OBJECTIVE: Keratin proteins have been utilized as biomaterials for decades, and are currently under investigation for a variety of tissue regeneration and trauma applications. It has been suggested that certain keratins may have the capacity to act as a colloid in fluid resuscitation applications, providing viscosity and oncotic properties that may be beneficial during acute ischemic events. Oxidized keratin derivatives, also known as keratoses, show good blood and cardiovascular compatibility and thus are the subject of this study. METHODS: The effects of keratose compounds will be assessed using a topload i.v. infusion model and observation of changes in the microvasculature of the cremaster muscle of rats. RESULTS: Keratose resuscitation fluid (KRF) administration resulted in significant vasodilation in the cremaster muscle. This effect was blocked with pretreatment of l-NA to inhibit NO. Another keratin fraction, alpha-keratose, which is the primary viscosic compound, was not found to induce vasodilation. CONCLUSIONS: The apparent mechanism of vasodilation was found to be NO-mediated and isolated to a particular purified fraction, the KAP.
OBJECTIVE: Keratin proteins have been utilized as biomaterials for decades, and are currently under investigation for a variety of tissue regeneration and trauma applications. It has been suggested that certain keratins may have the capacity to act as a colloid in fluid resuscitation applications, providing viscosity and oncotic properties that may be beneficial during acute ischemic events. Oxidized keratin derivatives, also known as keratoses, show good blood and cardiovascular compatibility and thus are the subject of this study. METHODS: The effects of keratose compounds will be assessed using a topload i.v. infusion model and observation of changes in the microvasculature of the cremaster muscle of rats. RESULTS: Keratose resuscitation fluid (KRF) administration resulted in significant vasodilation in the cremaster muscle. This effect was blocked with pretreatment of l-NA to inhibit NO. Another keratin fraction, alpha-keratose, which is the primary viscosic compound, was not found to induce vasodilation. CONCLUSIONS: The apparent mechanism of vasodilation was found to be NO-mediated and isolated to a particular purified fraction, the KAP.