Abstract P126: Effects of Carvedilol on Mortality and Inflammatory Responses to Hemorrhagic Cardiac Arrest in Rats

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Takumi Taniguchi ◽  
Hideo Inaba
Keyword(s):  
Cardiac Arrest ◽  
Treatment Group ◽  
Oral Administration ◽  
Hemorrhagic Shock ◽  
Beta Blocker ◽  
Inflammatory Responses ◽  
Tnf Alpha ◽  
Control Group ◽  
Sprague Dawley ◽  
Arterial Blood

Recent studies showed that beta-blocker is often used in hypertensive and/or cardiac failure patients because of its drug efficacy. Moreover, several papers reported that beta-blocker has the beneficial effects in patients with cardiogenic shock. However, there are few studies about the effects of beta-blocker during hemorrhagic shock and hemorrhagic cardiac arrest. To evaluate the effects of beta-blocker in an animal model of hemorrhagic cardiac arrest. Carvedilol was used as the beta-blocker agents. Twenty-four male Sprague Dawley rats were used. Animals were randomly assigned to one of two groups (n = 12 per group): control group, no medication; treatment group, oral administration of carvedilol (10 mg/kg/day) for 5 days. After then, all animals were anesthetized with pentobarbital ip. Hemorrhagic cardiac arrest was induced with removing of blood. After 8 minutes of cardiac arrest, the all removing blood was administered. There were no other therapies before, during or after cardiac arrest. Hemodynamics and arterial blood gases were recorded, and mortality were calculated for the 5-hr observation period and plasma cytokine (TNF-alpha and Interleukin-6) concentrations were measured at 5-hr after cardiac arrest. The mortality rates at 5hrs after cardiac arrest were 8% and 50% for control and treatment groups, respectively. The increases of base deficit and lactate concentrations were less for the control group than the treatment group. Moreover, the increases of TNF-alpha and IL-6 concentrations were less for the control group than the treatment group. The present study showed that oral administration of carvedilol had the disadvantage effects on mortality and inflammatory effects to hemorrhagic cardiac arrest in rats. These finding suggest that beta-blocker may worsen the recovery of hemorrhagic shock.

Abstract P14: Estradiol Does Not Improve Survival and Hemodynamic Parameters in Male Piglets after Hemorrhage and Ventricular Fibrillation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Egidijus Semenas ◽  
Lars Wiklund
Keyword(s):  
Gender Differences ◽  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Hemorrhagic Shock ◽  
Repeated Measures ◽  
Troponin I ◽  
Control Group ◽  
Hemodynamic Parameters ◽  
Start Time ◽  
Arterial Blood

Introduction: Gender differences in organ functions and survival have been described in animal models of trauma and hemorrhagic shock. The female gender is associated with better cardiac, hepatic and immune functions compared to males after hemorrhagic shock. However, data about gender differences in hypovolemic normothermic cardiac arrest is lacking. Hypothesis: We hypothesized that the estradiol given during cardiopulmonary resuscitation (CPR) will improve survival and hemodynamic response in hypovolemic cardiac arrest and subsequent CPR. Methods: Twenty anesthetized male piglets (with a weight of 25.7 ± 1.7 kg [mean ± SD]) were bled 30% via the right femoral artery to a mean arterial blood pressure of 35 mm during 15 minutes. In the end of bleeding period estradiol group (n=10) received 17â-estradiol 50 ìg/kg intravenously, while the control group received no estradiol (n=10). Later all piglets were subjected to 4 min of untreated ventricular fibrillation followed by up to 15 min of open chest CPR. At 5 min of cardiac arrest piglets received vasopressin 0.4 U/kg, amiodarone 0.5 mg/kg, and hypertonic-hyperoncotic solution 3 ml/kg infusion for 20 minutes. Internal defibrillation was attempted from 8 min of cardiac arrest to achieve restoration of spontaneous circulation (ROSC). The experiment was terminated at 3 hours after initial resuscitation. Data were analyzed using Fisher’s exact test, Kaplan-Meier and repeated measures ANOVA methods. Results: All piglets were successfully resuscitated. No significant differences were observed in survival between the groups (p=0.24). All piglets needed dobutamine infusion and no differences were observed in either total dobutamin dose, or infusion start time (p=0.05). No significant changes were observed in any hemodynamic parameters (p>0.05). Troponin I levels did not differ between groups (p>0.75). Conclusions: Intravenous 17â-estradiol does not improve survival and hemodynamic parameters in male piglets after experimental hypovolemic cardiac arrest.

