Transoesophageal Cardiac Pacing Research Articles

Effect of mild hypothermia combined with hydrogen-rich saline on cerebral injury after cardiac arrest and resuscitation in rats

Objective To evaluate the effect of mild hypothermia combined with hydrogen-rich saline on cerebral injury after cardiac arrest and resuscitation in rats. Methods Healthy male Sprague-Dawley rats, aged 7-8 weeks, weighing 280-320 g, were divided into 5 groups (n=33 each) using a random number table method: sham operation group (group S), cardiac arrest and resuscitation group(group CA-R), hydrogen-rich saline group (group H2), mild hypothermia group (group MH), and mild hypothermia plus hydrogen-rich saline group (group MH+ H2). Cardiac arrest was induced with transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the cerebral injury model.Hydrogen-rich saline 5 ml/kg was intraperitoneally injected immediately after return of spontaneous circulation (ROSC) in H2 and MH+ H2 groups, while the equal volume of normal saline was given instead in the other groups.The body temperature of rats was cooled down to 32-34℃ within 15 min starting from the time point immediately after ROSC and maintained for 4 h in MH and MH+ H2 groups.Fifteen rats were selected at 24 h after ROSC to assess the neurological function score (NDS). Eighteen rats in each group were sacrificed at 24 h after ROSC, and brains were removed for microscopic examination of the pathological changes in hippocampal CA1 region after hematoxylin and eosin staining and for determination of pyramidal cell count and expression of glucose-regulated protein 78 (GRP78), C/EBP-homologous protein (CHOP), caspase-12, caspase-3, Bcl-2 and Bax in hippocampal CA1 region (by Western blot). Results Compared with group S, the NDS was significantly decreased, the pyramidal cell count was reduced, the expression of GRP78, CHOP, caspase-12, caspase-3 and Bax was up-regulated, and the expression of Bcl-2 was down-regulated in the other four groups (P 0.05). Conclusion Combination of mild hypothermia and hydrogen-rich saline offers enhanced efficacy in reducing cerebral injury after cardiac arrest and resuscitation over mild hypothermia or hydrogen-rich saline alone in rats. Key words: Hypothermia, induced; Hydrogen; Heart arrest; Cardiopulmonary resuscitation; Reperfusion injury; Brain

Mild hypothermia combined with hydrogen sulfide alleviates hippocampal endoplasmic reticulum stress after global cerebral ischemia-reperfusion

Objective: To investigate the effect of mild hypothermia combined with hydrogen sulfide on hippocampal endoplasmic reticulum stress (ERS) after global cerebral ischemia-reperfusion (I/R) injury. Methods: Sixty healthy male Sprague-Dawley rats, 8-10 week old, weighing 280-320 g, were randomly divided into 5 groups (n=12) using a random number table: sham operation group (group Sham), global cerebral I/R group (group I/R), hydrogen sulfide group (group H(2)S), mild hypothermia group (group MH) and hydrogen sulfide + mild hypothermia group (group H(2)S+ MH). Cardiac arrest was induced with transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the global cerebral I/R model. The administration regimen for sodium hydrosulfide (NaHS) was as follows: Sodium hydrosulfide was intraperitoneal injection as a bolus of 2.5 mg/kg immediately restoration of spontaneous circulation. The implementation of mild hypothermia: wipe the body surface of rats with ethanol immediately after restoration of spontaneous circulation, and reduce the rectal temperature to 32-34 ℃ within 15 min, and maintain 6 h with the ice bag. At 72 h of reperfusion, neurological deficit was scored, and the rats were sacrificed (Neurological Deficit Scores, NDS), the expression of glucose-regulated protein 78 (GRP78), CHOP and Caspase-12 were detected by Western blot. After reperfusion 72 h, the hippocampal tissue were removed and stained with haematoxylin and eosin to examine the pathological findings in hippocampal CA1 area (under microscope). The apoptosis rate of hippocampal CA1 area cells was detected by TUNEL staining and the apoptosis index was calculated. Results: The expression levels of endoplasmic reticulum stress marker, GRP78, CHOP and Caspase-12, were upregulates during the global cerebral ischemia reperfusion injury, indicating activation of severe endoplasmic reticulum stress. The GRP78 contents of Sham group, I/R group, H(2)S group, MH group and H(2)S+ MH group were as follows: GRP78: 0.11±0.03, 1.11±0.10, 0.67±0.09, 0.66±0.08, 0.48±0.04, CHOP contents: 0.16±0.03, 1.60±0.11, 1.39±0.09, 1.34±0.08, 1.13±0.09, Caspase-12 contents: 0.09±0.02, 0.87±0.08, 0.65±0.08, 0.59±0.06, 0.45±0.06, the differences were statistically significant (F=147.569, 264.983, 119.356, all P<0.01). The apoptosis index of Sham group, I/R group, H(2)S group, MH group and H(2)S+ MH group were as follows: (1.83±0.75)%, (53.17±4.62)%, (35.17±2.14)%, (32.67±2.25)%, (17.83±2.79)%, the differences were statistically significant (F=284.962, P<0.01). The neurological deficit scores of Sham group, I/R group, H(2)S group, MH group and H(2)S+ MH group were as follows: 0%, (76±9)%, (54±5)%, (47±6)%, (35±6)%, the differences were statistically significant(F=135.218, P<0.01). Conclusion: Mild hypothermia combined with hydrogen sulfide alleviates hippocampal endoplasmic reticulum stress after global cerebral ischemia-reperfusion, and the combined effect is better than that of a single application.

