Volume 113  ·   Issue 08  ·  2000

Objective To evaluate the tissue Doppler acceleration imaging(TDAI)data which can be used to determine the intramural site of origin of myocardial contraction in response to electrical stimulation. Methods Six open-chest pigs with left ventricle(LV)pacing were evaluated with TDAI. An epicardial surface scanning method was used to collect short-axis views of the left ventricle. The electrode was implanted from the epicardium through the anterior free wall to an intramural position. Results During pacing, the intramural onset of myocardial acceleration occurred within 33 ms after electrical stimulation and always surrounded the embedded subendocardial end of the pacing needle. The observed short-axis diameter of the area of initial myocardial acceleration ranged from 2.9 mm to 5.0 mm(4.2±0.9 mm, n = 6). The onset of myocardial acceleration allowed appreciation of the initial intramural myocardial contraction. The spatial size and acceleration magnitude of the initial myocardial acceleration distribution were irregular. Conclusion Two-dimensional myocardial acceleration mapping can show the intramural site of origin of myocardial contraction in response to paced electrical stimulation. The location of myocardial acceleration conformed to the site of initial electrical stimulation. The delay to the earliest regional myocardial contraction, 33 ms after paced electrical stimulation, was related to the frame rate of image acquisition. Chin Med J 2000; 113(8): 763-768

Objective To determine whether diabetes recurs in their later life when women have a history of gestational diabetes mellitus(GDM)or abnormal glucose tolerance test(impaired glucose tolerance, IGT). Methods Three groups of women were investigated at 5-10 years postpartum. GDM group(n = 45)had been diagnosed as having GDM in their previous pregnancy. IGT group(n = 31)had a history of abnormal glucose tolerance test during previous pregnancy. Normal control group(n = 39)was normal previous pregnant population. Their previous obstetric and medical histories were thoroughly reviewed. Fasting plasma glucose(FPG)and oral glucose(75g)tolerance test(OGTT)were repeated in all women. Results Diabetes mellitus(DM)was diagnosed in 33.3% of patients in the GDM group, while in 9.7% in the IGT group and in 2.6% in the normal control group. Incidence of recurring DM in later life was significant higher in the GDM group(P = 0.017). When one or more blood glucose values exceeding WHO criteria for diagnosis of diabetes in their previous pregnancy, the incidence of DM in later life was 60%(3/5, including GDM in women having four abnormal OGTT values), 41.7%(5/12)in women having three, 25%(7/28)in women having two and 9.7%(3/31)in women having one. The women with DM, also with a history of GDM and abnormal OGTT in previous pregnancy, tends to have a high pregnant body mass index(BMI > 25 kg/m2). Conclusion The women suffering from GDM during previous pregnancy have a high risk of recurrence DM. Two or more abnormal OGTT values during pregnancy, blood glucose level exceeding the maximal values at 1 and 2 hours after oral glucose loading and high pregnant BMI are concluded to be useful factors in predicting the recurring DM in their later life. Chin Med J 2000; 113(8): 759-762

Objective To study the role of platelet activating factor(PAF)in the pathogenesis of intestinal mucosal injury and endotoxin/bacterial translocation in acute severe pancreatitis(ASP)in pigs. Methods ASP was induced by intraductal injection of a mixture of sodium taurocholate and trypsin. BN50739, a specific antagonist of PAF, was given 30 min prior to the induction of ASP. Mucosal blood flow, mucosal myeloperoxidase(MPO)and malondialdehyde(MDA)were determined. Intestinal injury was observed microscopically. Portal blood endotoxin levels and the bacterial counts in the portal blood, intestinal lymph nodes and the pancreas were determined. Results Prior antagonism of PAF by BN50739 reduced intestinal injury, increased intestinal mucosal blood flow, and reduced blood levels of endotoxin and bacterial counts in the portal blood, mesenteric lymph nodes and pancreas. Conclusions Intestinal mucosal injury developed in ASP. PAF is responsible for the injury. Antagonism of PAF by BN50739 can improve intestinal microcirculation and reduce the severity of intestinal mucosal injury, which may decrease endotoxin/bacterial translocation. Chin Med J 2000; 113(8): 756-758