Abstract 218: Therapeutic Hypothermia Alone and Combination With Preconditioning Blunt Inflammation in Experimental Hemorrhagic Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Jianru Shi ◽  
Wangde Dai ◽  
Juan Carreno ◽  
Sharon L Hale ◽  
Robert A Kloner
Keyword(s):  
Hemorrhagic Shock ◽  
Therapeutic Hypothermia ◽  
Absolute Lymphocyte Count ◽  
Control Group ◽  
Sprague Dawley ◽  
Term Survival ◽  
Shed Blood ◽  
Arterial Blood ◽  
The Absolute ◽  
Experimental Hemorrhagic Shock

Background: Recent studies by our group indicate that preconditioning, therapeutic hypothermia (TH) and TH combined with preconditioning improved long-term survival during resuscitation of hemorrhagic shock. The neutrophil-to-lymphocyte ratio (NLR) is a marker of inflammation associated with increased mortality in patients with severe hemorrhage shock. The aim of this study is to evaluate the effects of these three therapies on NLR level in rats with acute hemorrhagic shock. Methods and Results: In the preconditioning study, Sprague Dawley rats (both genders) were randomized to preconditioning (n=26) or control group (n=27); in the hypothermia study, rats were randomized to TH (n=16) or control group (n=15); in a combination study, rats were randomized to TH plus preconditioning (n=11) or control group (n=10). Rats were anesthetized with intraperitoneal Ketamine and xylazine. After heparinizing, hemorrhagic shock was induced by withdrawing blood to a fixed mean blood pressure (MBP) of 30 mmHg for 30 minutes and then shed blood was reinfused. Preconditioning was induced by 4 cycles of inflating small cuffs around the femoral arteries to 200 mmHg for 5 minutes, followed by 5-minute deflation of the cuffs prior to hemorrhagic shock. TH started at 5 minutes after MBP reached 30 mmHg. Core temperature was maintained at ~32 °C until blood volume was fully restored. In the control group, body temperature was maintained at ~ 37°C. Arterial blood samples were collected 1 hour after resuscitation. The NLR is an easily accessible biomarker, which is calculated by dividing the absolute neutrophil count by the absolute lymphocyte count. The NLR was significantly lower in TH group (0.20 ± 0.02) compared with the control group (0.32 ± 0.03; p=0.003). Similarly, the NLR level was significantly decreased in TH plus preconditioning group (0.19 ± 0.02) versus the control group (0.33 ± 0.02; p= 0.001). There was no difference in NLR level between the preconditioning group (0.41 ± 0.04) and the control group (0.41 ± 0.04; p=0.984). Conclusions: NLR is widely recognized inflammation marker associated with poor prognosis in severe hemorrhagic shock. TH alone and TH combined with preconditioning blunt the inflammation by decreasing the NLR level in experimental hemorrhagic shock.

Abstract 119: Influence of Anesthetics on the Hemodynamic Response in a Rat Model of Hemorrhagic Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Claudius Balzer ◽  
Franz J Baudenbacher ◽  
Susan S Eagle ◽  
Michele M Salzman ◽  
William J Cleveland ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Rat Model ◽  
Cardiovascular Response ◽  
Femoral Vein ◽  
Blood Pressure Measurement ◽  
Experimental Models ◽  
Sprague Dawley ◽  
Compensatory Mechanisms ◽  
Arterial Blood