Role of nuclear factor E2 related factor/heme oxygenase-1 pathway in hydrogen sulfide-induced reduction of blood brain barrier damage in rats with cardiac arrest

Objective To investigate whether the nuclear factor E2 related factor/heme synthase-1(Nrf2/HO-1) pathway is involved in the mechanism of hydrogen sulfide-induced reduction of blood brain barrier(BBB) injury in rats with cardiac arrest and the possible mechanism involved in the effect. Methods Cardiac arrest was induced with transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the cardiac arrest model and the time of ischemia was 4 min. 140 adult male SD rats were randomly divided into five groups: sham operation group(Sham group, n=20), cardiac arrest model group (CPR group, n=30), sodium hydrogen sulfide(NaHS) group(n=30), NaHS+solvent group[NaHS+dimethyl sulfoxide(DMSO) group, n=30], NaHS+Nrf2 inhibitor retinoic acid(RA) group(NaHS+RA group, n=30). In Sham group, only anesthesia was performed, and the trachea was inserted through the mouth, and the catheters were performed via femoral artery and vein. The other four groups were all induced cardiac arrest by electrical stimulation. NaHS group and NaHS+RA group, rats received NaHS (0.5 mg/kg) at the start of CPR intravenously, followed by a continuous infusion of NaHS(1.5 mg·kg-1·h-1) for 3 h. NaHS+RA group, RA was given i.p. daily at 10 mg/kg for 1 week before experiment and immediately after recovery. NaHS+DMSO group was given the same amount of solvent daily for 1 week before experiment and immediately after recovery. CPR group was given the same amount of normal saline at the start of CPR intravenously. After recovery, 7 days were observed continuously and the survival condition was recorded, and neurological function were evaluated at 1, 3 d, and 7 d after recovery, brain water content, BBB permeability and Nrf2, HO-1, BBB tight junction protein occludin expression was detected at 24 h after resuscitation, and the expression of matrix metalloproteinase-9(MMP-9) was detected by immunohistochemical staining. Results The survival rates, neurologic deficit scores(NDS), Nrf2 and HO-1 expression, and occludin expression in NaHS group were higher than CPR group(P 0.05). Conclusions Hydrogen sulfide could reduce the BBB damage in rats with cardiac arrest, which may be related to the activation of Nrf2/HO-1 pathway, inhibiting the expression of MMP-9 and decreasing the loss of occludin protein. Key words: Nuclear factor E2 related factor/heme oxygenase-1 pathway; Blood-brain barrier; Hydrogen sulfide; Cardiac arrest; Cardiopulmonary resuscitation

The efficiency of ventilation in out-of-hospital cardiopulmonary resuscitation: ananimal study

