background Sustained return of spontaneous circulation (ROSC) can be initially established in patients with out-of-hospital cardiac arrest (OHCA); however, the early postresuscitation hemodynamics can still be impaired by high levels of serum potassium (hyperkalemia). The impact of different potassium levels on early postresuscitation heart function has remained unclear. We aim to analyze the relationship between different levels of serum potassium and postresuscitation heart function during the early postresuscitation period (the first hour after achieving sustained ROSC). Methods Information on 479 nontraumatic OHCA patients with sustained ROSC was retrospectively obtained. Measures of early postresuscitation heart function (rate, blood pressure, and rhythm), hemodynamics (urine output and blood pH), and the duration of survival were analyzed in the case of different serum potassium levels (low: <3.5; normal: 3.5–5; high: >5 mmol/L). Results Most patients (59.9%, n = 287) had previously presented with high levels of potassium. Bradycardia, nonsinus rhythm, urine output <1 ml/kg/hr, and acidosis (pH < 7.35) were more common in patients with high levels of potassium (all p < 0.05). Compared with hyperkalemia, a normal potassium level was more likely to be associated with a normal heart rate (OR: 2.97, 95% CI: 1.74–5.08) and sinus rhythm (OR: 2.28, 95% CI: 1.45–3.58). A low level of potassium was more likely to be associated with tachycardia (OR: 3.54, 95% CI: 1.32–9.51), urine output >1 ml/kg/hr (OR: 5.35, 95% CI: 2.58–11.10), and nonacidosis (blood pH >7.35, OR: 7.74, 95% CI: 3.78–15.58). The duration of survival was shorter in patients with hyperkalemia than that in patients whose potassium levels were low or normal (p < 0.05). Conclusion Early postresuscitation heart function and hemodynamics were associated with the serum potassium level. A high potassium level was more likely to be associated with bradycardia, nonsinus rhythm, urine output <1 ml/kg/hr, and acidosis. More importantly, a high potassium level decreased the duration of survival.

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Novel Modification of Potassium Chloride Induced Cardiac Arrest Model for Aged Mice

Cited by 17 publications

References 39 publications

A novel ultrasound-guided mouse model of sudden cardiac arrest

A novel ultrasound-guided mouse model of sudden cardiac arrest

Aging Is Associated With Impaired Activation of Protein Homeostasis‐Related Pathways After Cardiac Arrest in Mice

Impact of Different Serum Potassium Levels on Postresuscitation Heart Function and Hemodynamics in Patients with Nontraumatic Out-of-Hospital Cardiac Arrest

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