Introduction: Experimental models of hemorrhagic shock (HS) in rats are important to test new treatments that may improve outcomes in humans, and general anesthesia is required during these experiments. The volatile anesthetic Isoflurane is known for its beneficial effects in rat HS models. Focusing on cardiovascular compensatory mechanisms, we wanted to evaluate Isoflurane versus the injectable anesthetic Pentobarbital in our rat model of mild HS (class 2). We hypothesize that Isoflurane during development of HS improves hemodynamics compared to Pentobarbital. Methods: Twelve Sprague-Dawley rats were initially anesthetized with an intraperitoneal (IP) injection of Pentobarbital (45 mg/kg) and intubated (1 L/min, FiO 2 0.25); heart rate (HR) was monitored by subcutaneous ECG needles. Femoral artery and vein were cannulated for continuous blood pressure measurement and delivery of fluids, respectively. In one group (n=7), anesthesia was continued with repeated IP injections of Pentobarbital (dose mg/kg), the other group (n=5) received continuous Isoflurane (1%). After 30 min of stabilization and administration of Heparin (100 IU/kg), HS was induced by removal of 1 ml of blood over 1 min via the femoral vein, repeated every 3 min until a volume of 5 ml of blood was removed. Mean arterial blood pressure (MAP) and HR were recorded and analyzed in LabChart. Results: During baseline, rats showed no significant differences in HR and MAP between both groups. After 5 ml of hemorrhage, both groups showed significant changes compared to baseline, with significantly higher MAP and HR in rats given only Pentobarbital. Conclusions: In our rat model of HS, Isoflurane dampens the physiologic response to compensate for mild hemorrhage. The cardiovascular response of rats in the Isoflurane group was a decrease of HR and MAP to every ml of hemorrhage, while rats given only Pentobarbital were able to maintain their MAP by raising their HR until decompensation.

RNA Sequencing Reveals the Wound Repair Mechanism of Cuyuxunxi Prescription in Surgical Patients with Anal Fistulas

2021 ◽  
Vol 24 ◽  
Author(s):  
Yin Qu ◽  
Zhijun Zhang ◽  
Yafeng Lu ◽  
De Zheng ◽  
Wei Yang
Keyword(s):  
Wound Healing ◽  
Treatment Group ◽  
Rna Sequencing ◽  
Anal Fistula ◽  
Wound Repair ◽  
Inflammatory Responses ◽  
Control Group ◽  
Surgical Wound ◽  
Anal Fistulas ◽  
Skin Development

Background: Anal fistula is one of the most common colorectal and perirectal diseases in the world. Cuyuxunxi (CYXX) prescription is an efficient herbal fumigant used to promote the surgical wound healing of anal fistulas. Objective: This study aimed to explore the underlying molecular mechanism of CYXX prescription on surgical wound healing of anal fistulas. Methods: Ten patients with anal fistula were randomized into a control group or treatment group. The wound surface of patients in the control group was rinsed by normal saline, while that in the treatment group was rinsed by CYXX prescription. The wound tissues of patients with anal fistulas seven days after the surgery were collected for hematoxylin-eosin (HE) staining and RNA sequencing. The expressions of differentially expressed genes (DEGs) were validated by real-time quantitative PCR (RT-qPCR). Results: HE staining showed that CYXX treatment reduced the infiltration of inflammatory cells. A total of 472 DEGs, including 141 up-regulated genes and 331 down-regulated genes, were identified. These genes were significantly related to skin development, xenobiotic stimulus, and inflammation. In addition, the consistency rate of RT-qPCR and sequencing results was 83.33%, which showed a high relative reliability of the sequencing results. Conclusion: CYXX prescription could improve epidermis repair and reduce inflammatory responses.

Abstract P790: Landiolol Attenuates Global Cerebral Edema Following Experimental Cardiac Arrest in Mice

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Tomoyuki Iwai ◽  
Shin Nakayama
Keyword(s):  
Cardiac Arrest ◽  
Water Content ◽  
Cerebral Edema ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
P Value ◽  
Brain Water Content ◽  
Arterial Blood ◽  
The Brain ◽  
Brain Water

