Download Myocardial Ischemia: From Mechanisms to Therapeutic by Dennis V. P. Cokkinos, C. Pantos, Gerd Heusch, H. Taegtmeyer PDF

By Dennis V. P. Cokkinos, C. Pantos, Gerd Heusch, H. Taegtmeyer

Great development has been made in figuring out the pathophysiology of ischemic middle sickness. for this reason, new healing methods for safeguarding the guts from ischemic damage are in improvement. This quantity will spotlight concerns referring to uncomplicated mechanisms of ischemia-reperfusion damage with regards to power healing innovations.

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Additional resources for Myocardial Ischemia: From Mechanisms to Therapeutic Potentials (Basic Science for the Cardiologist)

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Schematic of a Langendorff perftised rat heart model. Retrograde perfusion is established through the aorta. Perfusate oxygenated with 95% O2 and 5% COj is circulated by a peristaltic pump and the flow can be adjusted. Left ventricular pressure is monitored through a balloon which is inserted into the empty left ventricle. Heart rhythm is controlled by pacing. B. Recording of left ventricular developed pressure (LVDP is defined as the difference between systolic and diastolic left ventricular pressure) from Langendorff perfused heart after stabilization followed by complete flow cessation (zero-flow global ischemia) and flow re-establishment (reperfusion).

Figure 8. c) Receptors (GPCRs) which are coupled, inside the cell, to GTP-binding and hydrolyzing proteins, collectively termed G-proteins. g p^-adrenergic or P2-adrenergic receptor. Figure 10. Table 1. c-AMP diffuses to protein kinase A (PKA) which phosphorylates glycogen synthase, phosphorylase and the trancription factor CREB (transcribes genes for gluconeogenesis). ERK or Akt intracellular signaling can be regulated through receptors bound to Gi. Figure 9. g PIP2) generating the second messengers diacylglycerol (DAG) and inositol-triphosphate (IP3).

COKKINOS Voltage (mV) Voltage (mV) +10-10 - -30-50 NormoxJa +10-1 k^^ ,^^^^^ '""^^ \ -10 -30 \ -70-90 a-' t Duration Ischemia -50 -70-j -90Duration Figure 6. Resting membrane potential under normoxia (left) and ischemia (right). Increased outward potassium current during ischemia causes shortening of the resting membrane potential. Potassium currents activated under physiological conditions are inhibited under ischemia and several other new channels come to the operation (IK^^p, IK^^, IK^p^). Resting membrane potential is less negative due to the increased extracellular potassium and inward currents.

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