Objective To study the efficiency of ventilationin in out-of-hospital cardiopulmonary resuscitation(CPR) by performing compression-only CPR or conventional CPR in rats of different causes of cardiac arrest(CA). Methods Forty five SD rats were randomly divided into 5 groups: asphyxia-conventional group(group A, n=10), asphyxia-compression-only group(group B, n=10), ventricular fibrillation-conventional group(group C, n=10), ventricular fibrillation-compression-only group(group D, n=10), group sham(n=5). The model of asphyxial CA was made by clamping endotracheal tube at expiration in group A and group B. The model of ventricular fibrillation CA was made by transoesophageal cardiac pacing in group C and group D. Bystander CPR was initiated 4 min later. Conventional CPR(compression∶ventilation=30∶2) was performed in group A and group C, compression-only CPR was performed in group B and group D. For animals that did not attain return of spontaneous circulation(ROSC) during the 8 min bystander CPR period, advanced life support(ALS) was provided. The animals which did not attain ROSC after 10 min ALS should be given up. The pathological specimens of brain, ventricular wall and right lower lobe of the lung were collected after 24 h, and the samples were collected in the death of 24 h. Post-resuscitation treatment had been performed in all successfully resuscitated animals for 1 h. At 24 h after ROSC, rats were sacrificed for histological analysis. The vilai signs was monitored for 1 h in goup sham, rats were sacrificed for histological analysis after survival 24 h. The major outcome measure was rates of ROSC, and the secondary was the survival rates of 24 h. Blood samples were drawn for blood gas analysis during resuscitation in the pathologic findings. Results Rates of ROSC were higher in group A and group C compared with group B and group D, but the difference was not significant. Survival rates of 24 h were compared, group A and group C were significantly higher than group B and group D(P<0.05), and the tissue damage in group A and group C were milder than group B and group D. Conclusions Conventional bystander CPR was associated with a higher survival of 24 h than compression-only CPR. Conventional bystander CPR might be the preferable approach of resuscitation for adult patients with witnessed out-of-hospital CA, whether cardiogenic or non-cardiogenic CA. Key words: Cardiac arrest; Cardiopulmonary resuscitation; Artificial ventilation

Effect of hypothermia on expression of dynamin-related protein 1 in brain tissues during global cerebral ischemia-reperfusion in rats

Objective To evaluate the effect of hypothermia on the expression of dynamin-related protein 1(Drp1)in brain tissues during global cerebral ischemia-reperfusion(I/R)in rats. Methods Thirty-six healthy male Sprague-Dawley rats, weighing 280-320 g, were divided into 3 groups(n=12 each)using a random number table: sham operation group(group Sham), global cerebral I/R group(group I/R)and hypothermia group(group H). Cardiac arrest was induced by transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the global cerebral I/R model in anesthetized rats in I/R and H groups.In group H, the body temperature(rectal temperature)was cooled down to 32-34 ℃ within 15 min starting from the beginning of reperfusion, and maintained at this level for 6 h. At 72 h of reperfusion, neurological deficit was scored, and the rats were sacrificed, and the whole brain was removed for examination of the pathological changes in hippocampal CA1 region and for determination of normal pyramidal cell count and neuronal apoptosis in hippocampal CA1 region and expression of Drp1 and cytochrome c(Cyt c)in hippocampal tissues(by Western blot). The apoptosis rate was calculated. Results Compared with group S, the neurological deficit score and apoptosis rate were significantly increased, and the number of normal pyramidal cells was decreased in I/R and H groups, the expression of Drp1 and Cyt c in hippocampal tissues was significantly up-regulated in group I/R(P 0.05). Compared with group I/R, the neurological deficit score and apoptosis rate were significantly decreased, the number of normal pyramidal cells was increased, and the expression of Drp1 and Cyt c in hippocampal tissues was down-regulated in group H(P<0.05). Conclusion The mechanism by which hypothermia inhibits cell apoptosis during global cerebral I/R may be related to down-regulation of Drp1 expression in rats. Key words: Hypothermia, induced; Reperfusion injury; Brain; Dynamins

Changes in expression of cold-inducible RNA binding protein in hippocampus after cardiopulmonary resuscitation in a rat model of cardiac arrest