Introduction: Cerebral edema following cardiac arrest and cardiopulmonary resuscitation (CA/CPR) is associated with unfavorable neurologic outcome. The Na + -K + -2Cl - water cotransporter NKCC1 is suspected to be a critical mediator of edema formation after ischemia. It is reported that β1 adrenoreceptor antagonists protect neurons following brain ischemia in rodents. β1 adrenoreceptor antagonists inhibit the Na + -K + -ATPase, which can inhibit driving force of NKCC1 that theoretically reduces cerebral edema following ischemia-reperfusion injury. In this study, we examined whether landiolol, a selective β1 adrenoreceptor antagonist, attenuates cerebral edema following CA/CPR. Methods: Isoflurane-anesthetized adult male mice (C57BL/6J, 25-30g) were randomized into landiolol group or control group. After 7-min CA followed by CPR, landiolol (0.5ml, 830μg/ml) was administered by continuous infusion intravenously for 4 hours. Animals in control group were given normal saline (0.5ml) in the same manner. Twenty-four hours after CA/CPR, the brain was removed to assess brain water content using wet-to-dry method. The primary outcome was measurement of the brain water content. Heart rate and arterial blood pressure were recorded. Measured parameters were analyzed by one-way ANOVA with post hoc Tukey-Kramer test using SPSS® statistics 25. Differences were considered statistically significant at a P value < 0.05. Results: Brain water contents was increased in control group mice after CA/CPR (n=10) compared with those in sham operated mice (n=5) (79.5±0.85% vs 78.3±0.14%, P=0.003). Compared with control group, landiolol treatment significantly reduced brain water content in mice subjected to CA/CPR (n=12) (78.9±0.51% vs 79.5±0.85%, P=0.04). Conclusion: Landiolol attenuated brain edema following CA/CPR. These results may suggest selective β1-blocker could be alternative treatment for neuroprotection in patients who suffered CA/CPR.

scholarly journals Dynamic Changes in MMP1 and TIMP1 in the Antifibrotic Process of Dahuang Zhechong Pill in Rats with Liver Fibrosis

2019 ◽  
Vol 17 (1) ◽  
pp. 346-356
Author(s):  
Jiayu Lin ◽  
Chaowen Deng ◽  
Yanzhong Peng ◽  
Jie Zheng ◽  
Liya Wei ◽  
...  
Keyword(s):  
Treatment Group ◽  
Liver Fibrosis ◽  
Differentially Expressed ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Control Group ◽  
Model Group ◽  
Sprague Dawley ◽  
Dynamic Changes ◽  
Matrix Metalloproteinase 1 ◽  
Liver Tissues

AbstractOn the basis of carbon tetrachloride (CCl4)induced liver fibrosis in rats, this study aims to investigate the dynamic changes in matrix metalloproteinase 1 (MMP1) and the tissue inhibitor of metalloproteinase 1 (TIMP1) in the antifibrotic process of Dahuang Zhechong Pill (DHZCP). A total of 50 male Sprague Dawley rats, aged 8 weeks, were randomly divided into 3 groups: the control group, the model group (the group treated with CCl4), and the treatment group (the group treated with CCl4 and DHZCP). Rats were sacrificed at Weeks 4 and 8. Liver tissues were separated for RNA sequencing and bioinformatics analysis. Real-time PCR, Western blot analysis, and histological staining were conducted to confirm the gene expression and pathological change in liver tissues. Compared with control group, rats in model group showed poor mental state and slow weight gain. The liver tissues of the rats in the model group exhibited a damaged hepatic lobule structure, fibrous connective tissue hyperplasia, and inflammatory cell infiltration among the hyperplastic tissues. DHZCP could significantly improve the appearance of rats and alleviate CCl4-induced fibrosis. Compared to model group, 798 differentially expressed mRNAs were found in the treatment group, of which 120 were up-regulated and 678 were down-regulated. Differentially expressed mRNAs between the CCl4-induced group and the DHZCP-treated group were mainly focused on the following KEGG pathways: focal adhesion, phagosome, tight junction, and ECM–receptor interactions. Relative to those in the control group, MMP1 was downregulated, whereas, TIMP1 and Col1A1 were upregulated in the CCl4-induced group at Weeks 4 and 8. DHZCP could reverse MMP1, TIMP1, and Col1A1 expression.DHZCP protects against liver injury and exerts an antifibrotic effect on liver fibrosis induced by CCl4 in rats. Its mechanism may be related to the upregulation of MMP1, downregulation of TIMP1, and promotion of collagen degradation.

