Genomic Epidemiology of ST34 Monophasic Salmonella enterica Serovar Typhimurium from Clinical Patients from 2008 to 2017 in Henan,China

Salmonella enterica serovar 4,[5],12:i:-(S.4,[5],12:i:-)is a monophasic variant of Salmonella enterica serovar Typhimurium that has emerged as a global serovar causing public health concern.To date,the epidemiology and genomic characterization of this pathogen in China have not been well described.We investigated the prevalence,antimicrobial resistance(AMR)phenotypes,and population genomics of sequence type 34(ST34)S.4,[5],12:i:-among cases of human salmonellosis in Henan Province,China.A total of 100 ST34 S.4,[5],12:i:-isolates were studied from 2008 to 2017 and found mostly resistant to ampicillin(AMP),streptomycin(STR),sulfonamides(SUL),and tetracycline(TET)(ASSu T).Bayesian phylogenetic analysis demonstrated that isolates identified in China were mostly related to the European lineage and evolved into two major clades with different resistance genes and plasmid profiles.Notably,clade 1 showed a significantly higher rate of mutations in gyr A and plasmid-mediated quinolone resistance genes.The carrying of the resistance-containing region(encoding R-type ASSu T),including bla(conferring resistance to AMP),str AB(STR),sul2(SUL),and tet(B)(TET)inserted into the flj BA operon,was responsible for most of the monophasic variants in clade 2.Inc HI2 plasmids were the dominant multi-drug resistance mobile genetic elements accounting for the transmission of acquired resistance genes in this serovar,and these were more prevalent in clade 1.Our findings highlighted the increasing prevalence of multi-drug resistant S.4,[5],12:i:-in China,along with the differential characteristics of resistance gene acquisition among various lineages.Based on our data,control measures are required to address the spread of this zoonotic pathogen.Further owing to its potential origin in food-producing animals,a"One Health"approach,should be implemented to support surveillance whilst informing interventional strategies.

Cellular/dendritic transition,dendritic growth and microhardness in directionally solidified monophasic Sn-2%Sb alloy

Horizontal directional solidification experiments were carried out with a monophasic Sn-2%Sb（mass fraction） alloy to analyze the influence of solidification thermal parameters on the morphology and length scale of the microstructure. Continuous temperature measurements were made during solidification at different positions along the length of the casting and these temperature data were used to determine solidification thermal parameters, including the growth rate（VL） and the cooling rate（TR）. High cooling rate cells and dendrites are shown to characterize the microstructure in different regions of the casting, with a reverse dendrite-to-cell transition occurring for TR5.0 K/s. Cellular（λc） and primary dendrite arm spacings（λ1） are determined along the length of the directionally-solidified casting. Experimental growth laws relating λc and λ1 to VL and TR are proposed, and a comparative analysis with results from a vertical upward directional solidification experiment is carried out. The influence of morphology and length scale of the microstructure on microhardness is also analyzed.

Changes of Monophasic Action Potential Duration and Effective Refractory Period of Three Layers Myocardium of Canine during Acute Ischemia in Vivo

Summary： The effect of acute ischemia on the electrophysiological characteristics of the three layers myocardium of canine in vivo was investigated. Twelve canines were divided into two groups randomly： acute ischemia （AI） group and sham operation （SO） group. By using the monophasic action potential （MAP） technique, MAP and effective refractory period （ERP） of the three layers myocardium were measured by specially designed plunge needle electrodes and the transmural dispersion of repolarization （TDR） and transmural dispersion of ERP （TDE） were analyzed. The results showed that in the AI group, MAP duration （MAPD） was shortened from 201.67±21.42 ms to 169.50±13.81 ms （P〈0.05）, but ERP prolonged to varying degrees and TDE increased during ischemia. In the SO group, MAPD and ERP did not change almost. Among of the three layers myocardium of canine, MAPD was coincident in two groups. It was concluded that during acute ischemia, MAPD was shortened sharply, but there was no significant difference among of the three layers myocardium. The prolonged ERP was concomitant with increased TDE during acute ischemia, which may play an important role in the occurrence of arrhythmias induced by acute ischemia. These findings may have important implications in arrhythmogenesis.

