Persistence of Mammary Artery Branches and Blood Supply to the Left Anterior Descending Artery

Background. Partial harvesting of the left internal mammary artery (LIMA) is a widespread technique used during minimally invasive coronary operations performed through a left anterior small thoracotomy. The influence of persisting LIMA branches was investigated to evaluate their effect on the blood flow of the left anterior descending artery.

Methods. Thirty patients, 15 with totally (group A) and 15 with partially (group B) harvested LIMAs, were evaluated. All the patients underwent postoperative angiography, during which a flow map of the LIMA was performed. The average peak velocity and the diastolic-to-systolic peak velocity ratio were recorded. The LIMA graft flow pattern was recorded in the proximal and distal thirds of the artery. Intramammary adenosine (12 to 14 μg) was injected and the average peak velocities before and after injection were calculated.

Results. The average peak velocity was similar in both groups in the proximal and distal thirds of the LIMA (25 ± 7 and 26 ± 5 cm/sec, respectively, in group A versus 27 ± 5 and 25 ± 5 cm/sec, respectively in group B; p = NS). The diastolic-to-systolic peak velocity ratio was similar proximally (0.78 ± 0.3 in group A versus 0.69 ± 0.3 cm/s in group B; p = NS), but not distally (1.72 ± 0.1 in group A versus 0.97 ± 0.3 in group B; p < 0.0005). The LIMA graft flow reserve was similar both proximally and distally (2.6 ± 0.6 and 2.5 ± 0.3 cm/s, respectively, in group A versus 2.6 ± 0.5 and 2.6 ± 0.3 cm/s, respectively, in group B; p = NS).

Conclusions. The persistence of LIMA branches does not influence the blood flow of the left anterior descending artery after acute adenosine-induced myocardial hyperemia. If a left anterior small thoracotomy is used in left anterior descending artery direct revascularization, complete LIMA harvesting is not mandatory and depends on the personal preference of the surgeon.     

MRI of the brain in diabetes mellitus

We studied the MRI appearances of the brain in 159 patients with diabetes mellitus (DM) and 2566 agematched individuals without DM (controls). The images were reviewed for cerebral infarcts, hemorrhage, atrophy and subcortical arteriosclerotic encephalopathy. Cerebral atrophy was significantly more frequent in patients with DM than in controls (P>0.005) from the sixth to the eighth decade. The frequency of atrophy was 41.2% in the 6th decade, 60.0% in the 7th and 92.3% in the 8th decade in DM, and 19.8%, 38.9% and 56.8% respectively in controls. Unexpectedly, there was no statistically significant difference in the incidences of cerebrovascular diseases at any age.     

Hyperglycaemia compensates for the defects in insulin-mediated glucose metabolism and in the activation of glycogen synthase in the skeletal muscle of patients with Type 2 (non-insulin-dependent) diabetes mellitus

Summary Insulin resistance and a defective insulin activation of the enzyme glycogen synthase in skeletal muscle during euglycaemia may have important pathophysiological implications in Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia may serve to compensate for these defects in Type 2 diabetes by increasing glucose disposal through a mass action effect. In the present study, rates of whole-body glucose oxidation and glucose storage were measured during fasting hyperglycaemia and isoglycaemic insulin infusion (40 mU·m^–2min^–1, 3 h) in 12 patients with Type 2 diabetes. Eleven control subjects were studied during euglycaemia. Biopsies were taken from the vastus lateralis muscle. Fasting and insulin-stimulated glucose oxidation, glucose storage and muscle glycogen synthase activation were all fully compensated (normalized) during hyperglycaemia in the diabetic patients. The insulin-stimulated increase in muscle glycogen content was the same in the diabetic patients and in the control subjects. Besides hyperglycaemia, the diabetic patients had elevated muscle free glucose and glucose 6-phosphate concentrations. A positive correlation was demonstrated between intracellular free glucose concentration and muscle glycogen synthase fractional velocity insulin activation (0.1 mmol/l glucose 6-phosphate: r=0.65, p<0.02 and 0.0 mmol/l glucose 6-phosphate: r= 0.91, p<0.0001). In conclusion, this study indicates an important role for hyperglycaemia and elevated muscle free glucose and glucose 6-phosphate concentrations in compensating (normalizing) intracellular glucose metabolism and skeletal muscle glycogen synthase activation in Type 2 diabetes.     

