A quantitative study of the relation between intracellular pH and force in rat mesenteric vascular smooth muscle

Strips of rat mesenteric artery were loaded with carboxy-seminaphthorhodafluor (SNARF) to measure intracellular pH (pH_i) and force simultaneously. pH_i was altered by using weak acids and bases. Alkalinization produced an increase in force. For equal elevations of pH_i a greater and faster increase of force was obtained in depolarized (high K⁺) than in non-depolarised preparations. Acidification produced little change in force unless the tissue was contracted (high-K⁺), in which case it elicited relaxation. Examination of the relationship between pH_i and force in depolarized preparations showed that acidification produced a greater change in force than alkalinization. Removal of weak bases produced a transient acidification that was accompanied by a fall in force in all preparations. This was followed by a secondary contraction in depolarized preparations during the period over which pH_i was acidic and being restored to resting values. Some preparations demonstrated a hysteresis in the relation between pH_i and force. It is concluded that the relationship between pH_i and force in mesenteric vascular smooth muscle is not constant but depends on the previous history of the preparation, and may involve differences in the interactions between H⁺, Ca²⁺ and the contractile machinery.     

Reduction of open wound contraction in humans with a synthetic dressing

Summary Many articles have been written about wound contraction. The majority of these use animals as these experiments are impossible to repeat in humans for ethical reasons. Skin graft donor sites have been used in this study as repeatable controlled wounds. Wound contraction does occur in these wounds and it can be reduced by covering the wound with a synthetic dressing.     

组织胺及其1、2型受体阻断剂对贮脂细胞收缩的影响

目的　探讨组织胺及其1型受体(H1R)阻断剂、2型受体(H2R)阻断剂对贮脂细胞收缩的影响。方法　采用肝脏离体胶原酶灌注消化及密度梯度离心的方法来分离培养贮脂细胞；用二甲基多聚硅烷烧制聚硅酮膜；传代后的贮脂细胞在聚硅酮膜上培养3d后，随机分为5组A组(对照组)；B组(组织胺1×10-7mol/L组)；C组(组织胺1×10-6mol/L组)；D组(H1R阻断剂+组织胺1×10-6mol/L组)和E组(H2R阻断剂+组织胺1×10-6mol/L组)。各组于加药前及加药后20min摄相，在相片上分析同一视野细胞周围的聚硅酮膜皱纹变化，皱纹增多表明细胞收缩。结果　B组、C组的贮脂细胞收缩率分别为21.0%、34.2%，远高于A组的3.8%，并呈量效依赖关系（P＜0.001）；D组的贮脂细胞收缩率为17.7%，低于C组（P＜0.05）；E组的贮脂细胞收缩率为26.3%，与C组相比，差异无显著性（P＞0.05）。结论　组织胺通过H1R的介导促进贮脂细胞的收缩，可能在门静脉高压症的发生发展中起了一定的作用。     

稳心颗粒联合美托洛尔治疗心律失常随机平行对照研究

[目的]观察稳心颗粒联合美托洛尔治疗心律失常疗效。[方法]使用随机平行对照方法,将80例分为两组,均进行西药综合治疗,并停服其它抗心律失常药5个半衰期。对照组38例美托洛尔口服。治疗组42例在对照组基础上加服稳心颗粒9g,3次/d,冲服。均4周为1疗程。观察动态心电图与临床症状改善及不良反应。治疗4疗程(112d)判定疗效。[结果]动态心电图改善总有效率治疗组80.95%优于对照组63.16%(P<0.01),临床症状疗效总有效率治疗组92.86%优于对照组73.68%(P<0.05),不良反应治疗组低于对照组。[结论]稳心颗粒可抗心律失常,与美托洛尔联用可提高疗效,减少副反应。     

川芎嗪对几种致喘介质所致离体豚鼠气管条收缩作用的影响

观察川芎嗪对白三烯C_4、D_4、组织胺、前列腺素F_(2a)、乙酰胆碱等所致豚鼠离体气管条收缩作用的影响,发现除乙酰胆碱外,川芎嗪对其他几种致喘介质均有一定抑制作用,为非竞争性拮抗剂。本实验似可为川芎嗪的平喘作用提供了一定的理论基础。     