Structural and Magnetic Properties of Monophasic Maghemite (<i>γ</i>-Fe₂O₃) Nanocrystalline Powder

Structural and magnetic studies of monophasic maghemite (γ-Fe2O3) magnetic nanocrystallites (MNCs) synthesized by the co-precipitation chemical route are reported in this paper. For the synthesis, a starting precursor of magnetite (Fe3O4) in basic medium was oxidized at room temperature by adjusting the pH = 3.5 at 80°C in an acidic medium without surfactants. X-ray diffraction (XRD) pattern shows widened peaks indicating nanometric size and Rietveld Refinement confirms only one single-phase assigned to γ-Fe2O3 MNCs. High Resolution Transmission Electron Microscopy (HR-TEM) demonstrates the formation of nanoparticles with diameter around D ≈ 6.8 ± 0.1 nm which is in good agreement with Rietveld Refinement (6.4 ± 1 nm). A selected area electron diffraction pattern was carried out to complement the study of the crystalline structure of the γ-Fe2O3 MNCs. M(H) measurements taken at different temperatures show almost zero coercivity and remanence indicating superparamagnetic domain and high magnetic saturation.

Construction of Energy-Optimal Smooth Monophasic Defibrillation Pulse Waveforms Using Cardiomyocyte Membrane Model

The goal is to help create smooth energy-optimal monophasic pulse waveforms for defibrillation using the Luo-Rudy cardiomyocyte membrane computer model. The waveforms were described with the help of the piecewise linear function. Each line segment provides a transition from one present level of the transmembrane potential to the next with a minimal energy value. The duration of the last segment was defined as a minimum duration at which an action potential occurs. Monophasic waveforms of segments 3, 10 and 29 were built using different increments of the transmembrane potential. The pulse energy efficiency was evaluated according to their threshold energy ratios in mA2·ms/cm4. There was virtually no difference between the threshold energy ratios of the three waveforms constructed and those of the previously studied energy-optimal half- sine waveform: 241 - 242 and 243 mA2·ms/cm4. The pulse waveform constructed is characterized by a low rise and fall as the duration of the rise is ~1.5 times longer than that of the fall. Conclusion: Energy-optimal smooth monophasic pulse waveforms have the same threshold energy ratio as the optimal half-sine one which was studied before. The latter is equivalent to the first phase of biphasic quasisinusoidal Gurvich-Venin pulse which has been used in Russia since 1972. Thus, the use of the Luo-Rudy cardiomyocyte membrane model appears to offer no possibilities for a substantial increase in the energy efficiency (threshold energy ratio reduction) of the classical monophasic defibrillation pulse waveforms.

Effect of dexmedetomidine on monophasic action potential amplitude in myocardial ischemia-reperfusion and its correlation with myocardial injury

Objective: To study the effect of dexmedetomidine on monophasic action potential amplitude (MAPA) in myocardial ischemia-reperfusion and its correlation with myocardial injury. Methods: SD rats were selected as the experimental animals and randomly divided into control group, ischemia reperfusion group (I/R group) and dexmedetomidine group (Dex group);I/R group and Dex group were made into myocardial ischemia-reperfusion injury models, and Dex group were given exmedetomidine intervention;the MAPA of myocardial tunica intima layer, tunica media layer and tunica externa layer were measured in Langendorff perfusion system;myocardial tissue was collected to determine the contents of oxidative stress molecules and the expression of apoptosis genes. Results: The MAPA levels of myocardial tunica intima layer, tunica media layer and tunica externa layer as well as Klotho and SOD contents in myocardial tissue of I/R group were significantly lower than those of control group whereas CaMKII, NOX2, NOX4 and MDA contents as well as CaSR, USP14, JNK, Bax, Fas and Caspase-3 mRNA expression in myocardial tissue were significantly higher than those of control group;the MAPA levels of myocardial tunica intima layer, tunica media layer and tunica externa layer as well as Klotho and SOD contents in myocardial tissue of Dex group were significantly higher than those of I/R group whereas CaMKII, NOX2, NOX4 and MDA contents as well as CaSR, USP14, JNK, Bax, Fas and Caspase-3 mRNA expression in myocardial tissue were significantly lower than those of I/R group;Pearson test showed that the MAPA levels of myocardial tunica intima layer, tunica media layer and tunica externa layer were negatively correlated with CaMKII, NOX2, NOX4 and MDA contents as well as CaSR, USP14, JNK, Bax, Fas and Caspase-3 mRNA expression in myocardial tissue, and positively correlated with Klotho and SOD contents. Conclusion: Dexmedetomidine can increase the MAPA in myocardial ischemia-reperfusion process, and is closely related to the inhibition of oxidative stress response and apoptosis.