不同浓度的金属硫蛋白对离体豚鼠乳头肌缺氧、复氧电生理特性的影响

为探讨金属硫蛋白（MT）对豚鼠乳头肌缺血再灌注损伤所致心律失常的影响，利用标准玻璃微电极技术，采用缺氧及复氧豚鼠乳头肌模型，模拟体内缺血再灌注损伤，观察不同浓度MT对豚鼠乳头肌电生理特性的影响。结果显示低浓度的MT（0．002mmol／L）对正常及缺氧和复氧豚鼠乳头肌的动作电位（AP）有关参数及自律性均无影响；中等浓度的MT（0．02mmol／L）仅使正常乳头肌的AP复极达50％时程（APD50）缩短24％（P＜0．05），但使缺氧乳头肌的AP复极达20％时程（APD20）、APD50和AP复极达90％时程（APD90）分别缩短68％、56％和43％（P均＜0．01），并使静息电位（RP）、AP幅值（APA）和0相最大上升速率（Vmax）分别增加30％、30％和45％（P均＜0．01）；高浓度的MT（0．1mmol／L）使正常豚鼠乳头肌的APD20、APD50和APD90分别缩短57％、54％和50％（P均＜0．01），并且RP、APA及Vmax分别下降22％（P＜0．05）、28％（P＜0．01）和29％（P＜0．05），而使缺氧豚鼠乳头肌的APD20、APD50和APD90分别延长92％、78％和50％（P均＜0．01），对RP、APA及Vmax无明显影响。在复氧期间，0．02mmol／L的MT可使自律性的发生率从77．8％降至55．6％（P＜0．05）；而0．1mmol／L的MT则使自律性的发生率从77.8％降至22．2％（P     

脊髓萎缩（附2例报告）

本文报告了两例脊髓萎缩，并结合文献复习讨论了该病的好发部位、病因、临床表现、诊断和治疗。脊髓萎缩的病因多为继发性，也可为特发性。根据临床表现结合脊髓ＣＴ造影及ＭＲＩ检查，可以明确诊断。     

Different effects of halothane, isoflurane and sevoflurane on sarcoplasmic reticulum of vascular smooth muscle in dog mesenteric artery

Background: The direct effect of halothane on vascular smooth muscle is mediated in part via its effects on the sarcoplasmic reticulum (SR). Little information is available concerning the effects of other volatile anesthetics including isoflurane and sevoflurane, whose vascular effects differ from those of halothane. The aim of the present study was to compare the effects of halothane, isoflurane and sevoflurane on the SR by testing the contraction induced by caffeine in vascular smooth muscle. Methods: Rings without endothelium from isolated canine mesenteric artery were mounted in physiological saline solution (PSS) for isometric tension recording. After complete depletion of Ca²⁺ from the SR by adding 35 mM caffeine, the rings were exposed to normal Ca²⁺ containing PSS (Ca²⁺ loading), to Ca²⁺-free PSS for 10 min, and then to 15 mM caffeine to induce contraction. Anesthetics were administered during Ca²⁺ loading, the Ca²⁺-free phase and simultaneously with caffeine administration. Results: Halothane (0.5-2%) attenuated the caffeine-induced contraction of canine mesenteric artery when administered during Ca²⁺ loading in the SR (P<0.001), whereas isoflurane and sevoflurane (1–4%) failed to affect the contraction. When given simultaneously with caffeine, halothane (1–2%) potentiated the caffeine-induced contraction (P<0.05), but isoflurane and sevoflurane had no effect. When given before caffeine administration, halothane (0.5-2%), isoflurane (24%) and sevoflurane (4%) all potentiated the caffeine-induced contraction (P<0.05). Conclusion: It has been shown that halothane not only potentiates caffeine- induced Ca²⁺ release from the SR, but also induces contraction by releasing Ca²⁺ from the SR. We conclude that halothane decreases Ca²⁺ accumulation in the SR while exerting facilitative and additive effects on caffeine-induced Ca²⁺ release from the SR when applied before caffeine administration and simultaneously with caffeine, respectively, whereas isoflurane and sevoflurane lack both the ability to decrease Ca²⁺ accumulation and an additive effect on caffeine-induced Ca²⁺ release from the SR, but are able to facilitate Ca²⁺ release by caffeine.     

利多卡因对大鼠离体气管平滑肌的作用及机制

目的:研究利多卡因对气管平滑肌的作用及机制.方法:观察利多卡因对乙酰胆碱(ACh)和高钾预收缩大鼠离体气管的作用,对ACh、高钾和CaCl2诱发气管平滑肌收缩作用剂量反应曲线和ACh致两种收缩组分的影响并与维拉帕米进行比较.结果:利多卡因对ACh和高钾诱发的大鼠离体气管平滑肌标本收缩有舒张作用,并不被L-NAME和普萘洛尔阻断.利多卡因浓度依赖性地使ACh、KCl和CaCl2对大鼠离体气管条标本的量效反应曲线右移,最大反应降低.利多卡因0.69和3.45 mmol/L对ACh所致依赖细胞内钙收缩的抑制率及依赖细胞外钙收缩的抑制率差别均十分显著(P＜0.01).结论:利多卡因对离体大鼠气管平滑肌的舒张作用可能是通过非特异性地抑制细胞外钙经电压调节和受体调节钙通道向内流动及抑制细胞内钙释放来实现的.     

