What is the optimal dose of epinephrine during cardiopulmonary resuscitation in a rat model?

Objective

Because different species may require different doses of drug to produce the same physiologic response, we were provoked to evaluate the dose-response of epinephrine during cardiopulmonary resuscitation (CPR) and identify what is the optimal dose of epinephrine in a rat cardiac arrest model.

Methods

Rat cardiac arrest was induced via asphyxia, and then the effects of different doses of epinephrine (0.04, 0.2, and 0.4 mg/kg IV, respectively) and saline on the outcome of CPR were compared (n = 10/each group). The primary outcome measure was restoration of spontaneous circulation (ROSC), and the secondary was the change of spontaneous respiration and hemodynamics after ROSC.

Results

Rates of ROSC were 9 of 10, 8 of 10, 7 of 10, and 1 of 10 in the low-dose, medium-dose, and high-dose epinephrine groups and saline group, respectively. The rates of withdrawal from the ventilator within 60 minutes in the low-dose (7 of 9) and medium-dose epinephrine groups (7 of 8) were higher than in the high-dose epinephrine group (1 of 7, P < .05). Mean arterial pressures were comparable, but the heart rate in the high-dose epinephrine group was the lowest among epinephrine groups after ROSC. These differences in part of time points reached statistical significance (P < .05).

Conclusion

Different doses of epinephrine produced the similar rate of ROSC, but high-dose epinephrine inhibited the recovery of spontaneous ventilation and caused relative bradycardia after CPR in an asphyxial rat model. Therefore, low and medium doses of epinephrine were more optimal for CPR in a rat asphyxial cardiac arrest model.     

Effects of hyperbaric oxygen on intestinal mucosa apoptosis caused by ischemia-reperfusion injury in rats

BACKGROUND:

Hyperbaric oxygen (HBO) is an effective adjuvant therapy for ischemia- reperfusion (I/R) injury of the brain, small intestine and testis in addition to crushing injury. Studies have shown that HBO increases the activity of villi of the ileum 30 minutes after I/R injury. The present study aimed to observe the effect of HBO on apoptosis of epithelial cells in the small intestine during different periods of I/R and to elucidate the potential mechanisms.

METHODS:

Rats were subjected to 60-minute ischemia by clamping the superior mesenteric artery and 60-minute reperfusion by removal of clamping. The rats were randomly divided into four groups: I/R group, HBO precondition or HBO treatment before ischemia (HBO-P), HBO treatment during ischemia period (HBO-I), and HBO treatment during reperfusion (HBO-R). After 60-minute reperfusion, samples of the small intestine were prepared to measure the level of ATP by using the colorimetric method and immunochemical expression of caspase-3. The levels of TNF-α in intestinal tissue were measured using the enzyme-linked immunosorbent assay method (Elisa).

RESULTS:

TNF-α levels were significantly lower in the HBO-I group than in the HBO-P (P<0.05), HBO-R and I/R groups; there was no significant difference between the HBO-R and I/R groups (P>0.05). The expression of caspas-3 was significantly lower in the HBO-I group than in the HBO-P group (P<0.05); it was also significantly lower in the HBO-P group than in the I/R and HBO-R groups (P<0.05). ATP level was significantly lower in the HBO-I group than in the HBO-P group (P<0.05), and also it was significantly lower in the HBO-P group than in the I/R and HBO-R groups (P<0.05).

CONCLUSIONS:

There is an association between HBO, small intestinal I/R injury, and mucosa apoptosis. HBO maintains ATP and aerobic metabolism, inhibites TNF-α production, and thus prevents intestinal mucosa from apoptosis. Best results can be obtained when HBO is administered to patients in the period of ischemia, and no side effects are produced when HBO is given during the period of reperfusion.KEY WORDS: Hyperbaric oxygen, Ischemia-reperfusion injury, Apoptosis     

Mild hypothermia in improving multiple organ dysfunction after cardiac arrest

BACKGROUND:

Resuscitation after cardiac arrest (CA) with a whole-body ischemia–reperfusion injury causes brain injury and multiple organ dysfunction (MODS). This study aimed to determine whether mild systemic hypothermia could decrease multiple organ dysfunctions after resuscitation from cardiac arrest.

