DigitalUM :: Browsing by Subject "Heart"

Browsing by Subject "Heart"

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Open Access
A comparison of cyclosporine A and cyclosporine G in a rabbit heterotopic cardiac transplant model: graft outcome and histological findings
(Murcia : F. Hernández, 1996) Fryer, J.P.; Pascoe, E.A.; Yatscoff, R.W.; Thliveris, J.A.
Cervical heterotopic heart transplants were performed on 20 male New Zealand white rabbits comprising 4 treatment groups. Animals in each group were injected daily via the marginal ear vein and received one of the following regimes: Cyclosporine A, 10 mglkglday; Cyclosporine G, 15 mglkglday; cremophor-El, 3mllday; or normal saline. Measurement of 24 hour trough blood concentrations revealed no significant differences between the average concentrations of Cyclosporine A and Cyclosporine G. Animals were examined daily and the cervical allografts assessed by palpation for viabilitylrejection. The duration of the study ended for each animal when the graft stopped beating at which time the animals was euthanized and the transplanted heart and native kidneys harvested and processed for light microscopy evaluation of rejection and drug toxicity, respectively. Graft survival in the Cyclosporine A group significantly surpassed that seen in the Cyclosporine G group as well as the control groups, whereas in animals treated with Cyclosporine G, graft survival was not different from controls. In the native kidney, there were no differences in glomerular tuft area or volume density amongst drug-treated or control animals. In contrast, tubule atrophy and interstitial fibrosis were markedly greater in Cyclosporine A-treated vs Cyclosporine Gtreated animals. The results of this study indicate that, whereas Cyclosporine G is less nephrotoxic than Cyclosporine A, given equivalent blood concentrations Cyclosporine A delays rejection of a cardiac allograft significantly longer than Cyclosporine G in this animal species.
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Age-related changes in mitochondrial membrane composition of rainbow trout (Oncorhynchus mykiss) heart and brain
(Elsevier, 2012-05-22) Almaida Pagán, Pedro Francisco; Costa, J. de; Mendiola, P; Tocher, D R; Fisiología; Institute of Aquaculture, School of Natural Sciences, University of Stirling, Stirling FK9 4LA, Scotland, United Kingdom; Department of Physiology, Faculty of Biology, University of Murcia, 30100 Murcia, Spain
Membrane composition, particularly of mitochondria, could be a critical factor by determining the propaga-tion of reactions involved in mitochondrial function during periods of high oxidative stress such as rapid growth and aging. Considering that phospholipids not only contribute to the structural and physical properties of biological membranes, but also participate actively in cell signaling and apoptosis, changes affecting either class or fatty acid compositions could affect phospholipid properties and, thus, alter mitochondrial function and cell viability. In the present study, heart and brain mitochondrial membrane phospholipid compositions were analyzed in rainbow trout during the four first years of life, a period characterized by rapid growth and a sustained high metabolic rate. Specifically, farmed fish of three ages (1-, 2- and 4-years) were studied, and phospholipid class compositions of heart and brain mitochondria, and fatty acid compositions of individual phospholipid classes were determined. Rainbow trout heart and brain mitochon- dria showed different phospholipid compositions (class and fatty acid), likely related to tissue-specific functions. Furthermore, changes in phospholipid class and fatty acid compositions with age were also tissue-dependent. Heart mitochondria had lower proportions of cardiolipin (CL), phosphatidylserine (PS) and phosphatidylinositol, and higher levels of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) with age. Heart mitochondrial membranes became more unsaturated with age, with a significative increase of peroxidation index in CL, PS and sphingomyelin (SM). Therefore, heart mitochondria became more susceptible to oxidative damage with age. In contrast, brain mitochondrial PC and PS content decreased in 4-year-old animals while there was an increase in the proportion of SM. The three main phospholipid classes in brain (PC, PE and PS) showed decreased n−3 polyunsaturated fatty acids, docosahexaenoic acid and peroxidation index, which indicate a different response of brain mitochondrial lipids to rapid growth and maturation.
Open Access
Alterations induced by cyclosporine A in myocardial fibers and extracellular matrix in rat
(Murcia : F. Hernández, 2002) Rezzani, R.; Angoscini, P.; Rodella, L.F.; Bianchi, R.
