scholarly journals Therapeutic hypothermia promotes cerebral blood flow recovery and brain homeostasis after resuscitation from cardiac arrest in a rat model

2018 ◽  
Vol 39 (10) ◽  
pp. 1961-1973 ◽  
Author(s):  
Qihong Wang ◽  
Peng Miao ◽  
Hiren R Modi ◽  
Sahithi Garikapati ◽  
Raymond C Koehler ◽  
...  

Laboratory and clinical studies have demonstrated that therapeutic hypothermia (TH), when applied as soon as possible after resuscitation from cardiac arrest (CA), results in better neurological outcome. This study tested the hypothesis that TH would promote cerebral blood flow (CBF) restoration and its maintenance after return of spontaneous circulation (ROSC) from CA. Twelve Wistar rats resuscitated from 7-min asphyxial CA were randomized into two groups: hypothermia group (7 H, n = 6), treated with mild TH (33–34℃) immediately after ROSC and normothermia group (7 N, n = 6,37.0 ± 0.5℃). Multiple parameters including mean arterial pressure, CBF, electroencephalogram (EEG) were recorded. The neurological outcomes were evaluated using electrophysiological (information quantity, IQ, of EEG) methods and a comprehensive behavior examination (neurological deficit score, NDS). TH consistently promoted better CBF restoration approaching the baseline levels in the 7 H group as compared with the 7 N group. CBF during the first 5–30 min post ROSC of the two groups was 7 H:90.5% ± 3.4% versus 7 N:76.7% ± 3.5% ( P < 0.01). Subjects in the 7 H group showed significantly better IQ scores after ROSC and better NDS scores at 4 and 24 h. Early application of TH facilitates restoration of CBF back to baseline levels after CA, which in turn results in the restoration of brain electrical activity and improved neurological outcome.

2011 ◽  
Vol 68 (6) ◽  
pp. 495-499 ◽  
Author(s):  
Milovan Petrovic ◽  
Gordana Panic ◽  
Aleksandra Jovelic ◽  
Tibor Canji ◽  
Ilija Srdanovic ◽  
...  

Introduction/Aim. The most important clinically relevant cause of global cerebral ischemia is cardiac arrest. Clinical studies showed a marked neuroprotective effect of mild hypothermia in resuscitation. The aim of this study was to evaluate the impact of mild hypothermia on neurological outcome and survival of the patients in coma, after cardiac arrest and return of spontaneous circulation. Methods. The prospective study was conducted on consecutive comatose patients admitted to our clinic after cardiac arrest and return of spontaneous circulation, between February 2005 and May 2009. The patients were divided into two groups: the patients treated with mild hypothermia and the patients treated conservatively. The intravascular in combination with external method of cooling or only external cooling was used during the first 24 hours, after which spontaneous rewarming started. The endpoints were survival rate and neurological outcome. The neurological outcome was observed with Cerebral Performance Category Scale (CPC). Follow-up was 30 days. Results. The study was conducted on 82 patients: 45 patients (age 57.93 ? 14.08 years, 77.8% male) were treated with hypothermia, and 37 patients (age 62.00 ? 9.60 years, 67.6% male) were treated conservatively. In the group treated with therapeutic hypothermia protocol, 21 (46.7%) patients had full neurological restitution (CPC 1), 3 (6.7%) patients had good neurologic outcome (CPC 2), 1 (2.2%) patient remained in coma and 20 (44.4%) patients finally died (CPC 5). In the normothermic group 7 (18.9%) patients had full neurological restitution (CPC 1), and 30 (81.1%) patients remained in coma and finally died (CPC 5). Between the two therapeutic groups there was statistically significant difference in frequencies of different neurologic outcome (p = 0.006), specially between the patients with CPC 1 and CPC 5 outcome (p = 0.003). In the group treated with mild hypothermia 23 (51.1%) patients survived, and in the normothermic group 30 (81.1%) patients died, while in the group of survived patients 23 (76.7%) were treated with mild hypothermia (p = 0.003). Conclusion. Mild therapeutic hypothermia applied after cardiac arrest improved neurological outcome and reduced mortality in the studied group of comatose survivors.


1998 ◽  
Vol 274 (4) ◽  
pp. H1378-H1385 ◽  
Author(s):  
Charles L. Schleien ◽  
John W. Kuluz ◽  
Barry Gelman

