Insulin decreases circulating levels of IL-1p, IL-6, migration inhibitory factor, TNF-a, and increases levels of IL- 4 and IL-10 in thermally injured rats. In lipopo-lysaccharide-treated animals, insulin suppresses TNF-a in a dose-dependant manner. Furthermore, insulin reduces proinflammatory and increases antiinflammatory cytosolic signal transduction constituents. Insulin has been shown to enhance production of endothelial nitric oxide, suppress superoxide anion generation, and inhibit myocardial apoptotic death. Hence insulin appears to have antiinflammatory effects. Because of the local effects of insulin and through its suppression of FFAs, insulin infusions cause an increase in glucose uptake in both dysfunctional and normal myocardial regions.
Increased FFA levels are toxic to ischemic myocardium and are associated with increased membrane damage, arrhythmias, and decreased cardiac function. The anti-FFA effects of GIK may be especially beneficial in patients with high circulating levels of catecholamines, which increases serum FFA levels. Insulin infusions also increase the generation of adenosine triphosphate production from glycolysis. In the resting fasting state, glucose only accounts for approximately 30% of the energy production of the heart; suppression of FFA by insulin allows the myocardium to increase the utilization of glucose, which is a more efficient energy source. Why GIK infusions are beneficial in septic shock is unclear but is likely to involve a combination of antiinflammatory and metabolic mechanisms. http://birthcontroltab.com/buy-yasmin-online.html
Why GIK improved hemodynamics in our two patients is unclear. It is conceivable that patient 1 had unidentified coronary artery disease, and in a high output state myocardial energy demand was far greater than supply, hence supplementing the myocardium with glucose improved cardiac output. Although, there was no clear reduction in inotrope requirements on commencing antibiotics, it remains possible that some of the decrease in inotrope dose merely represented a response to antibiotic therapy. Both patients were adequately volume resuscitated by colloid, and GIK contributed to < 100 mL/h of the total volume load. This coupled with the magnitude and rate of response to GIK suggests that the hemodynamic improvements were unrelated to a simple volume-loading effect. “Tight” normoglycemic control is associated with improved mortality in intensive care and may have contributed to prolonged survival in the two described patients. However, mean and range of glucose levels were similar before and during GIK administration, suggesting a specific role for the combination of glucose, insulin, and potassium on the improvement in hemodynamic profile and withdrawal of inotropes.
We have described two cases of pressor-resistant hyp-odynamic septic shock that were possibly reversed by GIK.
The mechanism for this is unclear. Further evaluation of GIK in the management of pressor-resistant hypodynamic septic shock is necessary.