Cyclosporine A (CsA) is the first choice immunosuppressant universally used in allotransplantation. However, it has been demonstrated that this drug produces unwanted side effects in several organs and in particular in the kidney and in the heart. While the cardiac toxicity, due to alteration of myocardial prostanoid has been reported, no data are available about the effects of CsA on myocardial cytoarchitecture. We studied the CsA induced alterations of the myocardial structure and of the extracellular matrix components (ECM). To test the ECM enzymatic changes we studied a family of enzymes (matrix metalloproteinase-MMP), responsible for the degradation of extracellular matrix components. In particular we investigated MMP1, MMP2 and MMP9. The study was carried out on two groups of Wistar rats. The group I animals served as a control and were injected subcutaneously daily with castor oil for 21 days. Group II: animals were subcutaneously injected daily with CsA (dose: 15 mg/Kg in castor oil) for 21 days. The group I animals (control) had normal heart architecture and low levels of MMP1, MMP2 and MMP9. The group II animals showed degenerative changes with myocardial fibrosis, low levels of MMP1 and MMP9 but a clear increase in MMP2. We suggest that the myocardial fibrosis was a consequence of the cardiotoxic effect of CsA determining the alteration of the balance between synthesis and degradation of ECM. The increase in MMP2 suggests that this enzyme could play a protective role during myocardial damage and represent a compensatory mechanism for the excessive accumulation of collagen.
Open Access
Cardiac and pancreatic lesions in guinea pigs infected with encephalomyocarditis. EMC, virus
(Murcia : F. Hernández, 1991) Petruccelli, M.A.; Hirasawa, K.; Takeda, M.; Itagaki, S.; Doi, K.
Cardiac and pancreatic lesions were observed in guinea pigs infected with 2 variants (B and D) of encephalornyocarditis (EMC) virus. Cardiac changes were characterized by focal myocardial necrosis and subsequent replacement by immature granulation tissue. and the pancrcatic ones by vacuolar degeneration of acinar cells. In the electron microscopic esaminatioiis. tlie affected cardiornyocytes showed intracellular oedema. swelling andlor partial destruction of mitochondria, and distortion and disruption of myofihrils. Intracellular vacuolization and dilatation of roughsurfaced endoplasniic reticulurn (rER) were conspicuous in the damaged pancreatic acinar cells. In addition, intracisternal granules were found in dilated rER with a high frequency. These changes were common to animals infected with the B and D variants. On the contrary, B cell alterations: i.e. degranulation and degeneration of insulin granules, were detected only in animals infected with the D variant.
Open Access
Catecholamine-induced heart injury in mice: differential effects of isoproterenol and phenylephrine
(Murcia : F. Hernández, 2010) Navarro Sobrino, Míriam; Lorita, Jordi; Soley, María; Ramírez, Ignasi
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Open Access
“Corazón is in the air”: la expansión de la imagen del corazón en el paisaje urbano y digital contemporáneo.
(Universidad de Murcia, Servicio de Publicaciones, 2022) Sampietro, Agnese; Morant Marco, Ricardo
La imagen del corazón aparece constantemente en nuestro día a día: la encontramos en la decoración de multitud de objetos cotidianos, en la ropa, en las pintadas callejeras, en logotipos y escaparates, y es omnipresente en el mundo digital, donde el comando “me gusta” tiene a menudo forma de corazón. El presente trabajo tiene el objetivo de identificar las razones de esta predilección por la imagen cardíaca y las funciones que desempeña su representación. Para ello, hemos llevado a cabo un estudio de paisaje lingüístico y semiótico, recopilando y analizando un amplio corpus de imágenes de corazones, recogido en el espacio urbano y en internet. El análisis muestra que la imagen estudiada desempeña todas las funciones del lenguaje de Jakobson (1984); los principales contextos de uso del corazón son la expresión del sentimiento amoroso, la muestra de apreciación y la manifestación de agradecimiento. Comentamos en las conclusiones el “trasvase” de usos del corazón de la calle a la pantalla y viceversa.