METHODS:

The patients who had been resuscitated after cardiac arrest were reviewed. During the resuscitation they had been assigned to undergo therapeutic hypothermia (target temperature, 32°C to 34°C, measured in the rectum) over a period of 24 to 36 hours or to receive standard treatment with normothermia. Markers of different organ injury were evaluated for the first 72 hours after recovery of spontaneous circulation (ROSC).

RESULTS:

At 72 hours after ROSC, 23 patients in the hypothermia group for whom data were available had favorable neurologic, myocardial, hepatic and pulmonic outcomes as compared with 26 patients in the normothermia group. The values of renal function were not significantly different between the two groups. However, blood coagulation function was badly injured in the hypothermia group.

CONCLUSION:

In the patients who have been successfully resuscitated after cardiac arrest, therapeutic mild hypothermia can alleviate dysfunction after resuscitation from cardiac arrest.KEY WORDS: Cardiac arrest, Ischemia reperfusion injury, Mild hypothermia, Multiple organ dysfunction     

Protection of Long-Term Treatment With Huang-Lian-Jie-Du-Tang on Vascular Endothelium in Rats With Type 2 Diabetes Mellitus

Background

Huang-Lian-Jie-Du-Tang (HLJDT) is the classical traditional Chinese recipe for heat clearance and detoxification and is used in diabetic patients in the clinical practice of traditional Chinese medicine.

Objective

The aim of this study was to evaluate the protective effects of long-term treatment with HLJDT on vascular endothelial function in rats with type 2 diabetes mellitus (T2DM).

Methods

The male T2DM model rats were induced by intraperitoneal injection of low-dose streptozotocin plus a high-fat and high-calorie laboratory diet. The T2DM animals were randomly divided into the T2DM model group, the low-dose HLJDT group (0.42 g/kg/d), and the high-dose HLJDT group (1.25 g/kg/d).

Results

Administration of HLJDT (0.42 or 1.25 g/kg/d) for 8 weeks decreased the levels of serum fasting blood glucose, malondialdehyde, and vascular tissue interleukin 6 but raised the level of serum superoxide dismutase compared with the T2DM model group in a dose-dependent manner. In addition, HLJDT treatment restored the impaired endothelial-dependent vascular relaxation in aortic preparations from the T2DM model group in a dose-dependent manner.

Conclusions

Early and long-term treatments with HLJDT could have anti-inflammatory, antioxidant properties and could protect vascular endothelium from the cardiovascular complications associated with T2DM.Key words: aorta, Huang-Lian-Jie-Du-Tang, oxidative stress, type 2 diabetes mellitus rats, vasodilation     

Effect of tumor necrosis factor-α on ventricular arrhythmias in rats with acute myocardial infarction in vivo

BACKGROUND:

Acute myocardial infarction (AMI) is an acute cardiovascular emergency. This study was undertaken to assess the effect of tumor necrosis factor-α (TNF-α) on ventricular arrhythmias induced by AMI in rats in vivo.

METHODS:

Two hundred and forty male Wistar rats were randomized into a sham-operation group, an AMI group, and a recombinant human tumor necrosis factor receptor:Fc fusion protein(rhTNFR:Fc) group. Acute anterior wall myocardial infarction was produced in the AMI group by ligating the left anterior descending coronary artery (LAD), and there was no ligation but operation in the sham-operation group. The rhTNFR:Fc group was treated with rhTNFR:Fc(10 mg/kg), a TNF-α antagonist, 24 hours before LAD ligation. The spontaneous and induced programmed electrical stimulation ventricular arrhythmias were recorded at baseline and 10 minutes, 20 minutes, 30 minutes, 60 minutes, 3 hours, 6 hours and 12 hours after ligation. At the same time the protein and mRNA expression levels of TNF-α among different groups were detected by histochemistry and real-time fluorescent quantitative PCR.

RESULTS:

Expression of TNF-α increased markedly from 10 minutes after infarction, peaked at 20-30 minutes, and returned to baseline gradually in the AMI group and rhTNFR:Fc group. The time-windows of spontaneous and induced ventricular arrhythmias were similar. Compared with the AMI group, the rhTNFR:Fc group showed a lesser expression of TNF-α protein and a lower incidence of ventricular arrhythmias (P<0.05). There was no obvious change in the sham-operation group.