Correlation between myocardial ischemia-reperfusion-induced monophasic action potential amplitude change and myocardial damage

Objective:To study the correlation between myocardial ischemia-reperfusion-induced monophasic action potential amplitude (MAPA) change and myocardial damage.Methods:New Zealand rabbits were selected as experimental animals and randomly divided into control group and ischemia-reperfusion group (I/R group), myocardial ischemia-reperfusion injury models were established, then the heart was separated and the MAPA of myocardial intima layer, media layer and outer layer were determined in Langendorff perfusion system;serum samples and myocardial tissue were collected to determine the contents of myocardial injury molecules.Results: MAPA levels of myocardial intima layer, media layer and outer layer of I/R group were significantly lower than those of control group;CK-MB, cTnI, cTnT and MDA contents in serum as well as Bax, Caspase-3 and Caspase-9 mRNA expression in myocardial tissue of I/R group were significantly higher than those of control group and negatively correlated with MAPA levels of myocardial intima layer, media layer and outer layer while SOD, GSH-Px and HO-1 contents in serum as well as Bcl-2 and Bcl-xL mRNA expression in myocardial tissue were significantly lower than those of control group and positively correlated with MAPA levels of myocardial intima layer, media layer and outer layer.Conclusion:Myocardial ischemia - reperfusion can induce the decrease of MAPA and is closely related to myocardial oxidative stress injury and apoptosis.

Resolution of DL-phenylalanine by porcine pancreas lipase catalyzed transesterification in monophasic organic solvent

With recent development of enzyme engineering, the use of enzyme in organic solvents is rapidly increasing. The remarkable stereoselectivity and regioselectivity of reaction catalyzed by enzyme were used to resolve many racemic alcohols and esters. A number of results have also been reported about the resolution of amino acids in organic solvents. For example, DL-phenylalanine methyl ester was resolved by α-chymotrypsin in toluene/water biphasic system; in fact, this reaction was carried, out in water;transesterification of DL-phenylalanine propyl ester and methanol was catalyzed by α-chymotrypsin in methanol, and the enzyme used was dissolved in water and the

Experimental Study of the Effect of Autonomic Nervous System on the Transmural Dispersion of Ventricular Repolarization under Acute Myocardial Ischemia in Vivo

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization(TDR)under acute myocardial ischemia in intact canine was investigated.Using the monophasic action potential(MAP)recording technique,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 under acute myocardial ischemia in 12 open-chest dogs.MAPD 90 and TDR among three myocardial layers as well as the incidence of the early afterdepolarization(EAD)before autonomic nervous stimulation and during autonomic nervous stimulation were compared.It was found that 10 min after acute myocardial ischemia,TDR was increased from 55±8 ms to 86±15 ms during sympathetic stimulation(P<0.01).The TDR(53±9 ms)during parasympathetic stimulation was not significantly different from that of the control(55±8 ms)(P>0.05).The EAD was elicited in the Mid of 2 dogs(16%)10 min after acute myocardial ischemia,but the EAD were elicited in the Mid of 7 dogs(58%)during sympathetic stimulation(P<0.01).It was concluded that:(1)Sympathetic stimulation can increase the transmural dispersion of repolari-zation and induce early afterdepolarizations in the Mid under acute myocardial ischemia,which provide the opportunity for the ventricular arrhythmia developing;(2)Parasympathetic stimulation has no significant effect on the transmural dispersion of repolarization under myocardial ischemia.

Effect of Autonomic Nervous System on the Transmural Dispersion of Ventricular Repolarization in Intact Canine

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. MAPD 90 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 MAPD 90 of Epi, Mid and Endo before autonomic nervous stimulation were 278±11 ms, 316±16 ms and 270±12 ms respectively, the MAPD 90 of Mid was significantly longer than that of Epi or Endo ( P <0.01). MAPD 90 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 MAPD 90 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.