Open Access
Crim1–, a regulator of developmental organogenesis
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Iyer, Swati; Pennisi, David J.; Piper, Michael
The regulation of growth factor localization, availability and activity is critical during embryogenesis to ensure appropriate organogenesis. This process is regulated through the coordinated expression of growth factors and their cognate receptors, as well as via proteins that can bind, sequester or localize growth factors to distinct locations. One such protein is the transmembrane protein Crim1. This protein has been shown to be expressed broadly within the developing embryo, and to regulate organogenesis within the eye, kidney and placenta. Mechanistically, Crim1 has been revealed to mediate organogenesis via its interaction with growth factors including TGFβs, BMPs, VEGFs and PDFGs. More recently, Crim1 has been shown to influence cardiac development, providing further insights into the function of this protein. This review will provide an overview of the role of Crim1 in organogenesis, largely focusing on how this protein regulates growth factor signaling in the nascent heart. Moreover, we will address the challenges ahead relating to further elucidating how Crim1 functions during development.
Open Access
Crosstalk between G protein-coupled receptors (GPCRs) and tyrosine kinase receptor (TXR) in the heart after morphine withdrawal
(2013-12-27) Almela Rojo, Pilar; García-Carmona, Juan-Antonio; Martínez Laorden, Elena; Laorden Carrasco, María Luisa; Milanés Maquilón, María Victoria; Farmacología
Open Access
Early structural alterations of intrinsic cardiac ganglionated plexus in spontaneously hypertensive rats
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Ranceviene, Dalia; Rysevaite Kyguoliene, Kristina; Inokaitis, Hermanas; Saburkina, Inga; Plekhanova, Khrystyna; Sabeckiene, Deimante; Sabeckis, Ignas; Azukaite, Joana; Pauza, Dainius H; Pauziene, Neringa
Persistent arterial hypertension leads to structural and functional remodeling of the heart resulting in myocardial ischemia, fibrosis, hypertrophy, and eventually heart failure. Previous studies have shown that individual neurons composing the intracardiac ganglia are hypertrophied in the failing human, dog, and rat hearts, indicating that this process involves changes in cardiac innervation. However, despite a wealth of data on changes in intrinsic cardiac ganglionated plexus (GP) in late-stage disease models, little is known about the effects of hypertension on cardiac innervation during the early onset of heart failure development. Thus, we examined the impact of early hypertension on the structural organization of the intrinsic cardiac ganglionated plexus in juvenile (8-9 weeks) and adult (12-18 weeks) spontaneously hypertensive (SH) and age-matched Wistar-Kyoto (WKY) rats. GP was studied using a combination of immunofluorescence confocal microscopy and transmission electron microscopy in whole-mount preparations and tissue sections. Here, we report intrinsic cardiac GP of SH rats to display multiple structural alterations: (i) a decrease in the intracardiac neuronal number, (ii) a marked reduction in axonal diameters and their proportion within intracardiac nerves, (iii) an increased density of myocardial nerve fibers, and (iv) neuropathic abnormalities in cardiac glial cells. These findings represent early neurological changes of the intrinsic ganglionated plexus of the heart introduced by early-onset arterial hypertension in young adult SH rats.
Open Access
Effect of telmisartan on preexistent cardiac and renal lesions in spontaneously hypertensive mature rats
(Murcia : F. Hernández, 2004) Mandarim-de-Lacerda, Carlos A.; Pereira, L.M.M.
Fifteen adult male spontaneously hypertensive rats (one year old) (SHR) were separated into three groups (n=5 each) during 15 weeks as follows: initial control group (IC); final control group (FC); and telmisartan group (T) (1.2 mg/kg/day of telmisartan). Serum and urinary creatinine and proteinuria were not different comparing untreated and telmisartan-treated SHRs. FC rats showed a continuous BP increase during the study while T rats reached the 15th week with a significantly low BP. The LV mass index was significantly smaller in the T group than in the FC group, as was the glomerular hypertrophy. The cardiomyocyte nuclei density per area and the cardiomyocyte mean cross-sectional area were smaller in the T group than in both the IC and FC groups. Intramyocardial artery densities (per area and per volume) were greater in the T group than in untreated SHRs, but myocardial fibrosis was reduced. In conclusion, telmisartan monotherapy effects on BP and also on the hypertension target organs, heart and kidney, are favorable. Telmisartan is able to attenuate SHR cardiomyocyte and glomerular hypertrophies, and myocardial reactive fibrosis as well. It also is favorable to the intramyocardial microcirculation.
Open Access
Enfermería: atención y cuidados en el golpe de calor.
(Murcia : Servicio de Publicaciones de la Universidad de Murcia, 2005) Loro Sancho, N.; Sancho Sánchez, M.J.; Sancho Sánchez, M.T.; Peiró Andrés, A.; Martínez Hernández, E.
