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  • Book
    edited by Joaquín S. Lucena, Pablo García-Pavía, M. Paz Suarez-Mier, Luis A. Alonso-Pulpon.
    Summary: This atlas reviews the spectrum of pathologies affecting the structures of the cardiovascular (CV) system most frequently encountered in sudden cardiac deaths, and has been conceived as a first step for making CV pathology diagnoses. It is almost impossible to establish an accurate diagnosis based only on morphology, and therefore this atlas is to assemble knowledge and points of view from two medical specialties, cardiology and forensic pathology. It has been designed as a practical visual reference that includes a summary of clinical characteristics, many high quality images and clear tables containing the main morphological characteristics of each disease. Clinico-Pathological Atlas of Cardiovascular Diseases has been written by cardiologists and forensic pathologists and histopathologists, which enables a combination approach in each chapter, to produce a thorough resource that will be of relevance to a wide range of specialists, including cardiologists, cardiac surgeons, interventional cardiologists, forensic doctors, and pathologists.

    Contents:
    Methodology of cardiovascular autopsy
    Pulmonary Artery Pathology.- Pathology of Aorta
    Pathology of the pericardium.- Coronary atherosclerotic disease.- Non-atherosclerotic coronary disease
    Valve Pathology
    Cardiomyopathies
    Cardiac system pathology
    Cardiovascular pathology secondary to consumption of ethanol, drugs of abuse and medicaments
    Cardiac tumors.
    Digital Access Springer 2015
  • Article
    Minota S, Koketsu K.
    Jpn J Physiol. 1978;28(6):799-806.
    In a certain group (type 2 cells) of bullfrog sympathetic ganglion cells, an action potential exhibiting a triphasic after-potential was produced when the cells were activated by direct intracellular stimulation. This triphasic after-potential consisted of two different potential components, namely, a depolarizing response (DR) and an after-hyperpolarization. The amplitude of DR was increased by increasing the interval between stimuli. Large DRs exceeded the threshold of the cell membrane and produced repetitive firings of spike potentials. The DR was selectively depressed and eventually eliminated in a low-Ca solution. Eserine (10(-5) M) reversibly increased both the amplitude and duration of the DR, and d-tubocurarine reversibly depressed it. These results indicate that the DR of type 2 cells is the EPSP mediated by the nicotinic action of acetylcholine released from preganglionic nerve terminals. Preganglionic nerve fibers innervating type 2 cells are activated through some kind of recurrent pathway formed between them. Recurrent activation of type 2 cells seems to be thus induced when the cells are activated by direct intracellular stimulation.
    Digital Access Access Options