桂甘龙牡汤治疗室性早搏疗效及安全性的Meta分析

目的：系统评价桂甘龙牡汤治疗室性早搏的疗效及安全性。方法：检索中国期刊全文数据库、中国学术期刊数据库、中文科技期刊数据库、Cochrane Library、Pubmed、SinoMed、EMbase共7个数据库,搜集有关桂甘龙牡汤治疗室性早搏的随机对照试验（RCT）,检索时间限定为建库至2020年3月。由2名研究人员独立参与文献筛选、提取资料和风险评估过程,然后使用Revman 5.3软件进行Meta分析。结果：纳入18个RCT共1 377例患者。Meta分析结果显示：有效率RR=1.26,95%CI为1.18~1.34,P<0.000 01;临床症状疗效：RR=1.23,95%CI为1.14~1.33,P<0.000 01;动态心电图：MD=-424.99,95%CI为-640.98～-209.00）,P=0.000 1;中医症状疗效：MD=-4.45,95%CI为-5.83～-3.07）,P<0.000 01;不良反应：RR=0.39,95%CI为0.23~0.67）,P=0.000 7。结论：桂甘龙牡汤治疗室性早搏的疗效优于对照组,疗效及安全性兼具。受纳入研究的数量与质量限制,需要扩大样本量,开展更为严格的随机对照、多中心、双盲、前瞻性临床试验,为临床实践提供更多证据。     

Effects of prostaglandin E2 and indomethacin on the rebound of the guinea-pig taenia coli.

The effects of prostaglandin E₂ (0.2 μM) and indomethacin (50 μM) on the rebound of smooth muscle cells of the guinea-pig taenia coli were studied. Stimulation of the non-cholinergic, non-adrenergic, intramural nerves caused membrane hyperpolarizaiton, known as the inhibitory junction potential (I.J.P.). This hyperpolarization was followed by a rebound depolarization and a rather small rebound contraction in quiescent preparations; the rebound depolarization was often accompanied by action potentials, resulting in a pronounced rebound contration. The effects of prostaglandin E₂ (PGE₂) on the membrane were comparable with the phenomena observed during the rebound, i.e. membrane depolarization, development of action potentials and contraction of the smooth muscle cells. Furthermore, an increase in amplitude of the I.J.P., enhancement of the spike discharge and a concomitant increase in rebound contraction were observed in the presence of PGE₂. Indomethacin did not modify the membrane potential or the amplitude of the I.J.P., but inhibited the rebound contraction and suppressed the development of action potentials during the rebound. The action of PGE₂ on the smooth muscle cell membrane was not modified by indomethacin, but the rebound contraction in the presence of both compounds was decreased. These experimental results indicate: that the rebound contraction is accompanied by depolarization of the membrane following the hyperpolarization caused by stimulation of the non-cholinergic non-adrenergic nerves; that the rebound activity can be mimicked by PGE₂; that indomethacin does not interfere with the action of PGE₂ applied exogenously and that the observations are consistent with the assumption that prostaglandins might be involved in the rebound.     

Expression of Potassium Channels in Uterine Smooth Muscle Cells from Patients with Adenomyosis

Background:

Adenomyosis (AM) has impaired contraction. This study aimed to explore the expression of potassium channels related to contraction in myometrial smooth muscle cells (MSMCs) of AM.

Methods:

Uterine tissue samples from 22 patients (cases) with histologically confirmed AM and 12 (controls) with cervical intraepithelial neoplasia were collected for both immunohistochemistry and real-time polymerase chain reaction to detect the expression of large conductance calcium- and voltage-sensitive K⁺ channel (BKCa)-α/β subunits, voltage-gated potassium channel (Kv) 4.2, and Kv4.3. Student''s t-test was used to compare the expression.

Results:

The BKCa-α/β subunits, Kv4.2, and Kv4.3 were located in smooth muscle cells, glandular epithelium, and stromal cells. However, BKCa-β subunit expression in endometrial glands of the controls was weak, and Kv4.3 was almost undetectable in the controls. The expression of BKCa-α messenger RNA (mRNA) (0.62 ± 0.19-fold decrease, P < 0.05) and Kv4.3 mRNA (0.67 ± 0.20-fold decrease, P < 0.05) decreased significantly in the MSMCs of the control group compared with the AM group. However, there were no significant differences in BKCa-β subunit mRNA or Kv4.2 mRNA.