CONCLUSION:

The expression of TNF-α induced by AMI could contribute to the onset of ventricular arrhythmias.KEY WORDS: Acute myocardial infarction, Tumor necrosis factor-α, Ventricular arrhythmia, Recombinant human tumor necrosis factor receptor, Fc fusion protein (rhTNFR: Fc)     

Therapeutic effect of recombinant tissue plasminogen activator on acute cerebral infarction at different times

BACKGROUND:

The study aimed to compare the therapeutic effect of recombinant tissue plasminogen activator (rt-PA) on the onset of acute cerebral infarction (ACI) at different time points of the first 6 hours.

METHODS:

A retrospective analysis was conducted in 74 patients who received rt-PA thrombolysis treatment within 4.5 hours after ACI and another 15 patients who received rt-PA thrombolysis treatment between 4.5–6 hours after ACI.

RESULTS:

National Institute of Health Stroke Scale (NIHSS) scores were statistically decreased in both groups (P>0.05) at 24 hours and 7 days after ACI. There was no significant difference in modified ranking scores and mortality at 90 days after the treatment between the two groups (P>0.05).

CONCLUSIONS:

The therapeutic effect and mortality of rt-PA treatment in patients with ACI between 4.5–6 hours after the onset of the disease were similar to those in patients who received rt-PA within 4.5 hours after the onset of this disease. Therefore, intravenous thrombolytic therapy for ACI within 4.5–6 hours after ACI was effective and safe.KEY WORDS: Acute cerebral infarction, Thrombolysis, Recombinant tissue type plasminogen activator     

Upregulated expression of S100A8 in mice brain after focal cerebral ischemia reperfusion

BACKGROUND:

Recent studies have showed that S100A8 has been implicated in the pathobiology of inflammatory disorders, and that cerebral ischemia reperfusion (I/R) rapidly activates inflammation responses via Toll-like receptor 4 (TLR4). This study aimed to explore the expression of S100A8 and the relationship between S100A8 and TLR4 in focal cerebral ischemia reperfusion injury.

METHODS:

C3H/HeJ mice (n=30) and C3H/HeN mice (n=30) were divided randomly into a C3H/HeJ model group (n=18), a C3H/HeJ control group (n=12), a C3H/HeN model group (n=18), and a C3H/HeN control group (n=12). Middle cerebral artery I/R model in mice was produced using a thread embolism method. The brains of the mice were collected after ischemia for 1 hour and reperfusion for 12 hours. Stroke outcome was evaluated by determination of infarct volume and assessment of neurological impairment scores. Brain injury after cerebral I/R was observed by an optical microscope after TTC and HE dyeing. The immunofluorescence technique and real time PCR were used to test the expression level of S100A8 in brain damage.

RESULTS:

Compared with C3H/HeN mice, TLR4-deficient mice (C3H/HeJ) had lower infarct volumes and better outcomes in neurological tests. The levels of S100A8 increased sharply in the brains of mice after I/R injury. In addition, mice that lacked TLR4 (C3H/HeJ) had lower expression of I/R-induced S100A8 than C3H/HeN mice in the model group, indicating that a close relationship might exist between the levels of S100A8 and TLR4.

CONCLUSION:

S100A8 interaction with TLR4 might be involved in brain damage and in inflammation triggered by I/R injury.KEY WORDS: S100A8, Toll-like receptor 4, Cerebral ischemia reperfusion, Inflammation     

Post-conditioning with gradually increased reperfusion provides better cardioprotection in rats

BACKGROUND:

Rapid and complete reperfusion has been widely adopted in the treatment of patients with acute myocardial infarction (AMI), but this process sometimes can cause severe reperfusion injury. This study aimed to investigate different patterns of post-conditioning in acute myocardial ischemia-reperfusion injury, and to detect the role of mitogen activated protein kinase (MAPK) during the injury.

