The presence of cytoplasmic strings in human blastocysts is associated with the probability of clinical pregnancy with fetal heart.

PURPOSE: Is the presence of cytoplasmic strings (CS) in human blastocysts associated with the probability of clinical pregnancy with fetal heart (CPFH) after transfer. METHODS: This case-control study involved 300 single blastocyst transfers. 150 of these resulted in a CPFH (cases) while 150 did not (controls). All embryos were cultured in Embryoscope+ and AI software (IVY) was used to select the blastocyst with the highest score from the cohort for transfer. An embryologist, blind to the transfer outcome, recorded the CS number, location, and duration of their activity. RESULTS: There was a significant difference in the number of blastocysts that contained CS, with 97.3% of women's blastocysts resulting in +CPFH containing the CS compared to 88.7% of blastocysts in women who did not have a pregnancy (p = 0.007, OR; 4.67, CI 95% 1.5-14.2). CS appeared 2.4 h earlier in embryo development in the +CPFH group compared to their negative counterparts (p = 0.007). There was a significant difference in the average number of CS/blastocyst with a higher number being present in those that achieved a clinical pregnancy (mean: 6.2, SD 2.9) compared to those that did not (mean: 4.6, SD 3.0) (p ≤ 0.0001). There was a significant increase in the number of vesicles seen traveling along the CS with more seen in the blastocysts resulting in a +CPFH (mean: 4.3 SD 2.1) compared to those in the -CPFH group (mean: 3.1, SD 2.1). CONCLUSION: This study has shown that the presence of cytoplasmic strings in human blastocysts is associated with the probability of clinical pregnancy with fetal heart.

Geranylgeranyl pyrophosphate synthase facilitates the organization of cardiomyocytes during mid-gestation through modulating protein geranylgeranylation in mouse heart.

Aims: With the maturation of placenta, ventricular chamber maturation enhances cardiac contractile performance to adapt to the metabolic demand of growing embryo. The organization of cardiomyocytes is required for the morphological remodelling in ventricular chamber maturation. However, the mechanism governing the establishment of cardiac cytoarchitecture during ventricular chamber maturation is still poorly studied. Methods and results: Here, we found that the expression of geranylgeranyl pyrophosphate synthase (Ggpps), which mediates protein geranylgeranylation, increased in the mouse heart after the onset of placental function. By using different Cre lines, we found that the cardiac inactivation of Ggpps by the Nkx2.5Cre/+ line disrupted protein geranylgeranylation as early as E9.5, which affected ventricular chamber maturation and resulted in mid-gestational embryonic lethality. In contrast, α-SMA-Cre line mediated the disruption of protein geranylgeranylation from E13.5 did not affect embryonic heart development. Further analysis of Nkx2.5Cre/+; Ggppsfl/fl mutants showed that the loss of Ggpps caused disorganized cardiac cytoarchitecture as early as E11.5 by disturbing cell-cell junctions. Ggpps inactivation decreased Rho GTPase geranylgeranylation and their activity, which might account for the disruption of cell-cell junctions. Moreover, elevating the protein geranylgeranylation by supplement of geranylgeranyl pyrophosphate (GGPP) could recover the Ggpps deficient induced defects of cytoarchitecture and cell-cell junctions in vitro and in vivo. Conclusion: Our present study demonstrates that GGPPS-mediated protein geranylgeranylation plays an indispensable role in the ventricular chamber maturation and acts as a stage-specific signal to regulate the establishment of cardiac cytoarchitecture during mid-gestation.

Fetal cardiac cine magnetic resonance imaging in utero.

Fast magnetic resonance imaging (MRI) led to the emergence of 'cine MRI' techniques, which enable the visualization of the beating heart and the assessment of cardiac morphology and dynamics. However, established cine MRI methods are not suitable for fetal heart imaging in utero, where anatomical structures are considerably smaller and recording an electrocardiogram signal for synchronizing MRI data acquisition is difficult. Here we present a framework to overcome these challenges. We use methods for image acquisition and reconstruction that robustly produce images with sufficient spatial and temporal resolution to detect the heart contractions of the fetus, enabling a retrospective gating of the images and thus the generation of images of the beating heart. To underline the potential of our approach, we acquired in utero images in six pregnant patients and compared these with their echocardiograms. We found good agreement in terms of diameter and area measurements, and low inter- and intra- observer variability. These results establish MRI as a reliable modality for fetal cardiac imaging, with a substantial potential for prenatal evaluation of congenital heart defects.

