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ABSTRACT: The quality of cardiopulmonary resuscitation (CPR), especially adequate compression depth, is associated with return of spontaneous circulation (ROSC) and is therefore recommended to be measured routinely. In the current study, we investigated the relationship between changes of transthoracic impedance (TTI) measured through the defibrillation electrodes, chest compression depth and coronary perfusion pressure (CPP) in a porcine model of cardiac arrest.
In 14 male pigs weighing between 28 and 34kg, ventricular fibrillation (VF) was electrically induced and untreated for 6min. Animals were randomized to either optimal or suboptimal chest compression group. Optimal depth of manual compression in 7 pigs was defined as a decrease of 25% (50mm) in anterior posterior diameter of the chest, while suboptimal compression was defined as 70% of the optimal depth (35mm). After 2min of chest compression, defibrillation was attempted with a 120-J rectilinear biphasic shock.
There were no differences in baseline measurements between groups. All animals had ROSC after optimal compressions; this contrasted with suboptimal compressions, after which only 2 of the animals had ROSC (100% vs. 28.57%, p=0.021). The correlation coefficient was 0.89 between TTI amplitude and compression depth (p<0.001), 0.83 between TTI amplitude and CPP (p<0.001).
Amplitude change of TTI was correlated with compression depth and CPP in this porcine model of cardiac arrest. The TTI measured from defibrillator electrodes, therefore has the potential to serve as an indicator to monitor the quality of chest compression and estimate CPP during CPR.
Resuscitation 07/2012; 83(10):1281-6. · 3.60 Impact Factor
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ABSTRACT: Though mild hypothermia displays an optimistic alleviation of contractive failure in the ischemia/reperfusion myocardium, we still lacked answers to many questions about its potential mechanisms. Our hypothesis is that hypothermia (32°C) induced in ischemia can ease mitochondrial injury resulting in improvement of myocardial contractility even under the condition of a normothermic reperfusion. Fifty newly born 1-2 d Sprague-Dawley rats were executed and the primary cardiomyocytes were obtained and cultivated in vitro. Myocytes were randomized into three groups and then subjected to ischemia either at 32°C or 37°C, both prior to undergoing reperfusion at 37°C. Contractility was presented as frequency and velocity. Ultrastructural alterations of cardiomyocytes and mitochondrion underwent semi-quantitative analysis with transmission electron microscopy and respiratory function of mitochondria was further assessed simultaneously. During cooling ischemia and following reperfusion, cardiomyocytes acquired a more immediate restoration to baseline level and had a significant difference as compared with those in normothermia (P < 0.05). Furthermore, hypothermia preserved the ultrastructure of myocytes and mitochondrion after ischemia. However, measurement on Heart Injury Score and form factor revealed no differences after 2-h reperfusion either in hypothermia or normothermia. On the contrary, the surface area and respiratory function of mitochondrion in reperfusion differed significantly in both groups (P < 0.05) which had an accordance with the variation on contractile performance. Hypothermia only induced in ischemia can bring contractility benefit even under a normothermia reperfusion in cultured cardiomyocytes.
In Vitro Cellular & Developmental Biology - Animal 04/2012; 48(5):284-92. · 1.31 Impact Factor
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ABSTRACT: Though there is evidence to implicate that the mitochondrion may play an important role in the development of postresuscitation myocardial dysfunction, limited data are available regarding the ultrastructural alterations of the mitochondria, mitochondrial energy-producing ability, and their relationship to postresuscitation myocardial dysfunction. This study was designed to determine whether mitochondrial abnormalities contribute to the development of postresuscitation myocardial dysfunction.
Fifteen anesthetized male Sprague-Dawley rats were randomized to: (1) global myocardial ischemia/reperfusion, in which 8 min of ventricular fibrillation was induced and successful defibrillation was achieved after 6 min of cardiopulmonary resuscitation (CPR); (2) global myocardial ischemia, in which ventricular fibrillation and CPR were performed without defibrillation attempt; and (3) sham control.