Objective To detect the expression of intercellular adhesion molecule-1(ICAM-1)and human leucocyte antigen-DR(HLA-DR)on retroocular fibroblasts(RFs)by immunoglobulin G(IgG)from patients with Graves' ophthalmopathy(GO)and interferon gamma(IFN-γ)and to study the possible mechanism of humoral immunity and cellular immunity in the pathogenesis of GO. Methods Purified IgG was obtained from 23 patients(GO 10, Graves' disease 9, toxic multinodular goiter 4)and 8 normal persons. Cytokine IFN-γ and thyroid stimulating hormon(TSH)were incubated with normal human RF cultured in vitro. Antigen expression on RFs induced by stimulators was examined using immunofluoresence staining and a flow cytometer. Results RFs spontaneously expressed ICAM-1, but did not express HLA-DR. All IgGs from patients with GO and other thyroid diseases as well as from normal persons could not stimulate the expression of ICAM-1 on RFs. IFN-γ and TSH significantly enhanced the expression of ICAM-1 in dose-dependent manner(P<0.05). Only IFN-γ could stimulate RFs to express HLA-DR(P<0.05). Conclusions IgG from patients with GO did not stimulate the expression of ICAM-1 and HLA-DR on the surface of cultured normal human RFs. IFN-y was the important factor for initiating and promoting autoimmune reactions in GO. We need to pay more attention to TSH, as it may possibly play a promoting role in the pathogenesis in GO. Chin Med J 2000; 113(8): 752-755

Objective To study the mechanism of stress exacerbating psoriasis and the involvement effect of neuropeptides in psoriatic pathogenesis, we investigated the expression and secretion of calcitonin gene-related peptide(CGRP)in psoriatic lesions, then identified the target cells of CGRP, the characters of CGRP positive dendrite cells and the source of CGRP in psoriatic plaque lesions. Methods Specific radioimmunoassay(RIA)and immunohistochemistry staining methods were used to determine CGRP secretive content and the target cells of CGRP in psoriatic plaque lesion tissue of vulgaris psoriasis. Double immunofluorenscence staining was done on psoriatic plaque lesion sections by first using rabbit anti-human CGRP antibody and mouse anti-human CD1a antibody, second using PE-conjugated anti-mouse immunoglobulin and FITC-conjugated anti-rabbit immunoglobulin. Confocal laser microscope showed the psoriatic lesion sections. Then both digoxigenin labelled anti-sense and sense RNA probe of CGRP were synthesized to make sure the source of CGRP on the dendrite cells. The psoriatic lesion sections were studied by in situ hybridization. Results The content of CGRP in vulgaris psoriatic plaque lesions was higher than that of normal controls(P< 0.01). CGRP was also found on the dermal microvascular endothelial cells and the epidermal dendrite cells in psoriatic plague lesions. Further study showed that CGRP existed on the surface of epidermal CD1a+Langerhans cell in psoriatic plaque lesion. The CGRP mRNA expressed around the nucleus of the Langerhans cells in psoriatic lesion. Conclusions The pathogenesis of psoriatic plaque lesions was closely related to the overexpression of neuropeptide CGRP. The CGRP contacted with the dermal microvascular endothelial cells and epidermal dendrite cells in psoriatic plaque lesion. The CGRP positive epidermal dendrite cell was CD1 a+Langerhans cell. The Langerhans cell itself expressed CGRP mRNA. Chin Med J 2000; 113(8): 747-751

Objective To study the primary mutations of mitochondrial DNA(mtDNA)associated with Leber's hereditary optic neuropathy(LHON)in patients with optic neuropathy. Methods Seventy-nine patients with a variety of bilateral optic neuropathies were examined. Mutations at np3460, np11 778 and np14 484 of mtDNA were tested by PCR-restriction detection in peripheral blood DNA from 16 cases of clinically probable LHON, 44 cases of possible LHON, 2 cases of alcohol amblyopia, 4 cases of multiple sclerosis, 5 cases of autosomal dominant optic atrophy, 4 cases of primary open-angle glaucoma, 3 cases of spinocerebellar degeneration, and 1 case of ethambutol-induced optic neuropathy. Results The mutation at np11778 was identified in 31 cases(39.2%)to establish LHON, which consisted of: all 16 of clinically probable LHON cases, 13 cases(29.5%)of possible LHON, and 2 cases of alcohol amblyopia. The remaining 48 cases were negative for mtDNA mutations at np3460, np11 778, and npl4 484. Conclusion Assessment of mtDNA provides a useful diagnostic aid in the definition and exclusion of LHON, in particular family history-negative, otherwise undefined bilateral optic nerve inflammatory disease. Chin Med J 2000; 113(8): 743-746

Objectives To examine whether the expression of choline acetyltransferase(ChAT), a marker for cholinergic neurons, and growth-associated protein(GAP-43), a marker for synaptogenesis, occurs differently following compression vs. decompression of spinal cord, and whether the reactions have any relationship with the time course of behavioral recovery. Methods A spinal cord compression model was studied quantitatively with an immunohistochemical method. The behavioral recovery of the rat was assessed by combined behavior score(CBS). Results The rebound in the ChAT-positive cell ratio was higher in decompressed cord than in compressed one. The time course of the change in the ChAT-positive cell ratio coincided with the recovery of CBS in the two models. Increased GAP-43 expression was found in the region of injured cord in the two models. Increased GAP-43 expression was partially parallel to the recovery of CBS, both in the decompression and continuous compression groups. Conclusions The results indicate that there are ChAT reversible neurons in both the compressed and decompressed cord, the number of which is closely related to the recovery of behavior following cord injury. Synaptogenesis plays a limited role in behavior recovery. Chin Med J 2000; 113(8): 737-742