Effects of ramipril on ventricular arrhythmia after myocardial infarction in rabbits

BACKGROUND： Ventricular arrhythmia （VA） is one of the most common complications of myocardial infarction （MI）, and ventricular tachycardia and fibrillation are the main causes for sudden cardiac death. This study aimed to explore the effect of ramipril on the occurrence of VA and its mechanism after MI in rabbits. METHODS： Twenty-four New Zealand rabbits purchased from the Wuhan Laboratory Animal Research Center were divided into three groups： sham-operated （SHAM） group （n=8）, MI group （n=8） and MI with ramipril （RAM） group （n=8）. Rabbits in the SHAM group received a median sternotomy without ligation of the left ventricular coronary artery. Rabbits in the MI and RAM groups received a median sternotomy followed by ligation of the left coronary artery. The successful anterior MI was confirmed by elevation of the ST segment with more than 0.2 mV in lead II and II1. After MI, rabbits in the RAM group were fed with intragastric ramipril （1 mg/kg per day ） for 12 weeks. Before and 12 weeks after MI in the three groups, ventricular tachycardia or fibrillation （VT/VF） episodes and MAP in cadiocytes of the epicardium, mid-myocardium and endocardium were recorded by a multichannel physiograph. Student＇s t test and ANOVA were used for statistical analysis. RESULTS： VT/VF episodes were decreased more markedly in the RAM group than in the MI group after 12 weeks （2.6±0.8 vs. 12.±＋2.9, P〈0.05）. Twelve weeks after MI, the duration of repolarization for 90% （APD90） of three-tier ventricular myocytes in the MI group was longer than that before MI （258.2±21.1 vs. 230.1±23.2,278.0±23.8 vs. 245.8±25.4,242.6±22.7 vs. 227.0±21.7, P〈0.05）. However, the APD90 was not significantly different at 12 weeks before and after MI in the RAM group （P〉0.05）. Moreover, the transmural dispersion of repolarization （TDR） was increased more markedly 12 weeks after MI in the MI group than in the SHAM and RAM groups （36.2±10.2 vs. 18.7±6.2, 24.9±8.7, P〈0.05）. But the TDR was not significantly different between the RAM and SHAM groups （18.7±6.2 vs. 24.9±8.7, P〉0.05）. CONCLUSION： Ramipril may reduce the incidence of malignant ventricular arrhythmia via mprovement of transmembrance repolarization heterogeneity after MI.

Variability in local action potential durations, dispersion of repolarization and wavelength restitution in aged wild-type and Scn5a^＋/- mouse hearts modeling human Brugada syndrome

Brugada syndrome is a primary arrhythmia syndrome characterized by loss-of-function mutations in the SCN5A gene, which encodes for the cardiac Na^＋ channel. In affected individuals, the risk of developing malignant ventricular arrhythmias and sudden cardiac death are increased.

Reduction of muscle contraction and pain in electroporation-based treatments:An overview

BACKGROUND In the first studies of electrochemotherapy(ECT),small cutaneous metastases were treated and only mild or moderate pain was observed;therefore,pain was not considered a significant issue.As the procedure began to be applied to larger cutaneous metastases,pain was reported more frequently.For that reason,reduction of both muscle contractions and pain have been investigated over the years.AIM To present an overview of different protocols described in literature that aim to reduce muscle contractions and pain caused by the electroporation(EP)effect in both ECT and irreversible EP treatments.METHODS Thirty-three studies published between January 1999 and November 2020 were included.Different protocol designs and electrode geometries that reduce patient pain and the number of muscle contractions and their intensity were analysed.RESULTS The analysis showed that both high frequency and bipolar/biphasic pulses can be used to reduce pain and muscle contractions in patients who undergo EP treatments.Moreover,adequate electrode design can decrease EP-related morbidity.Particularly,needle length,diameter and configuration of the distance between the needles can be optimised so that the muscle volume crossed by the current is reduced as much as possible.Bipolar/biphasic pulses with an inadequate pulse length seem to have a less evident effect on the membrane permeability compared with the standard pulse protocol.For that reason,the number of pulses and the voltage amplitude,as well as the pulse duration and frequency,must be chosen so that the dose of delivered energy guarantees EP efficacy.CONCLUSION Pain reduction in EP-based treatments can be achieved by appropriately defining the protocol parameters and electrode design.Most results can be achieved with high frequency and/or bipolar/biphasic pulses.However,the efficacy of these alternative protocols remains a crucial point to be assessed further.