Myocardial function was significantly impaired after resuscitation. Mitochondria were massively swollen in global ischemic hearts and mildly swollen in the resuscitated hearts. Concomitantly, ATP levels abruptly declined during global ischemia and partially recovered after resuscitation. Furthermore, mitochondrial abnormalities were supported by the incapability of utilizing energy substrates manifested by the accumulations of intramyocellular lipid droplets and glycogen deposits.
In this model of cardiac arrest and CPR, the presence of ultrastructural mitochondrial abnormalities, further evidenced by the incapability of utilizing energy substrates and impairment of energy-production, might, in part, contribute to the development of postresuscitation myocardial dysfunction.
Resuscitation 08/2011; 83(3):386-94. · 3.60 Impact Factor
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ABSTRACT: We hypothesized that administration of allogeneic bone marrow mesenchymal stem cells (MSCs) by intravenous, intraventricular or intramyocardial injection could improve myocardial function after survival time after cardiopulmonary resuscitation in myocardial infarcted rats. Myocardial infarction was induced by ligation of the left anterior descending artery in 54 rats (6 groups, 9 rats for each group). Left ventricular remodeling was quantitated weekly by ejection fraction (EF) measurement. One month after ligation, animals were randomized to receive injection of either MSCs 5x10(6) labeled with PKH26 in phosphate buffer solution (PBS) or PBS alone as a placebo. MSCs or PBS were administered by injection into the right femoral vein, the left ventricular cavity, or into the infracted anterior ventricular free wall. Four weeks after MSC or PBS injection, ventricular fibrillation (VF) was induced and untreated for 6 min, followed by 6 min of CPR prior to defibrillation. Hemodynamics, including cardiac index (CI), left ventricular dP/dt40 (dP/dt40), left ventricular negative dP/dt (-dP/dt) and left ventricular diastolic pressure (LVDP) were measured at baseline and hourly following return of spontaneous circulation (ROSC). Labeled MSCs were observed in 5 microm sections obtained with a cryostat from each harvested heart. Independently of the site of injection of MSCs, EF, CI, dP/dt40, -dP/dt, and LVDP were significantly improved and sustained before and after CPR in the animals treated with MSCs and were associated with significantly increased survival time when compared with the corresponding PBS treated animals.
Journal of Molecular and Cellular Cardiology 01/2009; 46(3):378-84. · 5.17 Impact Factor
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ABSTRACT: Allogeneic bone marrow mesenchymal stem cells were previously shown to improve myocardial function when administered intravenously after resuscitation from cardiac arrest in rats. Coincidental evidence of improved brain function prompted the present study.
Prospective, randomized, controlled study.
University-affiliated research institute.
Male Sprague-Dawley rats.
Using an established model in 20 male Sprague-Dawley rats in which 6 mins of untreated cardiac arrest was followed by cardiopulmonary resuscitation, animals were randomized to receive 5 x 10(6) mesenchymal stem cells labeled with PKH26 in phosphate buffer solution or phosphate buffer solution alone as a placebo at 2 hrs after restoration of spontaneous circulation. The stem cells or buffer diluent were injected into a catheter advanced from the jugular vein into the right atrium.
Outcome measurements in addition to 35-day survival included somatosensor testing of capability for removal of an adhesive patch applied to both front paws, testing of motor function using a rotating cylinder, and observational scoring of the severity of neurologic impairment. Labeled mesenchymal stem cells were subsequently identified and counted in 5 microm sections obtained from defined sites in the harvested brain. Immunohistochemistry was used to identify neural cells differentiation of mesenchymal stem cells. Adhesive removal, motor function test, neurologic severity score, and 35-day survival were each significantly improved in comparison with control animals. Labeled mesenchymal stem cells were identified in the hippocampus, cortex, pons, medulla, and cerebellum and expressed protein markers phenotypic neural cells.
Mesenchymal stem cells injected into the right atrium of rats after resuscitation from cardiac arrest were identified in brains harvested 35 days later. Brain function was significantly improved. Accordingly, venous injection of mesenchymal stem cells after cardiopulmonary resuscitation has promise of minimizing the severity of postresuscitation neurologic impairment.