scholarly journals Diazoxide Attenuates Postresuscitation Brain Injury in a Rat Model of Asphyxial Cardiac Arrest by Opening Mitochondrial ATP-Sensitive Potassium Channels

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Haidong Wu ◽  
Peng Wang ◽  
Yi Li ◽  
Manhui Wu ◽  
Jiali Lin ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Brain Injury ◽  
Cell Apoptosis ◽  
Brain Cell ◽  
Vehicle Group ◽  
Control Group ◽  
Tunel Staining ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Mitokatp Channels

Objective. We investigated whether and how diazoxide can attenuate brain injury after cardiopulmonary resuscitation (CPR) by selective opening of mitochondrial ATP-sensitive potassium (mitoKATP) channels.Methods. Adult male Sprague-Dawley rats with induced cerebral ischemia (n=10per group) received an intraperitoneal injection of 0.1% dimethyl sulfoxide (1 mL; vehicle group), diazoxide (10 mg/kg; DZ group), or diazoxide (10 mg/kg) plus 5-hydroxydecanoate (5 mg/kg; DZ + 5-HD group) 30 min after CPR. The control group (sham group,n=5) underwent sham operation, without cardiac arrest. Mitochondrial respiratory control rate (RCR) was determined. Brain cell apoptosis was assessed using TUNEL staining. Expression of Bcl-2, Bax, and protein kinase C epsilon (PKCε) in the cerebral cortex was determined by Western blotting and immunohistochemistry.Results. The neurological deficit scores (NDS) in the vehicle group decreased significantly at 24 h and 48 h after CPR. Diazoxide significantly improved NDS and mitochondrial RCR after CPR at both time points; 5-HD cotreatment abolished these effects. Diazoxide decreased TUNEL-positive cells following CPR, upregulated Bcl-2 and PKCε, downregulated Bax, and increased the Bcl-2/Bax ratio; 5-HD cotreatment reversed these effects.Conclusions. Diazoxide attenuates postresuscitation brain injury, protects mitochondrial function, inhibits brain cell apoptosis, and activates the PKC pathway by opening mitoKATP channels.

Systemic and renal haemodynamic changes in renal schemia/reperfusion injury: impact of erythropoietin

2012 ◽  
Vol 90 (11) ◽  
pp. 1535-1543 ◽  
Author(s):  
Abdel-Aziz M. Hussein ◽  
Nashwa Barakat ◽  
Amira Awadalla ◽  
Ahmed A. Shokeir
Keyword(s):  
Renal Function ◽  
Renal Plasma Flow ◽  
Treated Group ◽  
Significant Rise ◽  
Control Group ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Group I ◽  
Haemodynamic Changes ◽  
Renal Vascular

The objective of this study was to investigate the effects of erythropoietin (EPO) on systemic and renal hemodynamics in a rat model of renal ischemic/reperfusion (I/R) injury. We used 30 male Sprague–Dawley rats distributed among the following 3 groups (10 rats per group): (i) the sham-operated group, (ii) the control group (I/R injury only), and (iii) the EPO-treated group (I/R injury with 1500 U EPO·(kg body mass)–1 on day 0, and 500 U·kg–1 on days 2 and 4 after ischemia). Renal function, arterial blood pressure (ABP), renal plasma flow (RPF), renal blood flow (RBF), and renal vascular resistance (RVR) were measured on days 1, 2, and 7 after ischemia. The expression of endothelial NO synthase (eNOS) and histopathology of kidney were evaluated on day 7. The contractility of aortic strips was recorded from the different groups. The results show that renal function and histopathology were significantly improved after treatment with EPO. Compared with the control group, the EPO-treated group showed a significant increase in RPF, RBF, haematocrite, ABP, eNOS expression, and a decrease in RVR (p < 0.05).The response of aortic strips to the relaxant effect of acetylcholine was improved in the EPO-treated group. In conclusion, treatment with EPO improves renal function and renal haemodynamics in renal I/R injury, and causes significant rise of ABP and haematocrite value.