Conclusions:

The BKCa-α mRNA and the Kv4.3 mRNA are expressed significantly higher in AM than those in the control group, that might cause the abnormal uterus smooth muscle contractility, change the microcirculation of uterus to accumulate the inflammatory factors, impair the endometrium further, and aggravate the pain.     

Reperfusion injury in dog hearts with permanent occlusion of a coronary artery, probably due to reperfusion via collateral vessels

To clarify whether or not reperfusion injury occurs in the permanent occlusion of a coronary artery, we analyzed quantitatively contraction band necrosis as an indicator of early recanalization, coagulation necrosis, infarct size and measured regional blood flow in dog hearts with collateral circulation. Fifty mongrel dogs were divided into four groups: 15 dogs with a 24-hour occlusion of the left anterior descending coronary artery just distal to the first diagonal branch (permanent occlusion group): 15 dogs a with 3-hour occlusion followed by 24-hour recanalization (recanalization group); 10 dogs with a 2-hour occlusion without recanalization (transient occlusion group); 10 dogs with a 4-hour occlusion without recanalization (transient occlusion group).

The regional blood flow in the subepicardium and subendocardium determined by the generated hydrogen gas clearance method was greatly decreased 30 minutes after occlusion (14 + 8%/12 ± 9%) and was relatively restored from 180 minutes (31 ± 21%/21 ± 14%) to 24 hours later (41 + 19%/26 + 16%) in spite of complete occlusion of the coronary artery. The percentage infarct area in the risk area was significantly greater in the permanent occlusion group (60 ± 26%) than in the recanalization group (35 ± 31%). Although most of the infarct was occupied by contraction band necrosis in the recanalization group (86 ± 12%), contraction band necrosis was diffusely seen even in the permanent occlusion group (54 ± 27%). In both the permanent and recanalization groups, contraction band necrosis was the main histological feature of small infarcts occupying less than 30% of the risk area, while coagulation necrosis was the main feature in very large infarcts occupying more than 80% of the risk area. In the occlusion groups without recanalization, the percentage area of contraction band necrosis in the risk area was 6 ± 8% after the 2-hour occlusion, 23 ± 17% after the 4-hour occlusion and 31 ± 21% after permanent occlusion; the difference between the 4-hour and permanent occlusion groups was not significant. In the permanent occlusion group, the percentage infarct area in the risk area was inversely correlated with regional blood flow during occlusion, an indicator of collateral flow. It was concluded that reperfusion injury occurs even in hearts without recanalization. The pathogenesis may involve reperfusion in the risk area via collateral circulation. Protection against reperfusion injury is important to minimize the infarct size even in hearts with permanent occlusion, although the presence of collateral flow is an important factor in limiting infarct size.     

Association Between Clinical Tests Related to Motor Control Dysfunction and Changes in Pain and Disability After Lumbar Stabilization Exercises in Individuals With Chronic Low Back Pain

ObjectiveTo investigate whether clinical tests used to detect motor control dysfunction can predict improvements in pain and disability in patients with chronic nonspecific low back pain (LBP) who have undergone an 8-week lumbar stabilization exercise program.Study DesignA prospective cohort study.SettingOutpatient physical therapy university clinic.ParticipantsSeventy people with chronic nonspecific LBP were recruited, and 64 completed the exercise program (N=64).InterventionsThe lumbar stabilization program was provided twice a week for 8 weeks.Main Outcome MeasuresPain intensity (11-point numerical rating scale) and disability (Roland Morris Disability Questionnaire) and clinical tests, such as the Deep Muscle Contraction (DMC) scale, Clinical Test of Thoracolumbar Dissociation (CTTD), and Passive Lumbar Extension (PLE) test. Univariate and multivariate linear regression models were used in the prediction analysis.ResultsMean changes in pain intensity and disability following the 8-week stabilization program were ?3.8 (95% confidence interval [CI], ?3.2 to ?4.4) and ?7.4 (95% CI, ?6.3 to ?8.5), respectively. Clinical test scores taken at baseline did not predict changes in pain and disability at 8-week follow-up.ConclusionOur findings revealed that the DMC scale, CTTD, PLE test, clinical tests used to assess motor control dysfunction, do not predict improvements in pain and disability in patients with chronic nonspecific LBP following an 8-week lumbar stabilization exercise program.