METHODS:

Rats were randomly divided into five groups: sham group, reperfusion injury (R/ I) group, gradually decreased reperfusion group (GDR group, 30/10-25/15-15/25-10/30 seconds of reperfusion/ischemia), equal reperfusion group (ER group, 20/20 seconds reperfusion/ischemia, 4 cycles), and gradually increased reperfusion group (GIR group, 10/30-15/25-25/15-30/10 seconds of reperfusion/ischemia). Acute myocardial infarction and ischemic post-conditioning models were established in the rats. Six hours after reperfusion, 3 rats from each group were sacrificed and myocardial tissues were taken to measure the expressions of phosphorylation of extracellular signal-regulated protein kinase (P-ERK), phosphorylated c-Jun N-terminal kinase (P-JNK), mitogen-activated protein kinase p38 (p38 MAPK), tumor necrosis factor-α (TNF-α), caspases-8 in the myocardial tissue, and cytochrome c in the cytosol using Western blot. Hemodynamics was measured at 24 hours after reperfusion, the blood was drawn for the determination of cardiac enzymes, and the heart tissue was collected for the measurement of apoptosis using TUNEL. One-way analysis of variance and the Q test were employed to determine differences in individual variables between the 5 groups.

RESULTS:

Three post-conditioning patterns were found to provide cardioprotection (P<0.05) compared with R/I without postconditioning. GIR provided the best cardioprotection effect, followed by ER and then GDR. Apoptotic index and serum marker levels were reduced more significantly in GIR than in ER (P<0.05). The enhanced cardioprotection provided by GIR was accompanied with significantly increased levels of P-ERK 1/2 (1.82±0.22 vs. 1.54±0.32, P<0.05), and lower levels of p-JNK, p38 MAPK, TNF-α, caspase-8, caspase-9 and cytochrome in the cytoplasm (P<0.05), compared with ER. The infarct size was smaller in the GIR group than in the ER group, but this difference was not significant (16.30%±5.22% vs. 20.57%±6.32%, P<0.05). All the measured variables were improved more significantly in the GIR group than in the GDR group (P<0.05).

CONCLUSION:

Gradually increased reperfusion in post-conditioning could attenuate reperfusion injury more significantly than routine method, thereby the MAPK pathway plays an important role in this process.KEY WORDS: Ischemia-reperfusion injury, Postconditioning, Apoptosis     

An assessment of antioxidant status in patients with carbon monoxide poisoning

BACKGROUND:

Carbon monoxide poisoning (COP) is an important cause of mortality and morbidity worldwide. This study was to investigate the levels of serum paraoxonase (PON), arylesterase (ARYL), ceruloplasmin (Cp), and sulfhydryl (-SH) in the treatment of COP, and to further understand the pathophysiology of COP.

METHODS:

This prospective study comprised 107 individuals with COP (group 1) and 50 healthy volunteers (group 2). Serum, plasma, and erythrocyte samples were taken on admission from all participants with COP. This process was repeated in the 90^th and 180^th minutes of treatment. Samples were taken from the control group only once. The levels of plasma PON, ARYL, Cp activity and -SH were measured in both groups.

RESULTS:

Age, gender, and carboxyhemoglobin level were not correlated with PON, ARYL, Cp, and -SH levels. PON, ARYL, and -SH levels were significantly decreased in group 1 compared with group 2. Conversely, Cp was significantly elevated in group 1 in contrast to group 2. Although ARYL was lower on admission in patients with COP than that was observed in the 90^th and 180^th minutes (P<0.001), Cp was higher on admission than at the other time points (P<0.001).

CONCLUSIONS:

Participants with COP had decreased levels of antioxidants (PON, ARLY, and -SH). COP represses the antioxidant system.KEY WORDS: Carbon monoxide poisoning, Paraoxonase, Arylesterase, Ceruloplasmin, Total sulfhydryl groups     

Pulmonary embolism due to exogenous estrogen intoxication

Objective

Pulmonary embolism is a relatively common clinical presentation of venous thromboembolism, which develops in relation to acute pulmonary arterial occlusion mostly caused by thrombi of the lower limbs.

Effect of ischemic preconditioning in skeletal muscle measured by functional magnetic resonance imaging and spectroscopy: a randomized crossover trial

Background

Nuclear magnetic resonance (NMR) imaging and spectroscopy have been applied to assess skeletal muscle oxidative metabolism. Therefore, in-vivo NMR may enable the characterization of ischemia-reperfusion injury. The goal of this study was to evaluate whether NMR could detect the effects of ischemic preconditioning (IPC) in healthy subjects.