El Diazepam altera la ultraestructura del atrio fetal de ratón / Diazepam alters the ultrastructure of fetal atrium in rat

El diazepam (DZ) es un tranquilizante menor sintético, utilizado en pacientes con trastornos psicológicos y psiquiátricos. Es sedante, miorrelajante, anticonvulsionante y antipsicótico. El DZ atraviesa la barrera placentaria humana y la del ratón. Mujeres jóvenes que son adictas al fármaco, si se embarazan y continúan utilizándolo, sobre todo durante el primer trimestre, exponen a sus hijos a presentar alteraciones psicomotoras. El propósito de este trabajo fue investigar si el DZ administrado durante la gestación,induce alteraciones ultraestructurales del miocardio fetal de ratón. El grupo (DZ) de hembras gestantes deratón de la cepa CD-1 fue tratado con dosis únicas diarias de 1,0 mg/kg/pc/sc del día 6 al 17 y un grupo (C)que recibió solución salina. El día 18 las hembras de ambos grupos se anestesiaron, los fetos se perfundieron por vía intracardiaca con paraformaldehído al 1 % y glutaraldehido al 2,5 %, se les extrajo el corazón, se disecó el atrio, se fijó en OsO4 al 1 % y se incluyó en resina epóxica. Los cortes finos se contrastaron conacetato de uranilo y citrato de plomo y se observaron en un microscopio electrónico de transmisión. En los miocitos de los fetos del grupo DZ las sarcómeras del miocardio compacto tenían menor longitud que las del grupo C. Se observaron zonas con miofibrillas desorganizadas. El retículo sarcoplásmico de algunos miocitos presentaba cisternas distendidas y fragmentadas, mitocondrias alteradas y se observaron abundantes polirribosomas. Los cambios podrían deberse al efecto del DZ sobre la síntesis de actina y miosina pesada y sobre los organelos citoplásmicos, mediados por receptores benzodiazepínicos periféricos presentes en la membrana externa de las mitocondrias y asociados a canales de calcio dependientes de voltaje. Las alteraciones ultraestructurales del miocardio atrial de fetos de ratones expuestos in utero a DZ podrían tener efectos posnatales.

Diazepam (DZ) is a syntheticminor tranquilizer, used in patients with psychologicaland psychiatric disorders. It is a relaxing sedative,anticonvulsant and antipsychotic. DZ crosses thehuman placental barrier in mouse. Young women who are addicted to the drug, if they become pregnantand continue to use it, particularly during the firsttrimester, expose their children to psychomotor disorders. The purpose of this study was to investigate whether DZ administered during pregnancy induces ultrastructural alterations of fetal mouse myocardium.The group (DZ) of pregnant female mice of the CD-1strain was treated with a single daily dose of 1.0 mg/ kg / pc / sc of day 6 to 17 and a group (C) that received saline solution. On day 18 females of bothgroups were anesthetized, the fetuses were perfusedby intracardiac route with 1 % paraformaldehyde and 2.5 % glutaraldehyde, the heart was removed, theatrium was dissected, fixed in 1 % OsO4, it wasimmersed in epoxy resin. The fine sections werecontrasted with uranyl acetate and lead citrate and observed in a transmission electron microscope. Inthe myocytes of the fetuses of the DZ group, the sarcomers of the compact myocardium were shorter than those of the C group. Areas with disorganized myofibrils were observed. The sarcoplasmic reticulumof some myocytes had distended and fragmented 996cisterns, altered mitochondria, and abundant polyribosomes were observed. The changes may bedue to the effect of DZ on the synthesis of actin and heavy myosin and on cytoplasmic organelles mediatedby peripheral benzodiazepine receptors present onthe outer membrane of the mitochondria and associated with voltage-dependent calcium channels.Ultrastructural alterations of the atrial myocardium of fetuses of mice exposed to DZ in utero may have postnatal effects.

The roadmap of WT1 protein expression in the human fetal heart.