Differential effect of oestrogen on post‐exercise cardiac muscle myeloperoxidase and calpain activities in female rats

The effects of oestrogen administration on 1 h post‐exercise cardiac muscle myeloperoxidase (MPO) and calpain activities were determined in female rats. Rats were ovariectomized and implanted for 2 weeks with either oestrogen (25 mg 17‐oestradiol) or placebo pellets or left with ovaries intact. Rats were then run for 1 h at 21 m min^–1, 12% grade, killed 1 h post‐exercise and cardiac muscle and blood samples were removed. Control animals from each group were killed without prior exercise. Serum oestrogen levels in the order of the highest to lowest were; ovariectomized oestrogen replaced rats > intact ovaries rats > ovariectomized placebo rats. Oestrogen induced significant (P < 0.05) elevations in cardiac MPO activity at rest and at 1 h post‐exercise in ovariectomized rats. No significant elevations in cardiac MPO activity were evident in placebo ovariectomized or normal ovary rats at rest or post‐exercise. Cardiac calpain activities were similar in all unexercised groups. Ovariectomized placebo and intact ovary rats had significantly (P < 0.05) elevated cardiac calpain activities 1 h post‐exercise while calpain activity was not significantly elevated in hearts from ovariectomized oestrogen rats. These results demonstrate that oestrogen supplementation in ovariectomized rats induces elevations in cardiac muscle MPO activities at rest and at 1 h post‐exercise. This is opposite to the effect of oestrogen in post‐exercise skeletal muscle and implies a greater neutrophil infiltration into cardiac muscle caused by oestrogen. This effect cannot be explained by changes in 1 h post‐exercise cardiac muscle calpain activity, the elevation of which was suppressed by oestrogen administration. Oestrogen influences cardiac calpain activity similarly to its effect in skeletal muscle. Thus, oestrogen administration to ovariectomized rats induces elevations in cardiac MPO activity while suppressing cardiac calpain activity.     

Canine Latissimus Dorsi Muscle: An Apparatus for Isometric Force Measurements

Abstract: This paper describes a device used to measure the isometric forces generated during electrical stimulation of the canine latissimus dorsi muscle in vivo with a preserved neurovascular supply. This device uses 2 strain gauge force sensors linked to a movable alignment frame to which the muscle is attached. The muscle length is controlled by the application of known weights to the system. The device has a frequency of response of 17.5 Hz and compliance of -0.1 mm N^-1, and its experimental performance was tested in the anesthetized mongrel dog.     

3,6-(二甲氨基)-二苯骈碘杂六环葡萄糖酸盐对AGEP引起的大鼠主动脉平滑肌细胞增殖及牛主动脉内皮细胞内皮素和一氧化氮改变的影响

目的 :观察 3 ,6 (二甲氨基 ) 二苯骈碘杂六环葡萄糖酸盐对AGEP引起的大鼠主动脉平滑肌细胞增殖及牛主动脉内皮细胞内皮素和一氧化氮改变的影响。方法 :采用牛血清白蛋白 (BSA)与不同浓度葡萄糖 (0 ,2 0 ,5 0 ,80mmol·L-1)体外孵育制备糖基化终产物 (AGEP) ,应用 [3 H] TdR掺入法和MTT比色法观察I-93对重度糖化的AGEP诱导的大鼠主动脉平滑肌细胞 (ASMC)增殖的影响 ;应用放射免疫技术及Greiss法观察I -93对AGEP引起的牛主动脉内皮细胞 (BAEC)释放内皮素 1(ET 1)和一氧化氮 (NO)的影响。结果 :I-93 10 -7～ 10 -5mol·L-1能明显抑制AGEP引起的ASMC增殖 ,其 [3 H] TdR掺入量和MTT比色法的最大抑制率分别为79 .4%和 44 .2 %。随AGEP糖浓度的增加 (2 0～ 80mmol·L-1) ,BAEC培养液中ET 1含量亦逐渐上升 [(4 93± 63 )～ (779± 10 5 )ng·L-1] ,I -93 10 -7～ 10 -5mol·L-1能明显抑制重度糖化的AGEP促进ET 1释放的作用 ;I -93对AGEP灭活NO的作用有剂量依赖性抑制效应。结论 :I -93有抑制ASMC增殖的作用 ;对AGEP诱导的BAEC释放ET 1和NO间平衡失调有调节作用 ,在防治阻塞性血管疾病方面I -93具有潜在的应用价值