scholarly journals Sustained Tau Phosphorylation and Microglial Activation Following Repetitive Traumatic Brain Injury

2020 ◽  
Vol 8 (A) ◽  
pp. 837-840
Author(s):  
Andre Marolop Pangihutan Siahaan ◽  
Rr Suzy Indharty ◽  
Jessy Chrestella ◽  
Wismaji Sadewo ◽  
Steven Tandean ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Treatment Group ◽  
Microglial Activation ◽  
Control Group ◽  
Sprague Dawley ◽  
Sham Control ◽  
Treatment Groups ◽  
Sham Control Group ◽  
Cd 68

BACKGROUND: Repetitive traumatic brain injury (TBI), even without acute sequela, can induce a delayed neurodegenerative with overexpression of phosphorylated tau (p-tau) as hallmark, caused by chronic inflammation mediated in part by microglial activation. AIM: The aim of this study was to examine the dynamics of p-tau accumulation and microglial activation following repetitive TBI. MATERIALS AND METHODS: Thirty Sprague–Dawley rats were randomized into a sham control group and two treatment groups receiving three successive closed-skull impacts (TBI model) from a 40-g mass dropped from a 1-m height on alternating days (days 0, 1, 3, and 7). The first treatment group was sacrificed on the last day of trauma and the second treatment group after 7 days of no trauma. The expression level of p-tau was evaluated by AT-8 antibody immunostaining and microglial activation by anti-CD-68 immunostaining. RESULTS: Immunoexpression of AT-8 was significantly elevated 7 days after TBI compared to the last day of trauma and compared to the sham control group, while CD-68 expression was significantly higher than sham controls on the last day of trauma and remained elevated for 7 days without trauma. CONCLUSION: The study showed that brain trauma can induce p-tau overexpression and microglial activation that is sustained during the non-trauma period.

scholarly journals The effect of high-dose intramuscular epinephrine on the recovery of spontaneous circulation in an asphyxia‐induced cardiac arrest rat model

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Daesung Lim ◽  
Soo Hoon Lee ◽  
Dong Hoon Kim ◽  
Changwoo Kang ◽  
Jin Hee Jeong ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Saline Group ◽  
Spontaneous Circulation ◽  
Rank Test ◽  
High Dose ◽  
Sprague Dawley ◽  
Epinephrine Administration ◽  
Arterial Blood ◽  
Induced Cardiac Arrest

Abstract Background Obtaining vascular access can be challenging during resuscitation following cardiac arrest, and it is particularly difficult and time-consuming in paediatric patients. We aimed to compare the efficacy of high-dose intramuscular (IM) versus intravascular (IV) epinephrine administration with regard to the return of spontaneous circulation (ROSC) in an asphyxia-induced cardiac arrest rat model. Methods Forty-five male Sprague-Dawley rats were used for these experiments. Cardiac arrest was induced by asphyxia, and defined as a decline in mean arterial pressure (MAP) to 20 mmHg. After asphyxia-induced cardiac arrest, the rats were randomly allocated into one of 3 groups (control saline group, IV epinephrine group, and IM epinephrine group). After 540 s of cardiac arrest, cardiopulmonary resuscitation was performed, and IV saline (0.01 cc/kg), IV (0.01 mg/kg, 1:100,000) epinephrine or IM (0.05 mg/kg, 1:100,000) epinephrine was administered. ROSC was defined as the achievement of an MAP above 40 mmHg for more than 1 minute. Rates of ROSC, haemodynamics, and arterial blood gas analysis were serially observed. Results The ROSC rate (61.5%) of the IM epinephrine group was less than that in the IV epinephrine group (100%) but was higher than that of the control saline group (15.4%) (log-rank test). There were no differences in MAP between the two groups, but HR in the IM epinephrine group (beta coefficient = 1.02) decreased to a lesser extent than that in the IV epinephrine group with time. Conclusions IM epinephrine induced better ROSC rates compared to the control saline group in asphyxia-induced cardiac arrest, but not compared to IV epinephrine. The IM route of epinephrine administration may be a promising option in an asphyxia-induced cardiac arrest.

Sign in / Sign up

Export Citation Format

Share Document