The transcription factor Wilms' Tumor-1 (WT1) is essential for cardiac development. Deletion of Wt1 in mice results in disturbed epicardial and myocardial formation and lack of cardiac vasculature, causing embryonic lethality. Little is known about the role of WT1 in the human fetal heart. Therefore, as a first step, we analyzed the expression pattern of WT1 protein during human cardiac development from week 4 till week 20. WT1 expression was apparent in epicardial, endothelial and endocardial cells in a spatiotemporal manner. The expression of WT1 follows a pattern starting at the epicardium and extending towards the lumen of the heart, with differences in timing and expression levels between the atria and ventricles. The expression of WT1 in cardiac arterial endothelial cells reduces in time, whereas WT1 expression in the endothelial cells of cardiac veins and capillaries remains present at all stages studied. This study provides for the first time a detailed description of the expression of WT1 protein during human cardiac development, which indicates an important role for WT1 also in human cardiogenesis.

[Cilia and heart morphogenesis]. / Cils et morphogenèse cardiaque.

After the seminal discovery in 2000 that primary cilia are functional organelles which are essential for embryonic development, several mouse models of ciliopathies have been generated. The heart is frequently affected, with a large spectrum of malformations. The cilia of the node are required early in development in the determination of the left/right laterality of the embryo, which has secondary consequences on the formation of the heart. Thus, abnormal looping of the heart is a recurrent phenotype in models of ciliopathies. However, the function of primary cilia in cardiac cells remains poorly understood. Receptors such as polycystins or hedgehog receptors are usually localized in the primary cilium, raising the possibility that these signalling pathways, which are important for the septation and the growth of the heart, are transduced in primary cilia of cardiac cells. Knowledge of the roles of primary cilia at different steps of heart development and in different cardiac cell types will be essential to better understand the origin of human cardiopathies associated with ciliopathies.

Three-dimensional fast acquisition with sonographically based volume computer-aided analysis for imaging of the fetal heart at 18 to 22 weeks' gestation.

OBJECTIVE: The purpose of this study was to determine how frequently cardiac images derived from 3-dimensional (3D) volume sets, acquired by fast acquisition and evaluated with sonographically based volume computer-aided analysis (sonoVCAD), were satisfactory for prenatal screening at 18 to 22 weeks' gestation. METHODS: A prospective study of 100 women with singleton pregnancies was undertaken. Three fast acquisition 3D volume sets were obtained from each patient. Four reviewers independently evaluated the 4-chamber and 5 extracted VCAD views. Factors contributing to unsatisfactory screening were also evaluated. RESULTS: The frequency with which adequate views for cardiac screening could be obtained varied widely; some single views, such as that of the stomach, were well seen frequently, whereas others, such as the ductal arch, were well seen significantly less frequently (P < .05). A satisfactory screening examination, defined as a visualized 4-chamber, left ventricular outflow tract, right ventricular outflow tract, and axial stomach view, was obtained for 43% to 65% of patients (dependent on reviewer). Logistic regression revealed that obesity (odds ratio, 3.0; 95% confidence interval, 1.7-5.0) and a fetus with the spine toward the maternal abdomen (odds ratio, 1.7; 95% confidence interval, 1.1-2.5) were independently associated with an unsatisfactory screening examination CONCLUSIONS: Three-dimensional fast acquisition volumes evaluated with sonoVCAD did not allow a satisfactory fetal cardiac screening examination to be obtained a high percentage of the time in a general obstetric population during the second trimester. Certain patient factors, such as body habitus and fetal position, are associated with unsatisfactory 3D imaging.

[Effect of hyperglycaemia on fetal heart in pregnant rats].

OBJECTIVE: To investigate the effect of hyperglycaemia on the cardiomyodial change of rat fetus. METHODS: Thirty clean SD pregnant rats were randomly dividing into group A, B and C, 10 in each group. Group A were injected intraperitoneally 50 mg/kg streptozotocin on the 6th day of pregnancy, Group B were injected the same dose on the 13th day of pregnancy, while Group C were injected intraperitoneally 0.1 mmol/L citrate buffer solution on the 6th day of pregnancy. All rats were killed on the 21st day of pregnancy, the total fetus, live fetus, weight, and length of fetus were recorded. The blood glucose in the fetal rats was measured, and the fetal hearts were collected. The fetal hearts were pathologically examined under light microscope and electron microscope. Immunohistochemical staining was applied to determine Caspase-3 in the heart of fetus. RESULTS: (1) The blood glucose of pregnant rats in the 3 groups showed no difference before intervening (P>0.05). There was significant difference between Group A and C, Group B and C after intervening (P<0.01), but no significant difference between Group A and B was found (P>0.05). (2 )The fetus in Group A and B was heavier and longer than in Group C, with significant difference (P<0.01), but not between Group A and B (P>0.05). The blood glucose of fetus in Group A and B was lower than that in Group C, with significant difference (P<0.01), but not between Group A and B (P>0.05). The rate of fetal death in Group A, B, and C were 31.96%,12.84%, and 3.88%, respectively. Significant deviation existed in the 3 groups (P<0.01). (3) Under light microscope, fetal hearts in Group A and B showed disorder, cardiac muscle cells swelled. There were vacuoles in cytolymph and necrosis in the myocardial tissue. Significant deviation in the integral of fetal necrosis existed in the 3 groups (P<0.01). (4) Caspase-3 was detected in the fetal hearts, the positive area ratio and mean OD value had significant deviation in the 3 groups (P<0.01).(5) Under the electron microscope, cardiomyocytes wrinkled, mitochondrion decreased, myofibril ruptured, while sarcomere blurred. The density of mitochondria in cardiamyocyte in Group A was lower than that in Group B and C (P<0.01), and the average volume of mitochondria of Group A and B was higher than that in Group C (P<0.01). CONCLUSION: There is apparent pathological change of fetal hearts in pregnant rats with hyperglycaemia. The longer the duration, the more obvious the change.

