By Zeljko J. Bosnjak, J. Thomas August, Joseph T. Coyle, M. W. Anders
Every one quantity of Advances in Pharmacology offers a wealthy number of experiences on well timed issues. quantity 31 offers with the mechanisms of anesthetic activities below basic stipulations in addition to pathophysiologic states.
* Covers anesthetics and cardiac function
* Addresses issues of the cardiovascular procedure and linked diseases
* Explains healing and pathophysiological implications
* info reflex legislation of peripheral circulation
* comprises complete descriptions of the newest methodologies
* Written by means of the world over famous specialists within the box of anesthesia learn
Read or Download Anesthesia and Cardiovascular Disease, Volume 31 PDF
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Additional info for Anesthesia and Cardiovascular Disease, Volume 31
Fluoride stimulation of slow Ca2+current in cardiac muscle. J . Mol. Cell. Cardiol. 9, 461-475. 20. , and Hofmann, F. (1982). Injection of subunits of cyclic AMP-dependent protein kinase into cardiac myocytes modulates Ca2+current. Nature (London) 298, 576-578. 21. , and Sperelakis, N. (1984). Injection of protein kinase inhibitor into cultured heart cells blocks calcium slow channels. A m . J. Physiol. 246, H630-H634. 22. , and Trautwein, W. (1986). On the mechanism of padrenergic regulation of the Ca2+channel in the guinea pig heart.
The muscle was depolarized in 22 mM [K], to voltage inactivate fast Na' channels. (A) Small graded response (stimulation rate 30imin). (B) Superimposed records showing the gradual appearance of slow APs on cAMP injection over a 25-sec period. (C) Presence of stable slow APs after injection for 1 min. (D) Gradual depression of slow APs over a period of 25 sec after stopping injection. (E) Complete decay of slow APs 30 sec after cessation of cAMP injection. All records are from one impaled cell. (Data from Ref.
Arrhythmias) of the heart. The slow Ca2+channels have some special properties, including functional dependence on metabolic energy, selective blockade by acidosis, and regulation by intracellular cyclic nucleotide levels. Because of these special properties of the slow channels, Ca2+influx into the myocardial cell can be controlled by extrinsic factors (such as autonomic nerve stimulation or circulating hormones) and by intrinsic factors (such as cellular pH or ATP level). The special properties also serve to protect the myocardial cells during periods of ischemia.
Anesthesia and Cardiovascular Disease, Volume 31 by Zeljko J. Bosnjak, J. Thomas August, Joseph T. Coyle, M. W. Anders