Objective:To systematically compare the analgesic efficacy of pericapsular nerve group (PENG) block and fascia iliaca compartment block (FICB) after hip fracture surgery.Methods:Databases including Pubmed, Embase, Cochrane, CNKI, Wanfang and VIP were searched for randomized controlled trials involving comparison of the analgesic efficacy of PENG block and FICB after hip fracture surgery from inception to August 2022. The primary outcome was the postoperative pain score, and the secondary outcome was the amount of postoperative analgesics and incidence of postoperative adverse reactions. The data were analyzed using Revman 5.4 software.Results:Eight studies were included ( n=374), and the pain score at rest 30 min after block was significantly lower in PENG group than in FICB group ( MD=-0.35, 95% CI -0.60--0.11, I2=14%, P<0.05). There was no statistically significant difference between PENG group and FICB group in pain scores at rest and during activity at 6, 12, 24 and 48 h after operation ( P>0.05). Compared with FICB group, the amount of analgesics used was significantly reduced at 24 and 48 h after operation in PENG group ( MD=-9.10, 95% CI -19.11-0.91, I2=95%, P<0.05). There was no statistically significant difference in the incidence of adverse reactions after operation between the two groups ( P>0.05). Conclusions:PENG block provides better efficacy when used for analgesia following hip fracture than FICB.

AIM: To investigate the PI3K/AKT/GSK-3β signaling pathway involved in the protective effect and mechanism of propofol on the cerebral ischemia-reperfusion injury in rats. METHODS: There were 72 healthy male SD rats. All rats established a model of focal cerebral ischemia-reperfusion injury according to the Zea Longa method and were randomly divided into six groups (n=12), A-sham operation group, B-model group (MCAO), C-Propofol group, D-Propofol+adenosine A1R antagonist group (DPCPX), E-Propofol group+PI3K specific inhibitor (LY294002), F-Propofol+GSK3β inhibitor group (SB216763). The neurological scores of rats 24 h after operation, LDF monitors changes in cerebral blood flow before and after embolization were observed. The TTC staining method was used to detect the cerebral infarction volume of rats in each group; HE staining method was used to observe the morphological changes of the rat brain tissue; Immunohistochemical method was used to detect Bcl-2 positive cells expression; TUNEL was used to detect cerebral cortex ischemia in each group. The percentage of neuronal apoptotic cells. RESULTS: Compared with group A, the behaviors, cerebral infarction volume, apoptosis rate, and Bcl-2 protein expression of rats in groups B, C, D, E, and F all increased (P<0.05); compared with group C, the behavioral scores, cerebral infarction volume and apoptosis rate of rats in groups B, D and E all increased significantly, and the expression of Bcl-2 protein was decreased significantly (P<0.01), but the expression of Bcl-2 protein in group F was increased, cell apoptosis rate decreased (P<0.05), behavior score and infarcts decreased (P<0.05). CONCLUSION: The neuroprotective effect of propofol mediated by adenosine A1R on ischemia-reperfusion injury in rats may be related to the PI3K/AKT/GSK-3β signal transduction pathway.

Objective To evaluate the effect of melatonin pretreament on cell apoptosis and autophagy during lung ischemia-reperfusion (I/R) in rats.Methods Thirty-six adult male Sprague-Dawley rats,weighing 230-280 g,were divided into 3 groups (n=12 each) using a random number table method:sham operation group (group Sham),pulmonary I/R group (LIR group) and melatonin pretreatment group (MLT group).Lung I/R injury model was established by clamping the left hilum of lung for 60 min followed by 2 h reperfusion in LIR and MLT groups.Melatonin 1 mg/100 g was intraperitoneally injected at 15 min before clamping the left hilum of lung in group MLT.The rats were sacrificed at the end of reperfusion,the left lung was lavaged and the broncho-alveolar lavage fluid (BALF) was colleted for determination of protein concentrations.Lungs were removed for microscopic examination of the pathological changes (with a light microscope) which were scored and for determination of wet to dry weight ratio (W/D ratio),cell apoptosis (by TUNEL) and expression of Bcl-2,Bax,microtubule-related protein 1 light chain 3B Ⅰ (LC3B Ⅰ),LC3B Ⅱ,Beclin-1 and phosphorylated mammal rapamycin target protein receptor (p-mTOR) (using Western blot).The apoptosis index,Bcl-2/Bax ratio and LC3B Ⅱ/LC3B Ⅰ ratio were calculated.Results Compared with Sham group,the protein concentration in BALF,W/D ratio of lung tissues,apoptosis index,LC3B Ⅱ/LC3B Ⅰ ratio and Beclin-1 expression were significantly increased,and Bcl-2/Bax ratio and p-mTOR expression were decreased in LIR and MLT groups (P＜0.05).Compared with LIR group,the protein concentration in BALF,W/D ratio of lung tissues,apoptosis index,LC3B Ⅱ/LC3B Ⅰ ratio and Beclin-1 expression were significantly decreased,and Bcl-2/Bax ratio and p-mTOR expression were increased in MLT group (P＜0.05).Conclusion The mechanism by which melatonin pretreatment mitigates lung I/R injury may be related to inhibiting cell apoptosis and autophagy in rats.