Heart-specific ablation of Prkar1a causes failure of heart development and myxomagenesis.

BACKGROUND: Protein kinase A signaling has long been known to play an important role in cardiac function. Dysregulation of the protein kinase A system, caused by mutation of the protein kinase A regulatory subunit gene PRKAR1A, causes the inherited tumor syndrome Carney complex, which includes cardiac myxomas as one of its cardinal features. Mouse models of this genetic defect have been unsatisfactory because homozygote null animals die early in development and heterozygotes do not exhibit a cardiac phenotype. METHODS AND RESULTS: To study the cardiac-specific effects resulting from complete loss of Prkar1a, we used cre-lox technology to generate mice lacking this protein specifically in cardiomyocytes. Conditional knockout mice died at day 11.5 to 12.5 of embryogenesis with thin-walled, dilated hearts. These hearts showed elevated protein kinase A activity and decreased cardiomyocyte proliferation before demise. Analysis of the expression of transcription factors required for cardiogenesis revealed downregulation of key cardiac transcription factors such as the serum response factor, Gata4, and Nkx2-5. Although heart wall thickness was reduced overall, specific areas exhibited morphological changes consistent with myxomatous degeneration in the walls of knockout hearts. CONCLUSIONS: Loss of Prkar1a from the heart causes a failure of proper myocardial development with subsequent cardiac failure and embryonic demise. These changes appear to be due to suppression of cardiac-specific transcription by increased protein kinase A activity. These biochemical changes lead to myxoma-like changes, indicating that these mice may be a good model with which to study the formation of these tumors.

[Structural changes of rat myocardium in the mother-fetus system exposed to cadmium].

Myocardium structure and the pattern of cardiomyocyte cellular and intracellular changes were studied in rats following the exposure of the mother-fetus system to cadmium. Rats were intraperitoneally injected with cadmium sulfate during days 1-16 of pregnancy. Myocardium of the left ventricle was studied in pregnant females and fetuses on day 20 of gestation. Myocardium changes in cadmium-exposed animals included the reduction of cardiomyocyte and blood vessels relative volume in mother and fetus. The damage of the nuclear and nucleolar apparatus was detected, together with the signs of diffuse edema of cardiomyocyte myofibrils and dilatation of intercellular spaces within the myocardium. This changes in cadmium-exposed animals are indicative of the development of regenerative-plastic myocardium insufficiency in the mother-fetus system.

Immediate and long-term effects of color Doppler ultrasound on myocardial cell apoptosis of fetal rats.

The objective of this article is to evaluate the safety of diagnostic color Doppler ultrasound (CDUS) on embryos by observing its effects on myocardial cell apoptosis of fetal rats. Pregnant Sprague-Dawley rats were divided into fetal group and neonatal group according to the sample-drawing time averagely and randomly, and each group was subdivided into control group and insonification group. The control group was sham-insonificated, and the insonification group was insonificated by diagnostic ultrasound (3.0 MHz, Tis = 1.8, MI = 1.6) for 30 minutes. The fetal rats' hearts were removed 24 hours after insonification and the neonatal rats' hearts were removed 10 days after birth. Apoptosis cells were detected with TUNEL (in situ terminal deoxynucleotidyl transferase-mediated D-UTP nick end labeling), and ultrastructural changes were observed with transmission electron microscope. Myocardial cell apoptosis was significantly higher in the fetal insonification group than in the fetal control group (P < 0.05), and it was significantly higher in the fetal groups than in the neonatal groups (P < 0.05), but there was no significant difference in myocardial cell apoptosis between the neonatal groups (P < 0.05). Apoptotic changes of myocardial cells in the fetal insonification group were observed with transmission electron microscope, which showed margination, condensation of the nuclear chromatin, etc. It is concluded that apoptosis and ultrastructural changes could be induced if fetal rat's heart was irradiated continuously over 30 minutes by diagnostic CDUS, but this phenomenon would disappear after birth.