Methods

Twenty-three participants were included in two randomized crossover protocols in which the effects of IPC were measured by NMR and muscle force assessments. Leg ischemia was administered for 20 minutes with or without a subsequent impaired reperfusion for 5 minutes (stenosis model). IPC was administered 4 or 48 hours prior to ischemia. Changes in ³¹phosphate NMR spectroscopy and blood oxygen level-dependent (BOLD) signals were recorded. 3-Tesla NMR data were compared to those obtained for isometric muscular strength.

Results

The phosphocreatine (PCr) signal decreased robustly during ischemia and recovered rapidly during reperfusion. In contrast to PCr, the recovery of muscular strength was slow. During post-ischemic stenosis, PCr increased only slightly. The BOLD signal intensity decreased during ischemia, ischemic exercise and post-ischemic stenosis but increased during hyperemic reperfusion. IPC 4 hours prior to ischemia significantly increased the maximal PCr reperfusion signal and mitigated the peak BOLD signal during reperfusion.

Conclusions

Ischemic preconditioning positively influenced muscle metabolism during reperfusion; this resulted in an increase in PCr production and higher oxygen consumption, thereby mitigating the peak BOLD signal. In addition, an impairment of energy replenishment during the low-flow reperfusion was detected in this model. Thus, functional NMR is capable of characterizing changes in reperfusion and in therapeutic interventions in vivo.

Trial Registration

ClinicalTrials.gov: {"type":"clinical-trial","attrs":{"text":"NCT00883467","term_id":"NCT00883467"}}NCT00883467     

Trends in high-dose opioid prescribing in Canada

Objective

To describe trends in rates of prescribing of high-dose opioid formulations and variations in opioid product selection across Canada.

Design

Population-based, cross-sectional study.

Setting

Canada.

Participants

Retail pharmacies dispensing opioids between January 1, 2006, and December 31, 2011.

Main outcome measures

Opioid dispensing rates, reported as the number of units dispensed per 1000 population, stratified by province and opioid type.

Results

The rate of dispensing high-dose opioid formulations increased 23.0%, from 781 units per 1000 population in 2006 to 961 units per 1000 population in 2011. Although these rates remained relatively stable in Alberta (6.3% increase) and British Columbia (8.4% increase), rates in Newfoundland and Labrador (84.7% increase) and Saskatchewan (54.0% increase) rose substantially. Ontario exhibited the highest annual rate of high-dose oxycodone and fentanyl dispensing (756 tablets and 112 patches per 1000 population, respectively), while Alberta’s rate of high-dose morphine dispensing was the highest in Canada (347 units per 1000 population). Two of the highest rates of high-dose hydromorphone dispensing were found in Saskatchewan and Nova Scotia (258 and 369 units per 1000 population, respectively). Conversely, Quebec had the lowest rate of high-dose oxycodone and morphine dispensing (98 and 53 units per 1000 population, respectively).

Conclusion

We found marked interprovincial variation in the dispensing of high-dose opioid formulations in Canada, emphasizing the need to understand the reasons for these differences, and to consider developing a national strategy to address opioid prescribing.     

Application of emergency severity index in pediatric emergency department

BACKGROUND:

The purpose of triage is to identify patients needing immediate resuscitation, to assign patients to a pre-designed patient care area, and to initiate diagnostic/therapeutic measures as appropriate. This study aimed to use emergency severity index (ESI) in a pediatric emergency room.

METHODS:

From July 2006 to August 2010, a total of 21 904 patients visited the International Department of Beijing Children’s Hospital. The ESI was measured by nurses and physicians, and compared using SPSS.

RESULTS:

Nurses of the hospital took approximately 2 minutes for triage. The results of triage made by nurses were similar to those made by doctors for ESI in levels 1-3 patients. This finding indicated that the nurses are able to identify severe pediatric cases.