El golpe de calor es una emergencia médica y causa tratable de fracaso multiorgánico. Se caracteriza por un incremento de la temperatura corporal central por encima de 40ºC. y alteraciones del sistema nervioso central donde predomina la encefalopatía y es típico el coma. Habitualmente las tareas que se realizan con el tiempo fresco son relativamente fáciles, pero éstas se vuelven muy difíciles si se tratan de hacer en un día caluroso. Los ajustes fisiológicos que mejoran la tolerancia del calor se denominan colectivamente de aclimatación al calor; la mayor aclimatación ocurre durante la primera semana de exposición y se complementa a los diez días. Los hombres, como animales homeotermos, para subsistir, tenemos que ser capaces de mantener nuestra temperatura corporal estable entre 36´8 y 37ºC., independientemente de la temperatura ambiente. La alteración de la temperatura origina profundos cambios en la economía del organismo. Puede tolerarse una temperatura interna de 10ºC. y con un aumento de sólo 5ºC. el fracaso de los mecanismos termorreguladores puede desencadenar la muerte. La carga térmica que debe soportar el organismo es una constante homeostática vital que se mueve en unos límites muy estrechos y que debe ser siempre cero. La temperatura interna está en equilibrio dinámico entre los factores que añaden calor corporal y los que lo substraen. Este equilibrio se mantiene mediante la integración de los mecanismos que derivan el calor a la periferia, regulan el enfriamiento por evaporación y varían su ritmo de producción por el organismo; si la ganancia excede a la pérdida, la temperatura interna aumenta; con el frío, la pérdida a menudo excede a la producción y la temperatura interna desciende. La temperatura corporal se incrementa debido a la absorción desde el ambiente a causa de la radiación solar y de determinados objetos que están más calientes que el propio cuerpo; también se incrementa por el calor producido en las reacciones del metabolismo, cuando los músculos se activan. El calor se pierde por los mecanismos físicos de irradiación, conducción, convección y la evaporación de la piel y las vías respiratorias.
Open Access
¿Es necesaria y efectiva la promoción de la salud en la escuela?. A propósito de una intervención sobre hábitos tóxicos.
(Murcia : Servicio de Publicaciones de la Universidad de Murcia, 2006) Navarro Moya, F.J.; Vigueras Lorente, Mª D.; Rodríguez González, Mª C.; Nicolás Vigueras, Mª D.; Nicolás Vigueras, A. B.
RESUMEN Introducción: La educación sanitaria en la comunidad es una de las actividades menos desarrolladas en A.P. Esta actividad es responsabilidad de la enfermería comunitaria y su objetivo es la prevención primaria de hábitos de vida poco saludables. Material y Método: Durante los años 2002-2003 desarrollamos un proyecto educativo con un colegio de la ZBS. Se impartieron sesiones de educación sanitaria a 251 alumnos de entre 10-12 años sobre el tema “Drogas, tabaco, alcohol”. Se utilizó una metodología expositiva-participativa con realización de una encuesta de conocimientos pre y post-sesión y otra sobre ambiente familiar y actitudes. Simultáneamente se realizó un experimento demostrativo de los efectos del tabaco. Resultados: Conocimientos: Los dos contenidos que menos conocen los escolares son las diferencias y semejanzas entre drogas legales e ilegales y el concepto de síndrome de abstinencia. Ambiente y actitudes: el 7% de los niños reconoce haber fumado. El 24 % tiene amigos que fuman. Han bebido alcohol el 54%. Todos conocen a algún fumador y el 87% conoce a alguien que beba alcohol. El 54% de los padres y el 9% de los hermanos fuman. Conclusiones: A pesar de que el colegio pertenece a una zona urbana de nivel adquisitivo medio-alto, preocupa el porcentaje de niños que han fumado o han bebido alcohol y el ambiente familiar poco saludable. Los conocimientos, satisfacción y motivación de los alumnos creció notablemente tras las sesiones, lo que debe animarnos a fomentar estas actividades educativas y a hacer un seguimiento prospectivo de la efectividad de las intervenciones.
Open Access
Exploring cyclosporine A-side effects and the protective role-played by antioxidants: the morphological and immunohistochemical studies
(Murcia : F. Hernández, 2006) Rezzani, R.