Prenatal study of fetal endocardial hyperrefringence and its relation to maternal toxoplasmosis.

OBJECTIVE: To compare a group of fetuses whose mothers had acute or recent toxoplasmosis with a group of fetuses whose mothers had no systemic disease, analyzing the presence of changes in endocardial refringence. METHODS: This study assessed 91 fetuses of mothers diagnosed with acute or recent toxoplasmosis, detected by seroconversion or the presence of elevated IgM and IgG titers, confirmed through the IgM-capture ELISA. They were compared with a control group comprising 182 fetuses selected from a low-risk population participating in a prenatal screening program for heart diseases. RESULTS: No significant difference was observed between the mean gestational (29.2+/-4.6 weeks; 29.2+/-4.6 weeks) and maternal (25.7+/-6.7 years; 26+/-5.4 years) ages in the 2 groups. Areas of endocardial hyperechogenicity were observed in 69 fetuses whose mothers had toxoplasmosis (75.8%) and in only 6 fetuses of the control group (3.3%) (P<0.001). In 52 patients of the group studied (75.4%), endocardial hyperrefringence was diffuse, and, in 17 (24.3%), it was focal. In the control group, focal distribution was observed in 5 fetuses (83.3%). CONCLUSION: The prenatal echocardiographic image of focal or diffuse endocardial hyperrefringence is more prevalent in pregnancies with maternal toxoplasmosis than in the healthy ones, and an association between fetal endocardial hyperechogenicity and maternal disease exists.

Notch activation results in phenotypic and functional changes consistent with endothelial-to-mesenchymal transformation.

Various studies have identified a critical role for Notch signaling in cardiovascular development. In this and other systems, Notch receptors and ligands are expressed in regions that undergo epithelial-to-mesenchymal transformation. However, there is no direct evidence that Notch activation can induce mesenchymal transdifferentiation. In this study we show that Notch activation in endothelial cells results in morphological, phenotypic, and functional changes consistent with mesenchymal transformation. These changes include downregulation of endothelial markers (vascular endothelial [VE]-cadherin, Tie1, Tie2, platelet-endothelial cell adhesion molecule-1, and endothelial NO synthase), upregulation of mesenchymal markers (alpha-smooth muscle actin, fibronectin, and platelet-derived growth factor receptors), and migration toward platelet-derived growth factor-BB. Notch-induced endothelial-to-mesenchymal transformation does not seem to require external regulation and is restricted to cells expressing activated Notch. Jagged1 stimulation of endothelial cells induces a similar mesenchymal transformation, and Jagged1, Notch1, and Notch4 are expressed in the ventricular outflow tract during stages of endocardial cushion formation. This is the first evidence that Jagged1-Notch interactions induce endothelial-to-mesenchymal transformation, and our findings suggest that Notch signaling may be required for proper endocardial cushion differentiation and/or vascular smooth muscle cell development.

Neonatal lupus: review of proposed pathogenesis and clinical data from the US-based Research Registry for Neonatal Lupus.

Congenital heart block (CHB), a life-threatening manifestation of neonatal lupus, offers aunique opportunity to study the effect or arm of immunity and define the pathogenicity of an autoantibody in mediating tissue injury. This review focuses on our recent in vitro model which supports a cascade from antibody insult to unchecked fibrosis. In brief, it is proposed that the fetal cardiac myocyte undergoes apoptosis which facilitates transfer of intracellular Ro and La antigens to the surface where they are bound by circulating maternal autoantibodies (anti-SSA/Ro-SSB/La antibodies). Scavenging macrophages phagocytose these inadvertently "opsonized" cardiocytes, leading to the secretion of pro-inflammatory and pro-fibrotic cytokines, the latter of which transdifferentiate fibroblasts into myofibroblasts and thereby promote scarring. Immunohistologic study of a heart from a neonate dying of CHB supports this model in that macrophages and myofibroblasts were demonstrated. To facilitate both basic and clinical research, a Research Registry for Neonatal Lupus was established in 1994 by the U.S. National Institute of Arthritis, Musculoskeletal and Skin Diseases. Maternal and fetal outcomes are addressed as well as recurrence rates. Laboratory evaluation and management decisions during pregnancy are provided.