CONCLUSION:

In pediatric emergency rooms, ESI is a suitable tool for identifying severe cases and then immediate interventions can be performed accordingly.KEY WORDS: Pediatrics, Emergency Department, Triage, Emergency severity index     

Urokinase-type plasminogen activator receptor as a predictor of poor outcome in patients with systemic inflammatory response syndrome

BACKGROUND:

Urokinase-type plasminogen activator (uPA) and urokinase-type plasminogen activator receptor (uPAR) are known as important factors, which mediate a variety of functions in terms of vascular homeostasis, inflammation and tissue repair. However, their role in systemic inflammatory response syndrome (SIRS) has been less well studied. This study aimed to test the hypothesis that the abnormalities of fibrinolysis and degradation of extracellular matrix mediated by uPA and uPAR are directly related to the patients with SIRS. We therefore analyzed their role and clinicopathological significance in patients with SIRS.

METHODS:

A case-control study was conducted with 85 patients who were divided into two groups according to the diagnostic criteria of SIRS: SIRS group (n=50) and non-SIRS group (n=35). The SIRS group was divided into MODS group (n=26) and non-MODS group (n=24) by their severity, and survival group (n=35) and non-survival group (n=15) by their prognosis. Another 30 healthy adults served as normal controls. uPA and uPAR in plasma were detected by commercial enzyme-linked immunosorbent assay (ELISA) kits.

RESULTS:

The plasma level of uPA was lower in the SIRS group than in the non-SIRS group and controls (P<0.001 and P<0.001). It was lower in sepsis patients and the MODS group than in the non-sepsis patients and the non-MODS patients (all P<0.05). However, there was no difference in uPA level between survivors and non-survivors (P>0.05). The plasma level of uPAR increased in the SIRS group compared with the non-SIRS group and controls (P<0.001 and P<0.001). There was a significant elevation of uPAR in sepsis patients, MODS patients and non-survivors as compared with non-sepsis patients, non-MODS patients and survivors respectively (all P<0.05). Plasma uPAR levels were positively correlated with APACHE II score (r=0.575, P<0.001) and SOFA score (r=0.349, P=0.013). AUCs for the prediction of SIRS mortality were 0.67 and 0.51, respectively, for uPA and uPAR.

CONCLUSION:

uPAR could be a predictor of poor outcome in patients with SIRS.KEY WORDS: Systemic inflammatory response syndrome, Multiple organ dysfunction syndrome, Urokinase-type plasminogen activator, Urokinase-type plasminogen activator receptor     

Effect of spironolactone on cardiac remodeling after acute myocardial infarction

BACKGROUND:

Few studies have reported the effect of aldosterone receptor antagonist (ARA) on myocardial remodeling after acute myocardial infarction (AMI). This study was undertaken to investigate the preventive effect of ARA on myocardial remodeling after AMI.

METHODS:

A total of 616 patients who had been admitted into the CCU of the First Affiliated Hospital of Harbin Medical University from January 2008 to January 2010 were studied prospectively. Only 528 patients were observed completely, including 266 of the control group and 262 of the treatment group. There was no statistical difference in age, gender, medical history, admission situation, and treatment between the two groups (P>0.05). The preventive effects of spironolactone on cardiac remodeling, left ventricular function, renal function and blood levels of potassium were evaluated by echocardiography, serum potassium and serum creatinine at one-month and one-year follow-up.

RESULTS:

The echocardiography indicators such as LVESD, LVEDD, LVEF, LAD-ML and LAD-SI were significantly improved in the treatment group compared with the control group at one year (P<0.05). In the treatment group, LVESD, LVEDD, LVPWT, LVEF, LAD-ML and LAD-SI were more significantly improved at one year than one month (P<0.05, P=0.007 to LVEF), and in the control group LVEF was more significantly improved at one year than one month (P=0.0277). There were no significant differences in serum potassium and serum creatinine levels between the two groups.

CONCLUSION:

On the basis of conventional treatment, the early combination of low-dose spironolactone (20 mg/d) could inhibit cardiac remodeling at late stage and prevent heart failure.KEY WORDS: Myocardial infarction, acute, Ventricular remodeling, Atrial remodeling, Aldosterone, Aldosterone blockade, Spironolactone, Cardiac function, Prognosis     

The Acinetobacter baumannii group: a systemic review

BACKGROUND:

The Acinetobacter baumannii group, including Acinetobacter baumannii, Acinetobacter genomospecies 3 and 13TU, is phenotypically indistinguishable and uniformly identified as Acinetobacter baumannii by laboratories of clinical microbiology. This review aimed to demonstrate the differences among them.

