By H. Zhang (auth.), Prof. Antonino Gullo M.D. (eds.)
The administration of seriously ailing sufferers has,in the previous few years, been a self-discipline on the leading edge of improvement which keeps to make development with the aid of uncomplicated and scientific learn within the broadest experience. the appliance of biotechnology during this specific quarter has printed itself to be crucial in an try to give you the most sensible interpretation of the bio-humoral and sensible changes found in a protracted sequence of frequently complicated scientific stipulations. The care of the significantly sick can be on the leading edge within the software of more and more subtle medical tracking platforms that still give a contribution to standardizing definite approaches, identify guidance, and evaluation the efficacy of healing interventions and their costs.
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Extra resources for Anaesthesia, Pain, Intensive Care and Emergency Medicine - A.P.I.C.E.: Proceedings of the 12th Postgraduate Course in Critical Care Medicine Trieste, Italy - November 19–21, 1997
Henderson JL, Statman R. Cunnigham IN et al ( 1994) The effects of nitric oxide inhibition on regional hemodynamics during hyperdynamic endotoxemia. Arch Surg 129: 1271-1275 30. Pastor CM. Payen DM ( 1994) Effect of modifying nitric oxide pathway on liver circulation in a rabbit endotoxin shock model. Shock 2: 196-202 31. Wang Y. Mathews WR, Guido DM et al (1995) Inhibition of nitric oxide synthesis aggravates reperfusion injury after hepatic ischemia and endotoxemia. Shock 4:282-288 32. Nishida J.
Schumacker PT, Kazaglis J, Connolly HV et al (1995) Systemic and gut O2 extraction during endotoxemia: role of nitric oxide synthesis. Am J Respir Crit Care Med 151: 107-115 100. Zhang H, Nguyen DN, Spapen H et al (1995) Sodium nitroprusside does not influence tissue oxygen extraction capabilities during a critical reduction in oxygen delivery. Cardiovasc Res 30:240-245 101. Payne D, Kubes P (1993) Nitric oxide donors reduce the rise in reperfusion-induced intestinal mucosal permeability. Am J Physiol265:G 189-G 195 102.
The resulting overproduction of inducible NO (iNOS) may exert deleterious hemodynamic effects including arterial hypotension , vascular hyporeactivity and myocardial depression  and or directly induce cellular damage . A number of investigators studied the role of NO by administering either NO blockers or NO donors during septic shock. This review will briefly summarize some experimental data on the use of NO antagonists and NO agonists during septic shock. Effects of NO antagonists Increased production of NO in sepsis has been well demonstrated both in animals and humans [4-10].
Anaesthesia, Pain, Intensive Care and Emergency Medicine - A.P.I.C.E.: Proceedings of the 12th Postgraduate Course in Critical Care Medicine Trieste, Italy - November 19–21, 1997 by H. Zhang (auth.), Prof. Antonino Gullo M.D. (eds.)