Using infant piglets, we studied the effects of nonspecific inhibition of nitric oxide (NO) synthase by N G-nitro-l-arginine methyl ester (l-NAME; 3 mg/kg) on vascular pressures, regional blood flow, and cerebral metabolism before 8 min of cardiac arrest, during 6 min of cardiopulmonary resuscitation (CPR), and at 10 and 60 min of reperfusion. We tested the hypotheses that nonspecific NO synthase inhibition 1) will attenuate early postreperfusion hyperemia while still allowing for successful resuscitation after cardiac arrest, 2) will allow for normalization of blood flow to the kidneys and intestines after cardiac arrest, and 3) will maintain cerebral metabolism in the face of altered cerebral blood flow after reperfusion. Before cardiac arrest, l-NAME increased vascular pressures and cardiac output and decreased blood flow to brain (by 18%), heart (by 36%), kidney (by 46%), and intestine (by 52%) compared with placebo. During CPR, myocardial flow was maintained in all groups to successfully resuscitate 24 of 28 animals [ P value not significant (NS)]. Significantly,l-NAME attenuated postresuscitation hyperemia in cerebellum, diencephalon, anterior cerebral, and anterior-middle watershed cortical brain regions and to the heart. Likewise, cerebral metabolic rates of glucose (CMRGluc) and of lactate production (CMRLac) were not elevated at 10 min of reperfusion. These cerebral blood flow and metabolic effects were reversed byl-arginine. Flows returned to baseline levels by 60 min of reperfusion. Kidney and intestinal flow, however, remained depressed throughout reperfusion in all three groups. Thus nonspecific inhibition of NO synthase did not adversely affect the rate of resuscitation from cardiac arrest while attenuating cerebral and myocardial hyperemia. Even though CMRGluc and CMRLac early after resuscitation were decreased, they were maintained at baseline levels. This may be clinically advantageous in protecting the brain and heart from the damaging effects of hyperemia, such as blood-brain barrier disruption.


2018 ◽  
Vol 5 (1) ◽  
pp. 33-38
Author(s):  
Atsushi Sakurai ◽  
Kosaku Kinoshita ◽  
Akira Utagawa ◽  
Junko Yamaguchi ◽  
Makoto Furukawa ◽  
...  

Objective: In order to clarify indications for therapeutic hypothermia, we retrospectively examined patients resuscitated after Out-of-Hospital Cardiac Arrest (OHCA) who recorded an Auditory Brainstem Response (ABR) wave V according to the Utstein-style guidelines. Methods: Patients who recorded an ABR wave V immediately after resuscitation from OHCA were kept at 34 °C for 48 hours. The cohort was divided into two groups: A favorable neurological outcome group (F group: N=12) and an unfavorable neurological outcome group (U group: N=14). Favorable neurological outcome was defined as Pittsburgh Cerebral-Performance Scale (CPC) 1 or 2 and unfavorable as CPC 3-5. Data used to compare the groups included whether CA was witnessed, if a bystander initiated cardiopulmonary resuscitation, presence of cardiac etiology, initial cardiac rhythm and elapsed time from emergency call receipt until Return of Spontaneous Circulation (ROSC). Results: Elapsed time from receipt of the emergency call until ROSC was significantly shorter in the F group than in the U group. ROC curve analysis indicated that the cut-off duration was 28 minutes for a favorable neurological outcome. Conclusion: For OHCA patients with an ABR wave V, elapsed time from receipt of emergency call until ROSC may be an important parameter within the Utstein-style guidelines to determine the usefulness of therapeutic hypothermia.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tadashi Kaneko ◽  
Shunji Kasaoka ◽  
Ken Nagao ◽  
Naohiro Yonemoto ◽  
Hiroyuki Yokoyama ◽  
...  

Introduction: Therapeutic hypothermia (TH) for post cardiac arrest syndrome (PCAS) patients is standard strategy to reduce brain damage. However, current randomized control study (TTM: Target temperature management study, N Engl J Med 2013) suggested that simple target temperature did not improve outcome. Furthermore, there is no evidence, whether target temperature would be changed for each status of PCAS patients. Hypothesis: Lower target temperature could improve neurological outcome in PCAS patients. Methods: Participants with J-PULSE-Hypo study database were divided into the L group (32.0-33.9°C) and the M group (34-35°C). The favorable neurological outcomes (%, CPC 1-2 on 30th day) were compared between L and M groups in all and each subgroups with propensity score analysis with IPTW (inverse probability of treatment weighting) method as multivariate analysis. The subgroups were ages and interval from collapse to ROSC (return of spontaneous circulation). Results: 477 participants were analyzed. The comparison of each groups for favorable neurological outcome were that all groups (L: 64%, n = 42, vs M: 55%, n= 424, P = 0.234, multivariate: P = 0.452), age (≤60 y.o.) (L: 70% vs M: 67%, P = 0.717, multivariate: P = 0.657), age (>60 y.o.) (L: 50% vs M: 44%, P = 0.665, multivariate: P = 0.061), interval from collapse to ROSC (≤30 min.) (L: 88% vs M: 64%, P = 0.022, multivariate: P = 0.007), and interval from collapse to ROSC (>30 min.) (L: 21% vs M: 29%, P = 0.567, multivariate: P = 0.449). Conclusions: The PCAS victims within 30 min. from collapse to ROSC, would be treated by TH with less than 34°C target temperature.


2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
J. M. D. van den Brule ◽  
J. G. van der Hoeven ◽  
C. W. E. Hoedemaekers

Out of hospital cardiac arrest is the leading cause of death in industrialized countries. Recovery of hemodynamics does not necessarily lead to recovery of cerebral perfusion. The neurological injury induced by a circulatory arrest mainly determines the prognosis of patients after cardiac arrest and rates of survival with a favourable neurological outcome are low. This review focuses on the temporal course of cerebral perfusion and changes in cerebral autoregulation after out of hospital cardiac arrest. In the early phase after cardiac arrest, patients have a low cerebral blood flow that gradually restores towards normal values during the first 72 hours after cardiac arrest. Whether modification of the cerebral blood flow after return of spontaneous circulation impacts patient outcome remains to be determined.


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