METHODS:

Literatures associated with the Acinetobacter baumannii group were identified and selected from PubMed databases and relevant journals.

RESULTS:

Acinetobacter genospecies 3 and 13TU possess a certain proportion in clinical isolates. There were considerable differences in epidemiologic features, clinical manifestations, antimicrobial resistances and therapeutic options among the Acinetobacter baumannii group. Compared with Acinetobacter genomospecies 3 and 13TU, Acinetobacter baumannii with a higher resistance to antimicrobial agents are easier to be treated inappropriately, and present a worse outcome in patients.

CONCLUSION:

The Acinetobacter baumannii group comprises three distinct clinical entities, and their clinical value are not equal.KEY WORDS: Acinetobacter baumannii, Acinetobacter genomospecies 3, Acinetobacter genomospecies 13TU, Difference     

Effect of exogenous phosphocreatine on cardiomycytic apoptosis and expression of Bcl-2 and Bax after cardiopulmonary resuscitation in rats

BACKGROUND:

Ischemia-reperfusion injury in the myocardium after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) is an important pathologic basis of post-cardiac arrest of syndrome (PCAS), and apoptosis is one of the major mechanisms in myocardial ischemia-reperfusion injury. To lessen myocardial ischemia-reperfusion injury after cardiac arrest and CPR, it is important to reduce energy consumption and to increase energy supply in the myocardium. This study aimed to observe changes of cell apoptosis and expression of Bcl-2 and Bax protein on the myocardium after CPR in rats, and the protective effects of different doses of exogenous phosphocreatine (creatine phosphate, CP) on them.

METHODS:

A total of 32 male adult Sprague-Dawley rats were randomly divided into 4 groups: control group (group A), CPR group (group B), low-dose CP group (group C, CP 0.5 g/kg at beginning of CPR and 1.0 g/kg at 2 hours after CPR) and high-dose CP group (group D, CP 1.0 g/kg at beginning of CPR and 2.0 g/kg at 2 hours after CPR). Cardiac arrest was induced by asphyxiation and CPR started at 7 minutes after asphyxiation in groups B, C and D. Myocardium samples were taken at 24 hours after CPR. Cardiomycytic apoptosis was detected by the TdT-mediated dUTP-biotin nick end labeling (TUNEL) method. The expression of Bcl-2 and Bax protein was measured by immunohistochemistry.

RESULTS:

Cardiomyocytic apoptosis index (AI) and expression of Bcl-2 and Bax protein increased more significantly in groups B, C and D than in group A (P<0.01), but Bcl-2/Bax ratio significantly decreased (P<0.01). Cardiomyocytic AI and expression of Bcl-2 and Bax protein decreased more significantly in groups C and D than in group B (P<0.01), but Bcl-2/Bax ratio increased more significantly (P<0.01). Cardiomyocytic AI and expression of Bcl-2 and Bax protein decreased more significantly in group D than in group C (P<0.05), but Bcl-2/Bax ratio increased more significantly (P<0.05).

CONCLUSION:

Exogenous phosphocreatine, especially at a large dose, could inhibit cardiomyocytic apoptosis and alleviate myocardial injury after CPR in rats.KEY WORDS: Cardiopulmonary resuscitation, Phosphocreatine, Apoptosis, Bcl-2, Bax, TUNEL     

Impact of the United States propofol ban on emergency providers’ procedural sedation agent choice and patient length of stay

BACKGROUND:

In the recent past, propofol was temporarily removed from the emergency department (ED) for use in procedural sedation. We sought to determine which agents replaced it in clinical practice and the impact this change had on turnaround times (TAT) for sedated patients.

METHODS:

This study is a retrospective chart review at a level one trauma center. Patients receiving sedative agents (propofol, ketamine, midazolam, and etomidate) were identified by pharmacy codes, and their charts were then reviewed for demographics and TAT. Propofol was unavailable in the emergency department (ED) between May 2010 and February 2011. The study period extended from May 2009 until May 2011. Patients receiving sedation by non-emergency medicine physicians and those receiving sedation related to intubation were excluded.