Cyclosporine A (CsA) is the immunosuppressor most frequently used in transplant surgery and in the treatment of autoimmune diseases, because of its specific inhibiting effect on the signal transduction pathways of cell T receptor. It has been shown that CsA is able to generate reactive oxygen species and lipid peroxidation, which are directly involved in the CsA nephrotoxicity, hepatotoxicity and cardiotoxicity. So, the use of antioxidants seems to be a useful tool in attempting to reduce CsA adverse effects. The aim of this review is to summarise the general aspect of CsA, the classification of antioxidants, their mechanism of action and their administration for improving CsA side effects. The protective role of different antioxidants has been evaluated on CsA-induced nephrotoxicity. It has been shown that the antioxidants, improved the morphological renal cytoarchitecture, increased the antioxidant enzyme content, decreased lipid peroxidation and reactive species oxygen (ROS). The protective role of antioxidants was also found in CsA hepatotoxicity and was related to the increase in antioxidant capacity of hepatic tissue, which was responsible for ameliorating hepatic morphology. Recently, it has been demonstrated that CsA induces side effects on the heart but the data to this purpose are very few and also the number of results on the protective role played by antioxidants it is very limited. In conclusion, not only do these observations provide insight into the intricate mechanism of CsA adverse effects, but they also present novel opportunities for the design and development of more effective therapeutic strategies against negative effects
Open Access
Heart matters: cardiac dysfunction and other autonomic changes in Parkinson’s disease
(SAGE Publications, 2021-02-15) Gonçalves, Valeria C. ; Cuenca Bermejo, Lorena; Fernández Villalba, Emiliano; Martin Balbuena, Sebastian; Fernandes, Maria Jose da Silva; Scorza, Carla A.; Herrero Ezquerro, María Trinidad; Medicina; Facultades de la UMU
It has been more than 200 years since James Parkinson made the first descriptions of the disease that bears his name. Since then, knowledge about Parkinson’s disease has been improved, and its pathophysiology, diagnosis, and treatments are well described in the scientific and medical literature. However, there is no way to prevent the disease from its progressive nature yet and only its symptoms can be minimized. It is known that the process of neurodegeneration begins before the onset of motor signs and symptoms of the disease, when diagnosis is usually made. Therefore, recognizing manifested non-motor symptoms can make an early diagnosis possible and lead to a better understanding of the disease. Autonomic dysfunctions are important non-motor manifestations of Parkinson’s disease and affect the majority of patients. Importantly, heart failure is the third leading cause of death in people suffering from Parkinson’s disease. Several evidences have shown the correlation between Parkinson’s disease and the preexistence of cardiovascular diseases. Therefore, cardiovascular monitoring and identification of its dysfunctions can have a prodromal role for Parkinson’s disease. This review presents studies of the literature that can lead to a better understanding of Parkinson’s disease with special attention to its relation to heart and cardiovascular parameters.
Open Access
Heart mitochondria in rats submitted to chronic hypoxia
(Murcia : F. Hernández, 1999) Cervós-Navarro, J.; Kunas, R.Ch.; Sampaolo, S.; Mansmann, U.
The effect of prolonged exposure to normobaric hypoxia on the mitochondria of myocard of rats exposed for several weeks to 8 and 7% O2 has been morphometrically evaluated. Twelve male Wistar rats housed in Nalgene cages (2 per cage) with a batch of six cages placed in plexiglass chambers were maintained in air/N2 mixtures containing different concentrations of 02. Six animals kept in similar cages under normoxia served as controls. When at day 60 the FIOZ was reduced to 8%, the weight increase stagnated and after the 81st test day, on which the hypoxic animals were subdivided into 8% and 7% groups the weight curve showed a decrease in the mean body weight for both groups. The arrest and the following loss of weight beyond the 85th day may be interpreted as the expression of a limit reached in the compensation capacity. In the 8%-group the shape of the mitochondria varied more markedly often with budding and furrowing of the surface. In the 7%-group bizarre shapes and wide variations in size with a decided shift towards larger mitochondria were noteworthy. While rats kept under 8% oxygen exhibited a numerical increase in myocardial mitochondria compared to controls, the mitochondria of the 7%-group were numerically reduced. The results suggest that hypoxia of 8% oxygen is compensatable, if only to some extent, by an increasing surface of mitochondrial membranes, and that further reduction of oxygen causes compensation mechanisms to fail as seen by the severe alterations of the mitochondrial population of the cardiomyocyte in the 7%-group.