CT-1-CP-induced Ventricular Electrical Remodeling in Mice

The chronic effects of carboxyl-terminal polypeptide of Cardiotrophin-1（CT-1-CP） on ventricular electrical remodeling were investigated. CT-1-CP, which contains 16 amino acids in sequence of the C-terminal of Cardiotrophin-1, was selected and synthesized, and then administered to Kunming mice（aged 5 weeks） by intraperitoneal injection（500 ng·g^-1·day^-1）（4 groups, n=10 and female： male=1：1 in each group） for 1, 2, 3 and 4 weeks, respectively. The control group（n=10, female：male=1：1） was injected by physiological saline for 4 weeks. The epicardial monophasic action potential（MAP） was recorded by using a contact-type MAP electrode placed vertically on the left ventricular（LV） epicardium surface, and the electrocardiogram（ECG） signal in lead Ⅱ was monitored synchronously. ECG intervals（RR, PR, QRS and QT） and the amplitude of MAP（Am）, the maximum upstroke velocity（Vmax）, as well as action potential durations（APDs） at different repolarization levels（APD30, APD50, APD70, and APD90） of MAP were determined and analyzed in detail. There were no significant differences in RR and P intervals between CT-1-CP-treated groups and control group, but the PR segment and the QRS complex were greater in the former than in the latter（F=2.681 and 5.462 respectively, P〈0.05）. Though QT interval and the corrected QT interval（QTc） were shorter in CT-1-CP-treated groups than in control group, the QT dispersion（QTd） of them was greater in the latter than in the former（F=3.090, P〈0.05） and increased with the time. The ECG monitoring synchronously with the MAP showed that the compression of MAP electrode on the left ventricular epicardium induced performance similar to myocardium ischemia. As compared with those before chest-opening, the PR segment and QT intervals remained basically unchanged in control group, but prolonged significantly in all CT-1-CP-treated groups and the prolongation of QT intervals increased gradually along with the time of exposure to CT-1-CP. The QRS complex had no significant change in control group, one-week and three-week CT-1-CP-treated groups, but prolonged significantly in two-week and four-week CT-1-CP-treated groups. Interestingly, the QTd after chest-opening was significantly greater than that before chest-opening in control group（t=5.242, P〈0.01）, but decreased along with the time in CT-1-CP-treated groups. The mean MAP amplitude, Vmax and APD were greater in CT-1-CP-treated groups than those in control group, and became more obvious along with the time. The APD in four CT-1-CP-treat groups was prolonged mainly in middle to final repolarization phase. The difference among these groups became significant in middle phase（APD50）（F=6.076, P〈0.01） and increased furthermore in late and final phases（APD70： F=10.054; APD90： F=18.691, P〈0.01） along with the time of injection of CT-1-CP. The chronic action of CT-1-CP might induce the adapting alteration in cardiac conductivity and ventricular repolarization. The amplitude and the Vmax of the anterior LV epicardial MAP increased obviously, and the APD prolonged mainly in late and final phase of repolarization.

Preparation and characterization of nanosized Gd_xBi_(0.95-x)VO_4:0.05Eu^(3+) solid solution as red phosphor

A complete solid solutions with monophasic zircon-type structure of vanadates of formula GdxBio.95-xVO4：0.05Eu3＋ （x = 04）.95） are synthesized by combined method of co-precipitation and hydrothermal synthesis. Their microstructures and morphologies are characterized by X-ray powder diffraction and transmission electronic microscope, and the results show that each of all the samples has a monophasic zircon-type structure. The absorption spectrum of the prepared phosphor shows a blue-shift of the fundamental absorption band edge with increasing the gadolinium content. Under UV-light and visible-light excitation, all the prepared phosphors show the typical luminescence properties of Eu3＋ in the zircon-type structure. The emission intensity of GdxBi0.95-xVO4：0.05Eu3＋ （x = 0.55） is strongest in all samples under UV-light and visible-light excitations. Finally, the mechanisms of luminescence of Eu3＋ in the GdxBi0.95-xVO4：0.05Eu3＋ （x = 0-0.95） solid solutions are analyzed and discussed.