ObjectiveTo investigate the effect of isoflurane preconditioning on calcitonin gene-related peptide (CGRP) and NF-kappa B following local cerebral ischemia/reperfusion (I/R) in rabbits.MethodsFiftyfour adult New Zealand white rabbits of both sexes weighing 2.0-2.5 kg were randomly divided into three groups (n ＝ 18 each):sham operation group (group S),group I/R and isoflurane preconditioning group(group I).After anesthesia induction with intramuscular injection of ketamine 70 mg/kg and scopolamine 0.006 mg/kg and maintenance of anesthesia with intravenous injection of midazolam 0.1 mg/kg,fentanyl 0.01 mg/kg and vecuronium 0.1 mg/kg,endotracheal intubation was performed and mechanical ventilation was employed.In groups I/R and S,midazolam at 0.1 mg·kg-1·h-1 was infused through the left ear vein.After the rabbits in group I inhaling 1.4％ isoflurane for 30 minutes,which was then eluted for 10 minutes,local cerebral ischemia was made in groups I/Rand I with thread ligation method and reperfusion was made 2 hours later,simultaneously midasolam at 0.1 mg·kg- 1 · h - 1 was injected.All the rabbits in three groups were infused with fentanyl at 0.05 mg· kg- 1 · h- 1 and vecurenium at 0.10 mg· kg-1 · h-1.After blood samples were collected from the central artery of the ear for determination of plasma CGRP before anesthesia,immediately before reperfusion,and 1,2,3,4,and 5 h of reperfusion,all the animals were sacrificed at the corresponding time points and brain tissues were obtained for determination of NF-κB activity and its expression with Western blotting and immunohistochemistry staining.ResultsThe plasma concentration of CGRP,the activity and expression of NF-κB were higher in group I/R than in group S ( P <0.05).The plasma concentration of CGRP was higher and the activity and expression of NF-κB were lower in group I than in group I/R ( P < 0.05 ).ConclusionIsoflurane preconditioning can reduce local cerebral I/R injury in rabbits through promoting CGRP release and inhibiting NF-κB function.

Objective To explore the changes of expression of platelet PECAM-1,P-selectin in patients with acute cerebral infarction.Methods The platelet expression levels of PECAM-1,P-selectin in 35 patients with acute cerebral infarction were serially measured with whole blood flow cytometry 24,48 hours and 5,7,14 days after the onset,and were compared with those of 30 normal controls.Results The platelet expression levels of PECAM-1 and P-selectin in patients with cerebral infarction 24 hours after the onset(78.35?10.48,7.75?3.04 respectively)were higher than those of controls(48.89?10.84,2.18?0.83 respectively,all P