Open Access
Immunolocalization of interleukin-1 receptor antagonist in healthy and infarcted myocardium
(Murcia : F. Hernández, 2008) Bonetti, A.; Marchini, M.; Ortolani, F.
Ischemic heart disease is a widespread cause of death. During infarction, myocardial injury is mediated by release of several pro-inflammatory cytokines including multifunctional interleukin-1 (IL-1). In various tissues, IL-1-mediated deleterious effects are known to be attenuated via the over-expression of natural anti-inflammatory cytokine IL-1 receptor antagonist (IL-1ra). In the present investigation, IL-1ra distribution in healthy and infarcted myocardium was studied by light and electron microscopy. After immunostaining, weak positivity resulted for cardiomyocytes in normal myocardium and, at higher degrees, in infarction border areas and ischemic ones. In ischemic areas, additional reactivity was displayed by the extracellular matrix and intravascular plasma. Immunogold labelling provided further details on intracytoplasmatic and extracellular distribution; in particular, noticeable gold particle distribution appeared on intercalated discs in normal and hypertrophic cardiomyocytes, as well as on thickened Z-lines for these latter. The present results suggest that cardiomyocytes represent a major source of IL-1ra in vivo, even though additional contribution by blood derived IL-1ra is to be taken in account in ischemic areas. In addition, ischemia-associated intracytoplasmic IL-1ra increase and its additional presence in the extracellular matrix is consistent with the concept that this cytokine plays a cardioprotective role at different levels and by distinct mechanisms.
Open Access
Inflammatory cytokines and antimicrobial peptides in acquired heart diseases
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2019) Vartina, Edite; Pilmane, Mara; Lacis, Romans
Introduction. One of the risk factors for cardiovascular disease is inflammation. The role that it plays in the pathogenesis of cardiovascular disease remains a topic of ongoing research. The aim of this study was to identify the appearance and distribution of inflammatory markers, interleukins 1α (Il-1α) and 10 (Il-10) and β defensins 2 (βD2), 3 (βD3), and 4 (βD4), in the right atrial tissue from different acquired heart diseases. Methods. During cardiac surgery, right atrial tissue fragments were taken from 23 patients with acquired heart diseases. Tissue fragments were stained for immunohistochemical detection of Il-1α, Il-10, βD2, βD3 and βD4. Results. Few to a moderate number of Il-1α-positive cells and a moderate to great number of Il-10-, βD2- and βD3-positive cells were detected in right atrial tissue. There was a positive correlation between the level of CRP and the number of βD3-positive cardiomyocytes (rs 0.463; p 0.026). We found a negative correlation between the left ventricular ejection fraction and the number of βD2-positive cells in connective tissue (rs -0.524; p 0.012). Conclusions. The rich expression of antimicrobial peptides and its association with CRP support the idea that an inflammatory process is involved in the pathogenesis of acquired heart diseases. The worst preoperative condition is associated with increased antimicrobial peptide expression in the right atrial cells.