Taxol inhibits stretch-induced electrophysiological alterations in isolated rat hearts with acute myocardial infarction

Mechanosensitive channels have been determined to work as transducers of mechanoelectric feedback in the heart, which is associated with the generation of arrhythmias. Recent studies have investigated the role of the cytoskeleton in ion channels control. This study explored the ability of taxol to inhibit stretch-induced electrophysiological alterations in the ischemic myocardium. Thirty-two Wistar rats were randomly divided into four groups: normal control group (n=9), taxol group (n=7), myocardial infarction (MI) group (n=9), and MI+taxol group (n=7). After Langendorff perfusion, the isolated hearts were stretched for 5 s by balloon inflation to 0.2 or 0.3 mL. The effects of stretching on 90% monophasic action potential duration (MAPD90), premature ventricular beats (PVB), and ventricular tachycardia (VT) were observed for 30 s. Stretching increased MAPD90 in both the normal control and MI groups, but MAPD90 increased more in the MI group for the same degree of stretch. Taxol (5 μmol L?1) had no effect on MAPD90 under baseline, unstretched conditions, but MAPD90 in the taxol group was slightly increased after stretching compared with the normal control group (P】0.05). However, taxol reduced MAPD90 in infarcted myocardium (P【0.05 at V=0.3 mL). The incidences of PVB and VT in the MI group were higher than in the normal control group (both P【0.01). Taxol had no effect on the occurrence of arrhythmias in normal myocardium, but it inhibited PVB and VT in infarcted hearts (both P【0.01). Thus changes in MAPD and the occurrence of arrhythmias caused by mechanical stretching of the myocardium could be inhibited by taxol in isolated rat hearts during AMI, indicating the involvement of tubulin in mechanoelectric feedback in AMI.

Streptomycin inhibits electrophysiological changes induced by stretching of chronically infarcted rat hearts

Objective： To investigate stretch-induced electrophysiological changes in chronically infarcted hearts and the effect of streptomycin （SM） on these changes in vivo. Methods： Sixty Wistar rats were divided randomly into four groups： a control group （n=15）, an SM group （n=15）, a myocardial infarction （MI） group （n=15）, and an MI＋SM group （n=15）. Chronic MI was obtained by ligating the left anterior descending branch （LAD） of rat hearts for eight weeks. The in vivo blockade of stretch-activated ion channels （SACs） was achieved by intramuscular injection of SM （180 mg/（kg·d）） for seven days after operation. The hearts were stretched for 5 s by occlusion of the aortic arch. Suction electrodes were placed on the anterior wall of left ventricle to record the monophasic action potential （MAP）. The effect of stretching was examined by assessing the 90% monophasic action potential duration （MAPD90）, premature ventricular beats （PVBs）, and ventricular tachycardia （VT）. Results： The MAPD90 decreased during stretching in both the control （from （50.27±5.61） ms to （46.27±4.51） ms, P〈0.05） and MI groups （from （65.47±6.38） ms to （57.47±5.76 ms）, P〈0.01 ）. SM inhibited the decrease in MAPD90 during inflation （（46.27±4.51） ms vs. （49.53±3.52） ms, P〈0.05 in normal hearts; （57.47±5.76） ms vs. （61.87±5.33） ms, P〈0.05 in MI hearts）. The occurrence of PVBs and VT in the MI group increased compared with that in the control group （PVB： 7.93±1.66 vs. 1.80±0.86, P〈0.01; VT： 7 vs. 1, P〈0.05）. SM decreased the occurrence of PVBs in both normal and MI hearts （0.93±0.59 vs. 1.80±0.86 in normal hearts, P〈0.05; 5.40±1.18 vs. 7.93±1.66 in MI hearts, P〈0.01）. Conclusions： Stretch-induced MAPD90 changes and arrhythmias were observed in chronically infarcted myocardium. The use of SM in vivo decreased the incidence of PVBs but not of VT. This suggests that SACs may be involved in mechanoelectric feedback （MEF）, but that there might be other mechanisms involved in causing VT in chronic MI.