Critical care medicine 11/2008; 36(11 Suppl):S486-91. · 6.37 Impact Factor
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ABSTRACT: We investigated the effects of three different sites for delivery of bone marrow mesenchymal stem cells (MSCs) in a rat model of myocardial ischemia.
Prospective, randomized, controlled study.
University affiliated research institute.
Male Sprague-Dawley rats.
A thoracotomy was performed under general anesthesia. Myocardial ischemia was induced by ligation of the left anterior descending coronary artery. One month later, animals were randomized to receive 5 x 10(6) MSCs labeled with PKH26 in phosphate buffer solution or phosphate buffer solution alone as a placebo by injection into right femoral vein, directly into the left ventricular (LV) cavity, or into the ischemic zone in the anterior ventricular free wall.
Echocardiographically measured myocardial function, including ejection fraction and fractional shortening, was quantitated 2 wks and 4 wks after administering MSCs or phosphate buffer solution. Hemodynamics, including cardiac index, LV dP/dt40, LV negative dP/dt, and LV diastolic pressure were measured 4 wks after administering MSCs or phosphate buffer solution. MSCs were counted in 5-microm sections obtained with cryostat from each harvested heart. Significant improvements in ejection fraction, fractional shortening, cardiac index, LV dP/dt40, LV negative dP/dt, and LV diastolic pressure followed injection of MSCs, regardless of the site of injection. However, the number of MSCs counted in the heart sections was significantly greater after direct myocardial injection.
Independently of the site of injection and regardless of the different concentration of bone marrow mesenchymal stem cells identified in the myocardium, myocardial function was comparably improved in all groups of animals treated with MSCs.
Critical Care Medicine 12/2007; 35(11):2587-93. · 6.33 Impact Factor
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ABSTRACT: The membrane (M) protein of severe acute respiratory syndrome coronavirus (SARS-CoV) is a major glycoprotein with multiple biological functions. In this study, we found that memory T cells against M protein were persistent in recovered SARS patients by detecting gamma interferon (IFN-gamma) production using ELISA and ELISpot assays. Flow cytometric analysis showed that both CD4+ and CD8+ T cells were involved in cellular responses to SARS-CoV M antigen. Furthermore, memory CD8+ T cells displayed an effector memory cell phenotype expressing CD45RO- CCR7- CD62L-. In contrast, the majority of IFN-gamma+ CD4+ T cells were central memory cells with the expression of CD45RO+ CCR7+ CD62L-. The epitope screening from 30 synthetic overlapping peptides that cover the entire SARS-CoV M protein identified four human T-cell immunodominant peptides, p21-44, p65-91, p117-140 and p200-220. All four immunodominant peptides could elicit cellular immunity with a predominance of CD8+ T-cell response. This data may have important implication for developing SARS vaccines.
Journal of General Virology 11/2007; 88(Pt 10):2740-8. · 3.36 Impact Factor
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ABSTRACT: Our group has developed a rat model of cardiac arrest and cardiopulmonary resuscitation (CPR). However, the current rat model uses healthy adult animals. In an effort to more closely reproduce the event of cardiac arrest and CPR in humans with chronic coronary disease, a rat model of coronary artery constriction was investigated during cardiac arrest and CPR. Left coronary artery constriction was induced surgically in anesthetized, mechanically ventilated Sprague-Dawley rats. Echocardiography was used to measure global cardiac performance before surgery and 4 wk postsurgery. Coronary constriction provoked significant decreases in ejection fraction, increases in left ventricular end-diastolic volume, and increases left ventricular end-systolic volume at 4 wk postintervention, just before induction of ventricular fibrillation (VF). After 6 min of untreated VF, CPR was initiated on three groups: 1) coronary artery constriction group, 2) sham-operated group, and 3) control group (without preceding surgery). Defibrillation was attempted after 6 min of CPR. All the animals were resuscitated. Postresuscitation myocardial function as measured by rate of left ventricular pressure increase at 40 mmHg and the rate of left ventricular pressure decline was more significantly impaired and left ventricular end-diastolic pressure was greater in the coronary artery constriction group compared with the sham-operated group and the control group. There were no differences in the total shock energy required for successful resuscitation and duration of survival among the groups. In summary, this rat model of chronic myocardial ischemia was associated with ventricular remodeling and left ventricular myocardial dysfunction 4 wk postintervention and subsequently with severe postresuscitation myocardial dysfunction. This model would suggest further clinically relevant investigation on cardiac arrest and CPR.