This study evaluated the effects of adenovirus vector mediated human vascular endothelial growth factor-165 (hVEGF165) gene on prevention of restenosis after angioplasty. Rabbit models of bilateral carotid artery injury were established by balloon denudation. The recombinant adenoviruses containing hVEGF165 cDNA was directly injected into left side of the injured carotid arteries. On day 3 and week 3 after transfection the expression of VEGF was observed by RT-PCR and immunohistochemistry. The thrombokinesis, reendothelialization (rET) and intimal hyperplasia in carotid arteries were evaluated by computerized image analysis system 3 weeks after gene transfer. The changes in the VEGF gene-treated side were compared with the control side. Our results showed that 3 days and 3 weeks after hVEGF165 gene transfer the VEGF mRNA and antigen expression were detected in vivo. 3 weeks after the transfer, the carotid artery rET was markedly better in the VEGF gene-treated group compared with the control. The thrombokinesis, intima area/media area (I/M), maximal intimal and medial thicknesses (ITmax and MTmax) demonstrated a statistically significant decrease in arteries treated with VEGF gene as compared with the control group. It is concluded that VEGF gene transfer could be achieved by intra-arterial injection of recombinant adenoviruses. It might accelerate the restoration of endothelial integrity, inhibit thrombokinesis and attenuate intimal hyperplasia in the injured arteries after VEGF gene transfer. This procedure could be useful in preventing restenosis after angioplasty.
Adenoviridae ; genetics ; metabolism ; Angioplasty, Balloon ; adverse effects ; Animals ; Carotid Artery Injuries ; pathology ; Carotid Stenosis ; physiopathology ; prevention & control ; Cell Division ; drug effects ; Endothelium, Vascular ; injuries ; pathology ; Genetic Therapy ; Hyperplasia ; prevention & control ; Male ; Muscle, Smooth, Vascular ; cytology ; RNA, Messenger ; biosynthesis ; genetics ; Rabbits ; Recombination, Genetic ; Transfection ; methods ; Vascular Endothelial Growth Factor A ; biosynthesis ; genetics

To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), the changes of action potential duration (APD), transient outward potassium current (Ito), delayed rectifier potassium current (IK) and inward rectifier potassium current (IK1) of left ventricular myocytes in non-infarcted zone of HMI were investigated. Rabbits were randomly assigned into two groups: HMI group, in which animals were subjected to thoracotomy and ligation of the circumflex coronary and sham-operated group, in which rabbits underwent thoracotomy but no conorary ligation. 3 months after the operation, the whole myocyte patch clamp technique was used to record APD, Ito, IK, and IK1 of ventricular myocytes in non-infarcted zone. Our results showed that the membrane capacitance was larger in HMI group than in sham-operated group. Action potential duration was significantly lengthened in HMI group and early afterdepolarization (EAD) appeared in HMI group. The densities of Ito, I(K, tail), and IK1 were reduced significantly in HMI group, from 6.72 +/- 0.42 pA/pF, 1.54 +/- 0.13 pA/pF and 25.6 +/- 2.6 pA/pF in sham-operated group to 4.03 +/- 0.33 pA/pF, 1.14 +/- 0.11 pA/pF and 17.6 +/- 2.3 pA/pF, respectively. It is concluded that the reduced densities of Ito, I(K, tail) and IK1 in ventricular myocytes of non-infarcted zone in HMI were responsible for the prolongation of APD and the presentation of EAD which played important roles in the development of malignant arrhythmia in HMI.
Action Potentials ; Animals ; Arrhythmias, Cardiac ; etiology ; Female ; Heart Ventricles ; metabolism ; Male ; Myocardial Infarction ; complications ; metabolism ; pathology ; Myocytes, Cardiac ; cytology ; Patch-Clamp Techniques ; Potassium Channels ; metabolism ; Rabbits

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization in intact canine was investigated. By using the monophasic action potential (MAP) recording technique, monophasic action potentials (MAPs) of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall in 12 open-chest dogs. MAPD90 and transmural dispersion of repolarization among three myocardial layers as well as the incidence of the EAD before autonomic nervous stimulation and during autonomic nervous stimulation were compared. The results showed that the MAPD90 of Epi, Mid and Endo before autonomic nervous stimulation were 278 +/- 11 ms, 316 +/- 16 ms and 270 +/- 12 ms respectively, the MAPD90 of Mid was significantly longer than that of Epi or Endo (P<0.01). MAPD90 of Epi, Mid and Endo were shortened by 19 +/- 4 ms, 45 +/- 6 ms, 18 +/- 3 ms respectively during sympathetic stimulation. Compared with that of the control, the transmural dispersion of repolarization during sympathetic stimulation was shortened from 44 +/- 4 ms to 15 +/- 3 ms (P<0.01), but early afterdepolarizations were elicited in the Mid of 5 dogs (41%) during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD90 in the three layers. It is concluded that there is the transmural dispersion of ventricular repolarization in intact canine. Sympathetic stimulation can reduce transmural dispersion of repolarization, but it can produce early afterdepolarizations in the Mid. Parasympathetic stimulation does not significantly affect the transmural dispersion of ventricular repolarization.
Action Potentials ; physiology ; Animals ; Autonomic Nervous System ; physiology ; Dogs ; Electric Stimulation ; Electrocardiography ; Electrodes ; Endocardium ; innervation ; physiology ; Heart Ventricles ; innervation ; Myocardium ; cytology ; Neuromuscular Junction ; Pericardium ; innervation ; physiology ; Ventricular Function