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Naloxone-precipitated morphine withdrawal evokes phosphorylation of heat shock protein 27 in rat heart through extracellular signal-regulated kinase
(Elsevier, 2011-04-17) Almela, P.; Martínez Laorden, Elena; Atucha, N.M.; Laorden Carrasco, María Luisa; Milanés Maquilón, María Victoria; Farmacología; Facultades de la UMU
Heat shock protein 27 (Hsp27) is a well-known stress response protein that becomes phosphorylated through extracellular signal-regulated kinase (ERK). Different drugs of abuse, such as morphine and/or its withdrawal, induce severe stress situations. In this study, we investigated Hsp27 and phospho-Hsp27 expression during morphine dependence and withdrawal and evaluated the involvement of ERK in the phosphorylation of Hsp27 in the rat right ventricle. Dependence on morphine was induced by a 7-day s.c. implantation of morphine pellets. Morphine withdrawal was precipitated on day 8 by injection of naloxone (2 mg/kg, s.c.). ERK1/2, Hsp27 and phospho-Hsp27 at Ser15 were determined by quantitative blot immunolabeling using specific antibodies. Hsp27 expression was increased 30, 60, 90 and 120 min (144.5 ± 14.2%, P < 0.0001; 128.9 ± 4.6%, P = 0.04; 177.4 ± 12.7, P < 0.0001; and 136.2 ± 11.0%, P = 0.042, respectively) after saline injection to rats dependent on morphine. Naloxone-precipitated morphine withdrawal also increased the phosphorylation of Hsp27 at Ser15 at those time points (146.8 ± 19.8%, P = 0.034; 143.9 ± 17.9%, P = 0.032; 161.2 ± 33.3%, P = 0.029; and 152.2 ± 25.5%, P = 0.008, respectively). However, there were no changes in Hsp27 phosphorylation in the morphine dependent group injected with saline. In addition, there was an increase in the phosphorylation of ERK 60 min after naloxone injection in morphine dependent rats (pERK1: 116.3 ± 4.2%, P = 0.015 and pERK2: 117.2 ± 1.5%, P = 0.05). Pretreatment with SL327, an inhibitor of ERK phosphorylation, decreased activation (phosphorylation) of both ERK and Hsp27 (pERK1: 4.5 ± 3.6%, P < 0.0001; pERK2: 42.3 ± 3.3%, P < 0.0001; and pHsp27: 97.6 ± 1.5%, P = 0.008), suggesting that ERK activation triggers Hsp27 phosphorylation. The present findings demonstrate that morphine withdrawal is capable of inducing the activation of Hsp27 in the heart and suggest that phosphorylation of Hsp27 is closely linked to and also dependent on the ERK pathway.
Open Access
Nuclear relocation of DGKζ in cardiomyocytes under conditions of ischemia/reperfusion
(F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Akiyama, Hideyuki; Hozumi, Yasukazu; Nakano, Tomoyuki; Kubota, Isao; Goto, Kaoru
Diacylglycerol (DG) and phosphatidic acid (PA) are generated under various conditions, such as ligand stimulation and several stresses. They serve as second messengers to respond to pathophysiological conditions. DG kinase (DGK) catalyzes DG to produce PA. It is regarded as a regulator of these lipid messengers. Previous studies show that DGKζ, a nuclear isozyme, translocates from the nucleus to the cytoplasm in hippocampal neurons under transient ischemia and never relocates to the nucleus after reperfusion. This study examined whether a similar phenomenon is observed in cardiomyocytes, which represent another type of postmitotic, terminally differentiated cell. We performed immunostaining on ischemic hearts induced by occlusion of the left anterior descending coronary artery and on primary cultured cardiomyocytes under oxygen-glucose deprivation (OGD). In the animal model, 10 min ischemia is sufficient to cause DGKζ to disappear from the nucleus in cardiomyocytes. However, DGKζ is observed again in the nucleus at 10 min following reperfusion after 10 min ischemia, which contrasts sharply with ischemic hippocampal neurons. Similar results were obtained from experiments using primary cultured cardiomyocytes under OGD conditions, except that DGKζ relocates autonomously, if at all, to the nucleus, even under continuous OGD conditions. Results suggest that DGKζ is involved in the acute phase of cellular response to ischemic stress in cardiomyocytes in a similar, but not identical, manner to that of neurons.
Open Access
The heart of the killer whale: description of a plastinated specimen and review of the available literature
(MDPI, 2022-01-31) Latorre Reviriego, Rafael Manuel; Graïc, Jean Marie; Raverty, Stephen A.; Soria Gálvez, Federico; Cozzi, Bruno; López Albors, Octavio Miguel; Anatomía y Anatomía Patológica Comparada
The killer whale (Orcinus orca, Linnaeus, 1958) is the largest extant delphinid. Despite its worldwide distribution in the wild and in dolphinariums, its anatomy remains relatively poorly described. In the present study, we describe the detailed morphology of a plastinated killer whale heart. The gross description of the arteries and veins reaching the organ and its coronary vessels are reported. Additional endoscopy and CT (computed tomography) scanning were performed to provide extensive measurements of its parts. In many aspects, the killer whale heart conformed to other delphinid heart descriptions, including position, relative size and shape and specific features such as extensive papillary muscles, trabecular endocardium and trabecula septomarginalis. These characteristics are representative of the delphinid family, suggesting that its functions and capacities are similar to that of other, smaller, dolphins and help understand the conditions in which these predators exert their remarkable physical performance necessary for their survival.