Objective To evaluate the changes in the expression of cold-inducible RNA binding protein (CIRP) in the hippocampus after cardiopulmonary resuscitation (CPR) in a rat model of cardiac arrest. Methods Eighty-five male Sprague-Dawley rats, weighing 280–320 g, aged 3 months, were randomly divided into 3 groups using a random number table: control (group C, n=15), sham operation group (group S, n=15) and CPR group (n=55). Cardiac arrest was induced through ventricular fibrillation caused by transoesophageal cardiac pacing, and then CPR was performed in group CPR.At 6 h, 12 h, and 1, 3 and 7 days after CPR, and the hippocampi were removed for detection of the expression of CIRP mRNA (using real-time reverse transcriptase polymerase chain reaction) and CIRP protein (using Western blot). The brain tissues were also obtained at 3 days after CPR for detection of CIRP expression in the hippocampal CA1 region by immunohistochemistry. Results Compared with group C, the expression of CIRP mRNA was significantly up-regulated at 1, 3, and 7 days after CPR, and the expression of CIRP was up-regulated at 1 and 3 days after CPR in group CRP (P 0.05). Compared with the values at 3 days after CPB, the expression of CIRP mRNA was significantly down-regulated at each time point after CPR, and the expression of CIRP was down-regulated at 6 h, 12 h, and 7 days after CPR in group CRP (P<0.05). CIRP was mainly expressed in the nucleus of pyramidal cells in the hippocampal CA1 region. Conclusion Up-regulated expression of hippocampal CIRP is one of the endogenous mechanisms that inhibit cell apoptosis in the brain tissues of rats. Key words: Heart arrest, induced; Cardiopulmonary resuscitation; RNA-binding proteins; Hippocampus

Effect of mild hypothermia on expression of hippocampal microRNA-210 during global cerebral ischemia-reperfusion in rats

Objective To evaluate the effect of mild hypothermia on expression of hippocampal microRNA-210 (miR-210) during global cerebral ischemia-reperfusion (I/R) in rats.Methods Sixty healthy male Sprague-Dawley rats,aged 9-10 weeks,weighing 280-320g,were randomly divided into 3 groups (n =20 each):sham operation group (group S),group I/R,and mild hypothermia group (group H).Ventricular fibrillation (VF) was induced with transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the global cerebral I/R model.In group H,the rectal temperature was cooled down to 32-34 ℃ by rubbing body surface with ethanol within 10 min starting from onset of reperfusion and maintained at this level for 6 h.In the other groups,the rectal temperature was maintained at 36-37 ℃ with a heating blanket.Rats were sacrificed at 24 h of reperfusion,and then the bilateral hippocampi were removed for detection of miR-210 expression (using RT-PCR) and apoptosis (by TUNEL).Results Compared with group S,the expression of miR-210 was up-regulated,and apoptosis rate was increased in group I/R.Compared with group I/R,the expression of miR-210 was down-regulated,and apoptosis rate was decreased in group H.Conclusion Mild hypothermia playes a role in cerebral resuscitation possibly by down-regulating miR-210 expression and reducing apoptosis in hippocampal cells of rats. Key words: MicroRNAs; Hypothermia, induced; Brain; Reperfusion injury; Hippocampus

Ventricular fibrillation induced by transoesophageal cardiac pacing: A new model of cardiac arrest in rats

To investigate whether transoesophageal cardiac pacing can induce ventricular fibrillation (VF) and how long the cardiac pacing has to be sustained to prevent the reversion of the VF induced. A pacing electrode was inserted orally into the oesophagus and high-frequency ventricular pacing was performed so as to elicit VF in 25 Sprague-Dawley rats. Incidences of VF and time of cardiac pacing were observed and recorded. Four minutes after onset of VF cardiopulmonary resuscitation (CPR) was initiated. A short interval of high-frequency ventricular pacing caused an immediate drop of blood pressure, loss of pulse and increase of right atrial pressure in the same time frame. When the cardiac pacing was terminated, VF was elicited at least once or more than once in all of the 25 rats. However, the VF elicited by the burst stimulation could be defibrillated spontaneously. With the prolongation (120-180 s) of cardiac pacing, the incidence of defibrillation of VF decreased from 100 to 0%. VF persisted in 19 of 25 animals, developed into asystole in 5 of 25 animals and converted into pulseless electrical activity in 1 of 25 animals prior to CPR. Following CPR 22 of 25 animals were resuscitated. Transoesophageal cardiac pacing can induce VF in rats. However, the cardiac pacing is required for at least 120-180 s to ensure that VF does not spontaneously convert. We can use the technique to establish a new and simpler rat cardiac arrest (CA) model, which may facilitate experimental investigation on CPR.