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization in intact canine was investigated. By using the monophasic action potential (MAP) recording technique, monophasic action potentials (MAPs) of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall in 12 open-chest dogs. MAPD90 and transmural dispersion of repolarization among three myocardial layers as well as the incidence of the EAD before autonomic nervous stimulation and during autonomic nervous stimulation were compared. The results showed that the MAPD90 of Epi, Mid and Endo before autonomic nervous stimulation were 278 +/- 11 ms, 316 +/- 16 ms and 270 +/- 12 ms respectively, the MAPD90 of Mid was significantly longer than that of Epi or Endo (P<0.01). MAPD90 of Epi, Mid and Endo were shortened by 19 +/- 4 ms, 45 +/- 6 ms, 18 +/- 3 ms respectively during sympathetic stimulation. Compared with that of the control, the transmural dispersion of repolarization during sympathetic stimulation was shortened from 44 +/- 4 ms to 15 +/- 3 ms (P<0.01), but early afterdepolarizations were elicited in the Mid of 5 dogs (41%) during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD90 in the three layers. It is concluded that there is the transmural dispersion of ventricular repolarization in intact canine. Sympathetic stimulation can reduce transmural dispersion of repolarization, but it can produce early afterdepolarizations in the Mid. Parasympathetic stimulation does not significantly affect the transmural dispersion of ventricular repolarization.
Action Potentials/physiology ; Autonomic Nervous System/*physiology ; Electric Stimulation ; Electrocardiography ; Electrodes ; Endocardium/innervation ; Endocardium/physiology ; Heart Ventricles/innervation ; Heart Ventricles/*physiology ; Myocardium/cytology ; Neuromuscular Junction ; Pericardium/innervation ; Pericardium/physiology

To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), the changes of action potential duration (APD), transient outward potassium current (Ito), delayed rectifier potassium current (IK) and inward rectifier potassium current (IK1) of left ventricular myocytes in non-infarcted zone of HMI were investigated. Rabbits were randomly assigned into two groups: HMI group, in which animals were subjected to thoracotomy and ligation of the circumflex coronary and sham-operated group, in which rabbits underwent thoracotomy but no conorary ligation. 3 months after the operation, the whole myocyte patch clamp technique was used to record APD, Ito, IK, and IK1 of ventricular myocytes in non-infarcted zone. Our results showed that the membrane capacitance was larger in HMI group than in sham-operated group. Action potential duration was significantly lengthened in HMI group and early afterdepolarization (EAD) appeared in HMI group. The densities of Ito, I(K, tail), and IK1 were reduced significantly in HMI group, from 6.72 +/- 0.42 pA/pF, 1.54 +/- 0.13 pA/pF and 25.6 +/- 2.6 pA/pF in sham-operated group to 4.03 +/- 0.33 pA/pF, 1.14 +/- 0.11 pA/pF and 17.6 +/- 2.3 pA/pF, respectively. It is concluded that the reduced densities of Ito, I(K, tail) and IK1 in ventricular myocytes of non-infarcted zone in HMI were responsible for the prolongation of APD and the presentation of EAD which played important roles in the development of malignant arrhythmia in HMI.
Action Potentials ; Arrhythmia/*etiology ; Heart Ventricles/metabolism ; Myocardial Infarction/complications ; Myocardial Infarction/metabolism ; Myocardial Infarction/*pathology ; Myocytes, Cardiac/*cytology ; Patch-Clamp Techniques ; Potassium Channels/*metabolism