Teratogen-induced activation of the mitochondrial apoptotic pathway in the yolk sac of day 9 mouse embryos.

BACKGROUND: Using vital dyes, we have previously shown that while hyperthermia (HS), 4-hydroperoxycyclophosphamide (4CP), and staurosporine (ST) induce cell death within specific tissues (e.g., neuroepithelium) of day 9 mouse embryos, cells of the heart are resistant to the cell death-inducing potential of these teratogens. Subsequent work has shown that teratogen-induced cell death is associated with activation of the mitochondrial apoptotic pathway, i.e., release of cytochrome c from mitochondria, activation/cleavage of procaspase-9, -3, and -2, inactivation of poly(ADP-ribose) polymerase, and internucleosomal fragmentation of DNA, whereas resistance to teratogen-induced cell death in the heart is associated with a failure to activate this pathway. Teratogen-induced activation of the mitochondrial apoptotic pathway is initiated between 2.5 and 5 hr after teratogens are added to the culture medium. Because both the heart and the surrounding yolk sac are essential to successful development of mouse embryos during early postimplantation mouse development, we hypothesized that cells of the yolk sac are also resistant to teratogen-induced cell death. METHODS: To test our hypothesis, we cultured day 8.5 mouse conceptuses (embryo plus yolk sac) in whole embryo culture. On the morning of day 9, conceptuses were exposed to HS (43 degrees C for 15 min and then returned to 37 degrees C), 4CP (40 microM, 5-10 hr), or ST (0.5 microM 5-10 hr). At 5 and 10 hr after addition of teratogen, conceptuses were removed from culture and dissected into embryo and yolk sac. Activation of the mitochondrial apoptotic pathway was then assessed separately in embryos and yolk sacs using Western blot analysis to detect activation of procaspase-9, -3, and -2, enzyme assays to measure caspase-3-like activity, and immunohistochemistry to detect caspase-3 activation/cleavage in yolk sac cells. RESULTS: Although Western blot analysis revealed that procaspase-9, -3, and -2 were activated/cleaved in the embryo as early as the 5-hr time point, activation/cleavage of these caspases could not be detected in the yolk sac at either the 5- or 10-hr time point. Using an enzyme assay, we determined that caspase-3-like activity in the yolk sac was induced 1.7-fold by HS, 4.4-fold by 4CP, and 3.3-fold by ST. This compares to the embryo in which caspase-3-like activity was induced 45-fold by HS, 26-fold by 4CP, and 45-fold by ST. Using an antibody specific for the active p17 subunit of caspase-3 and immunohistochemistry, we were able to detect a small number of yolk sac cells showing caspase-3 activation. Thus, the low-level induction of caspase-3-like activity in the yolk sac is in part related to activation/cleavage of procaspase-3. CONCLUSIONS: Results presented indicate that cells of the extraembryonic yolk sac, like cells of the embryonic heart, are substantially more resistant to teratogen-induced activation of the mitochondrial apoptotic pathway and subsequent apoptosis compared to other embryonic tissues, particularly cells of the neuroepithelium.

[Image analysis of cardiac muscle cytoskeleton under simulated microgravity based on gray-level co-occurrence matrix (GLCM)].

OBJECTIVE: To study morphological changes of the cytoskeleton-microtubule (MT) of the fetal rat cardiac myocytes under simulated microgravity, and to quantify its image by utilizing the gray level co-occurrence matrix (GLCM) parameters of the image. METHOD: Cytoskeleton images, including cellular microphotographs taken under normal or microgravity (clinostat) conditions, were quantified by gray level co-occurrence matrix parameters, and the pharmacological counter effect of quercetin against the influences of microgravity was estimated with these parameters. RESULT: The results showed that the texture of microtubules in the image became worse under simulated microgravity environment. It also showed that quercetin has certain counter effect against the influence of microgravity. CONCLUSION: The microtubule of the cardiac myocytes cytoskeleton becomes diffused under microgravity, and the GLCM parameters can well describe these variation. Quercetin has certain counter-effect against the influence of microgravity.