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These results indicate that Neiguan EA may improve cardiac function by modulating neurons in the RVLM and the SON in surgically traumatized rats.
Based on our preliminary results, we may conclude that both EP and OD regimens may improve cardiac performance and age related dysfunctions.
They also suggest that glutathione supplementation may improve cardiac cell preservation in cardiac diseases, and be a complement to contemporary treatments.
Conversely, use of ASA in the chronic phase of disease may improve cardiac function suggesting the same COX-1 products that mediate host-survival during the acute disease are likely to contribute to the progression of cardiac damage and heart failure in the chronic phase.
Inhaled nitric oxide may improve cardiac function via extrapulmonary effects.
Therefore, HS may improve cardiac contractile function via maintenance of intracellular Ca2+ homeostasis.
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Previous evidence has suggested that high-dose allopurinol may be associated with reduced risk of mortality and cardiovascular events through its patho-physiological pathway [ 16] by the following two mechanisms: higher doses of allopurinol may have an increased ability to improve endothelial function; and higher doses may also improve cardiac structure [ 17].
IGF-1 may also improve cardiac function in diabetic patients [ 41- 45] and rat models of myocardial infarction and reperfusion [ 26].
Moreover, recent studies using animal species and in humans have provided accumulating evidence suggesting that mild therapeutic hypothermia may also improve cardiac performance [ 5, 6].
Those investigators concluded that hypertonic saline/dextran solution improved cardiovascular performance and resuscitated severely septic patients through a volume effect, but may also directly improve cardiac function.
As demonstrated recently [ 32, 53], GIK infusion may salvage myocardium, improve cardiac function, and decrease mortality by an absolute 10%, provided that hyperglycemia is prevented.
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