Journal of Applied Physiology 11/2006; 101(4):1091-6. · 3.75 Impact Factor
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ABSTRACT: Postresuscitation myocardial dysfunction has been recognized as a leading cause of early death after initially successful cardiopulmonary resuscitation. We have previously demonstrated that opening adenosine triphosphate (ATP)-sensitive K (KATP) channels or activation of delta-opioid receptors minimized the severity of postresuscitation myocardial dysfunction and increased the duration of postresuscitation survival. In the present study, we investigated the potential mechanism of myocardial protection following delta-opioid receptor activation in a rat model of cardiac arrest and cardiopulmonary resuscitation.
Randomized prospective animal study.
Animal research laboratory.
Male Sprague-Dawley rats.
Ventricular fibrillation was induced in 24 Sprague-Dawley rats. Mechanical ventilation and precordial compression were initiated after 8 mins of untreated ventricular fibrillation. Defibrillation was attempted after 6 mins of cardiopulmonary resuscitation. The animals were randomized to four groups: a) pentazocine (0.3 mg/kg), a delta-opioid receptor agonist; b) pentazocine pretreated with KATP channel blocker, glibenclamide (0.3 mg/kg), administered 45 mins before induction of ventricular fibrillation; c) glibenclamide pretreated alone 45 mins before induction of ventricular fibrillation; and d) placebo. Pentazocine or saline placebo was injected into the right atrium after 5 mins of untreated ventricular fibrillation.
Postresuscitation myocardial function, as measured by the rate of left ventricular pressure increase at 40 mm Hg, left ventricular end-diastolic pressure, and cardiac index, was significantly improved in pentazocine-treated animals. This was associated with significantly prolonged duration of survival. Except for ease of defibrillation, the beneficial effects of pentazocine were abolished by pretreatment with the KATP channel blocker glibenclamide.
The postresuscitation myocardial protective effects provided by activation of delta-opioid receptor may be mediated via opening KATP channels.
Critical Care Medicine 11/2006; 34(10):2607-12. · 6.33 Impact Factor
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Shanping Jiang,
Liwen Huang,
Xilong Chen,
Jingfeng Wang,
Wei Wu,
Songmei Yin,
Weixian Chen,
Jun Zhan,
Li Yan,
Liping Ma,
Jianguo Li, Zitong Huang
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ABSTRACT: To identify valid measures for preventing outbreaks of severe acute respiratory syndrome (SARS) among protected healthcare workers in isolation units.
Architectural factors, admitted SARS cases and infection of healthcare workers in different isolation wards between January 30 and March 30, 2003 were analyzed.
Four types of isolation wards were analyzed, including the ward where the thirty-first bed was located on the twelfth floor, the laminar flow ward in the Intensive Care Unit where the tenth bed was located on the fifteenth floor, the ward where the twenty-seventh bed was located on the thirteenth floor of the Lingnan Building, and thirty wards on the fourteenth to eighteenth floors of the Zhongshan Building. The ratios (m(2)/m(3)) of the area of the ventilation windows to the volume of the rooms were 0, 0, 1:95 and 1:40, respectively. Numbers of SARS cases in the wards mentioned above were 1, 1, 1 and 96, respectively. Total times of hospitalization were 43, 168, 110 and 1272 hours, respectively. The infection rates of the healthcare workers in the areas mentioned above were 73.2%, 32.1%, 27.5% and 1.7%, respectively. The difference in the infection rates was of statistical significance.
Isolating SARS cases in wards with good ventilation could reduce the viral load of the ward and might be the key to preventing outbreaks of SARS among healthcare workers along with strict personal protection measures in isolation units.