RESULTS:

In total 2466 charts were reviewed and 209 met inclusion criteria. When propofol was available, the most commonly used sedative agent was etomidate (40%), followed by propofol (28%), ketamine (20%), and midazolam (6%). When propofol was unavailable, etomidate remained the most commonly used agent (43%), followed by ketamine (41%), and midazolam (11%). When propofol was available, the median TAT for sedated patients was 163 minutes compared to 178 minutes when propofol was unavailable (P=0.83). When propofol was the primary sedative agent used, the median TAT was 166 minutes as compared with a median TAT of 172 minutes for all other sedative agents combined (P=0.87).

CONCLUSION:

When propofol was unavailable, ketamine became a preferred ED sedation agent. Removal of propofol from the sedation armamentarium did not affect ED TAT.KEY WORDS: Procedural sedation, Turnaround time, Propofol, Ketamine, Etomidate, Midazolam     

Expression of heat shock protein 70 in lung tissues of acute paraquat poisoned rats and intervention of ulinastatin

BACKGROUND:

Paraquat (PQ) is an effective herbicide and is widely used in agricultural production, but PQ poisoning is frequently seen in humans with the lung as the target organ. Clinically pulmonary pathological changes are often used to predict the severity and prognosis of the patients. In this study, we observed the expression of heat shock protein 70 (HSP70) in rat lung after PQ poisoning and to investigate the therapeutic effects of ulinastatin.

METHODS:

Seventy-two adult healthy SD rats were randomly divided into a control group (group A, n=24), a poisoning group (group B, n=24), and an ulinastatin group (group C, n=24). The rat models of acute PQ poisoning were established by intra-gastric administration of 80 mg/kg PQ to rats of groups B and C, and the rats of group C were intra-peritoneally injected with 100 000 IU/kg ulinastatin 30 minutes after poisoning. The expression of HSP70 in lung tissue was observed, and W/D and histopathological changes in the lung tissue were compared 12, 24, 48 and 72 hours after poisoning. The expression of HSP70 in the lung tissue was assayed by using RT-PCR. All quantitative data were processed with one-way analysis of variance to compare multiple sample means.

RESULTS:

Compared to group A, the expression of HSP70 in the lung of rats in groups B and C increased significantly at all intervals (P<0.05). The pathological changes in lung tissue of rats with PQ poisoning included congestion, leukocytes infiltration and local hemorrhage, whereas those of group C were significantly lessened.

CONCLUSION:

Ulinastatin may ameliorate acute lung injury to some extent after PQ poisoning in rats by enhancing the expression of HSP70.KEY WORDS: Paraquat, Poisoning, Ulilnastatin, Heat shock protein, Acute lung injury     

Lean techniques for the improvement of patients’ flow in emergency department

BACKGROUND:

Emergency departments (EDs) face problems with overcrowding, access block, cost containment, and increasing demand from patients. In order to resolve these problems, there is rising interest to an approach called “lean” management. This study aims to (1) evaluate the current patient flow in ED, (2) to identify and eliminate the non-valued added process, and (3) to modify the existing process.

METHODS:

It was a quantitative, pre- and post-lean design study with a series of lean management work implemented to improve the admission and blood result waiting time. These included structured re-design process, priority admission triage (PAT) program, enhanced communication with medical department, and use of new high sensitivity troponin-T (hsTnT) blood test. Triage waiting time, consultation waiting time, blood result time, admission waiting time, total processing time and ED length of stay were compared.

RESULTS:

Among all the processes carried out in ED, the most time consuming processes were to wait for an admission bed (38.24 minutes; SD 66.35) and blood testing result (mean 52.73 minutes, SD 24.03). The triage waiting time and end waiting time for consultation were significantly decreased. The admission waiting time of emergency medical ward (EMW) was significantly decreased from 54.76 minutes to 24.45 minutes after implementation of PAT program (P<0.05).

CONCLUSION:

The application of lean management can improve the patient flow in ED. Acquiescence to the principle of lean is crucial to enhance high quality emergency care and patient satisfaction.KEYWORDS: Lean, Triage, Waiting time, Patient flow, Emergency department