A comparison of transoesophageal cardiac pacing and epinephrine for cardiopulmonary resuscitation

The use of cardiac pacing to deal with bradycardia is well established. There is debate as to the benefits during cardiopulmonary resuscitation (CPR). This study was performed to compare the effects of transoesophageal cardiac pacing and high-dose epinephrine on the benefits of cardiopulmonary resuscitation after asphyxial cardiac arrest in rats. Thirty Sprague-Dawley rats of both sexes were randomly selected to a saline group (Sal-gro, treated with normal saline 1 mL IV, n = 10), an epinephrine group (Epi-gro, treated with epinephrine 0.4 mg/kg IV, n = 10), or a pacing group (Pac-gro, treated with normal saline 1 mL IV combined with transoesophageal cardiac pacing, n = 10) in a blinded fashion during resuscitation after 10 minutes of asphyxial cardiac arrest. Manual chest compression was in all cases performed using the same methodology by the same personnel who was blinded to hemodynamic monitor tracings. The rate of restoration of spontaneous circulation was 1 (10%), 7 (70%), and 8 (80%) of 10 in Sal-gro, Epi-gro, and Pac-gro, respectively. The rate of ventilator withdrawal within 60 minuets after resuscitation in Pac-gro was higher than that of Epi-gro (8/8 vs 1/7, respectively; P = .001); the survival rate after 2 hours in Pac-gro was significantly higher than that in Epi-gro (7/8 vs 1/7, respectively; P = .01). The data demonstrate that both epinephrine and transoesophageal cardiac pacing are effective within 10 minutes of asphyxia in rats. It is worth noting that transoesophageal cardiac pacing produced a better outcome with respiration and longer survival time compared with epinephrine after restoration of spontaneous circulation.

Transoesophageal cardiac pacing is effective for cardiopulmonary resuscitation in a rat of asphyxial model

To investigate effectiveness of transoesophageal cardiac pacing in a rat model of asphyxial cardiac arrest. Ten minutes after the tracheal tube had been clamped, cardiac arrest (CA) occurred in 20 Sprague-Dawley rats, and the rats were assigned randomly to receive cardiopulmonary resuscitation (CPR) in a control group or CPR combined with transoesophageal cardiac pacing in a pacing group. Restoration of spontaneous circulation (ROSC) was defined as an unassisted pulse with a mean arterial pressure (MAP) of >or=20 mmHg for >or=1 min. ROSC was significantly more frequent in the pacing group compared with the control group (7/10 versus 1/10, P<0.05). Faster ROSC and longer survival trend in the pacing group were seen compared with the control group. Transoesophageal cardiac pacing is effective for CPR in a rat of asphyxial model. However, the precise mechanism is not clear and further experiments will be necessary.

Cardiac pacemakers and implantable cardioverter-defibrillators in the perioperative phase

Recent developments have changed the techniques and indications for different methods of temporary cardiac pacing. Temporary transvenous pacing involves endocardial right ventricular stimulation by a bipolar electrode, introduced directly via a vein, or through a "paceport" pulmonary artery catheter. A "multipurpose" pulmonary artery catheter permits both atrial and ventricular sensing and pacing. Noninvasive transcutaneous cardiac pacing is safe, fast, and easily applicable. However, pain and discomfort from cutaneous nerve or muscle stimulation may be intolerable for unsedated patients. Transoesophageal cardiac pacing is usually successful only for atrial stimulation, e.g., in sinus node bradycardia, but is not indicated in patients with impaired AV-conduction. In patients with implanted pacemakers, temporary cardiac pacing can both impair or improve the haemodynamic situation. Implanted pacemakers should always be checked following surgery involving electrocautery. Preoperatively, rate-responsive pacemakers should be re-programmed so as to avoid activation of the rate-responsive function. Automatic implantable cardioverter-defibrillators should be deactivated to avoid delivery of inappropriate shocks. In patients with implanted epicardial patch electrodes, transthoracic defibrillation can be difficult with routine defibrillation protocols and may require positioning of the paddles on the lateral chest wall. However, emergency noninvasive transcutaneous cardiac pacing is possible in such patients with normal thresholds.

Successful emergency transoesophageal cardiac pacing with subsequent endoscopy

Successful emergency transoesophageal cardiac pacing with subsequent endoscopy

Successful emergency transoesophageal cardiac pacing with subsequent endoscopy.

Successful emergency transoesophageal cardiac pacing with subsequent endoscopy.