Chinese medical journal 10/2003; 116(9):1293-7. · 0.86 Impact Factor
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ABSTRACT: To explore digestive system manifestations in patients with severe acute respiratory syndrome (SARS).
The clinical data of 96 cases with SARS admitted into our hospital from February 6, 2003 to March 28, 2003 were retrospectively analyzed.
Among the 96 cases, 26 cases (27%) had diarrhea, 17 (18%) had nausea, 6 (6%) had vomiting, 16 (17%) had bellyache, and 8 (8%) had ALT elevation.
Patients with SARS may have digestive system manifestations; diarrhea is the most common symptom.
Chinese medical journal 09/2003; 116(8):1265-6. · 0.86 Impact Factor
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Wei Wu,
Jingfeng Wang,
Pinming Liu,
Weixian Chen,
Songmei Yin,
Shanping Jiang,
Li Yan,
Jun Zhan,
Xilong Chen,
Jianguo Li, Zitong Huang,
Hongzhang Huang
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ABSTRACT: To describe a hospital outbreak of severe acute respiratory syndrome (SARS) and summarize its clinical features and therapeutic approaches.
The outbreak started with a SARS patient from the community, and a total of 96 people (76 women and 20 men, mean age (29.5 +/- 10.3) years, 93.8% of whom were health care workers) who had exposure to this source patient became infected in a short time. Clinical data in this cohort were collected prospectively as they were identified.
(1) The incubation period ranged from 1 to 20 (mean: 5.9 +/- 3.5) days. The duration of hospitalization was (17.2 +/- 8.0) days. (2) The initial temperature was (38.3 +/- 0.6) degrees C, while the highest was (39.2 +/- 0.6) degrees C (P < 0.001), with fever duration of (9.0 +/- 4.2) days. (3) Other most common symptoms included fatigue (93.8%), cough (85.4%), mild sputum production (66.7%), chills (55.2%), headache (39.6%), general malaise (35.4%) and myalgia (21.9%). (4) The radiographic changes were predominantly bilateral in the middle or lower lung zones. The number of affected lung fields was 1.2 +/- 0.8 on presentation, which increased to 2.9 +/- 1.4 after admission (P < 0.001). The interval from the beginning of fever to the onset of abnormal chest radiographs was (3.5 +/- 2.3) days, which increased in size, extent, and severity to the maximum (6.7 +/- 3.5) days later. The time before the lung opacities were basically absorbed was (14.9 +/- 7.8) days. (5) Leukopenia was observed in 67.7% of this cohort. The time between the onset of fever and leukopenia was (4.4 +/- 2.3) days, with the lowest white blood cell count of (2.80 +/- 0.72) x 10(9)/L. (6) The lowest arterial oxygen saturation was (94.8 +/- 3.1)% with supplementary oxygen. (7) Antibiotical therapies included tetracyclines (91.0%), aminoglycosides (83.3%), quinolones (79.2%); 18.8% of the patients received a combination of tetracyclines and aminoglycosides, while 11.5% received a combination of tetracyclines and quinolones, and 63.5% received a combination of tetracyclines, aminoglycosides and quinolones. Vancomycin was used in 13.5% of the patients. (8) 68.8% of the patients were treated with methylprednisolones for a mean interval of (4.9 +/- 2.4) days. The initial dose was (67.3 +/- 28.2) mg/d and the maximal dose was (82.4 +/- 30.5) mg/d. (9) Human gamma-globulin, interferon-alpha, antiviral drugs (oral ribavirin or oseltamivir) were used respectively in 68.6%, 46.9% and 92.7% of the patients. (10) Ninety-five patients (99.0%) had a complete clinical recovery, and only 1 patient (1.0%) died.
SARS appears to be quickly infectious and potentially lethal among health care workers, characterized by acute onset and rapid progression, and mostly bilateral lung involvement on chest radiographs. Proper administration of glucocorticosteroids seems to be of some benefits. Antibiotics, human gamma-globulin, interferon-alpha, and antiviral drugs, although empirically, might be useful to shorten the clinical course.
Chinese medical journal 06/2003; 116(6):811-8. · 0.86 Impact Factor