Objective To observe the clinical efficacy and safety of intravenous thrombolytic therapy using an accelerated streptokinase(SK)regimen in acute myocardial infarction(AMI). Methods Data were collected from 40 hospitals during April 1996 to July 1997. Clinical therapeutic efficacy, five-week mortality, and adverse events were analyzed in 527 patients with AMI treated with an accelerated SK regimen(1.5 million IU within 30 min). Results The reperfusion rate of infarct-related arteries(IRAs)was 79.7%(421/528)assessed by clinical signs. The total mortality in the first 5 weeks was 6.6%(35/527). The incidence of allergic reactions and hypotension was 3.8%(20/528)and 4.2%(22/528), respectively. The incidence of bleeding was 2.7%(14/528), including cerebral bleeding 0.8%(4/528)and other major bleeding 0.8%(4/528). Conclusion Intravenous accelerated SK therapy can markedly improve reperfusion rate without increasing adverse events such as bleeding, allergic reactions and hypotension. Chin Med J 2000; 113(8): 733-736

Objective To explore the involvement of metabotropic glutamate receptors(mGluRs)in the formation of cerebral edema. Methods Male Wistar rats weighing from 250 g to 300 g were used. Trans-1-aminocyclopentane-1, 3-diacarboxylic acid(tACPD), an agonist of mGluRs, was microinjected into the right caudatum. Brain water content was determined by a wet weight/dry weight technique and Na+, K+ and Ca2+ contents were measured by Inductive Couple Plasma-9000 at 6 h, 24 h and 48 h post-injection. Extravasation of Evan's blue(EB)into the brain was determined as an indicator of disturbance in the blood-brain barrier(BBB)and endothelial cells. Histologic studies were performed under a Leitz microscope and a Philips EM208s electron microscope. Results Dose-dependent and time-related increase of brain water was induced after tACPD(10, 50, 500 and 1000 nmol)injection. A significant increase in Na+ and K+ content but not in Ca2+ content was observed. EB extravasation showed no blue stain, indicating no increase in BBB permeability induced by tACPD-injection. Electron microscope study confirmed this finding and revealed remarkable swelling of astrocytes especially endfoot processes of astrocytes around capillaries at 6 h after tACPD-injection. In addition, all changes mentioned above occurred in both caudatum. Conclusion These results indicate that activation of mGluRs by tACPD injected into the caudatum induced cytotoxic brain edema and interfered with astrocyte K+buffering. This may provide new clues for therapeutic intervention. Chin Med J 2000; 113(8): 728-732

Objective To study the feasibility of adenovirus mediated gene transfer into vein grafts and the role of the prourokinase gene in protecting vein grafts from thrombosis. Methods Fifty-two Wistar rats underwent implantation of reversed autologous jugular vein interposition grafts in the common carotid arteries. Jugular veins were excised and distended with solution containing three different adenovirus vectors(Adv5-CMV, group I; Adv5-CMV/LacZ, group Ⅱ; Adv5-CMV/Pro-UK, group Ⅲ)for 30 min, then the jugular veins werereversed and interposed into the divided carotid arteries, and end-to-end anastomoses were performed. The amount of 51 Cr-labeled platelets in vein grafts of group I and group Ⅲ was counted 24 hours postoperatively. On the 14th day, the vein grafts were harvested to examine β-galactosidase activity and prourokinase(Pro-UK)activity and observe thrombosis in vein grafts. Results Extensive blue coloration in the area of intima and media of each vein graft in group Ⅱ was observed. No blue coloration was seen in group I. Pro-UK activity was not detected in the vein grafts of group I. In group Ⅲ, the amount of Pro-UK gene expression was 308 IU/g tissue. The amount of 51 Cr labeled platelets in group I and group Ⅱ was(123.7±19.4)×106/g dry wt,(34.4±5.3)×106/g dry wt, respectively. The thrombosis rate and occlusion rate of the vein grafts in group I were 30%and 10%, respectively. In group Ⅲ, all vein grafts were patent and free of thrombosis. Conclusions Ex vivo gene transfer before vein grafting is feasible using replication deficient recombinant adenovirus and results in a high level of gene expression in vivo. Direct transfer of the Pro-UK gene into vein grafts may prevent thrombosis. Chin. Med J 2000; 113(8): 725-727