Spinal cord injury results in a permanent neurological deficit due to tissue damage. Such a lesion is a barrier for “communication” between the brain and peripheral tissues, effectors as well as receptors. One of the primary goal s of tissue engineering is to bridge the spinal cord injury and re-establish the damaged connections. Hydrogels are biocompatible implants used in spinal cord injury repair. They can create a permissive environment and bridge the lesion cavities by providing a scaffold for the regeneration of neurons and their axons, glia and other tissue elements. The advantage of using artificial materials is the possibility to modify their physical and chemical properties in order to develop the best implant suitable for spinal cord injury repair. As a result, several types of hydrogels have been tested in experimental studies so far. We review our work that has been done during the last 5 years with various types of hydrogels and their applications in experimental spinal cord injury repair., A. Hejčl, P. Lesný, M. Přádný, J. Michálek, P. Jendelová, J. Štulík, E. Syková., and Obsahuje bibliografii a bibliografické odkazy
Neurogenic pulmonary edema is a life-threatening complication, known for almost 100 years, but its etiopathogenesis is still not completely understood. This review summarizes current knowledge about the etiology and pathophysiology of neurogenic pulmonary edema. The roles of systemic sympathetic discharge, central nervous system trigger zones, intracranial pressure, inflammation and anesthesia in the etiopathogenesis of neurogenic pulmonary edema are considered in detail. The management of the patient and experimental models of neurogenic pulmonary edema are also discussed., J. Šedý, J. Zicha, J. Kuneš, P. Jendelová, E. Syková., and Obsahuje bibliografii a bibliografické odkazy
The development of neurogenic pulmonary edema (NPE) can be elicited by an immediate epidural balloon compression of the thoracic spinal cord. To evaluate whether a slower balloon inflation could prevent NPE development, we examined the extent of NPE in animals lesioned with a rapid (5 μl - 5 μl - 5 μl) or slow rate (3 μl - 2 μl - 2 μl - 2 μl - 2 μl - 2 μl - 2 μl) of balloon inflation. These groups were compared with the NPE model (immediate inflation to 15 μl) and with healthy controls. Slow balloon inflation prevented NPE development, whereas the pulmonary index and histology revealed a massive pulmonary edema in the group with a rapid rate of balloon inflation. Pulmonary edema was preceded by a considerable decrease in heart rate during the inflation procedure. Moreover, rapid inflation of balloon in spinal channel to either 5 μl or 10 μl did not cause NPE. Thus, a slow rate of balloon inflation in the thoracic epidural space prevents the development of neurogenic pulmonary edema, most likely due to the better adaptation of the organism to acute circulatory changes (rapid elevation of systemic blood pressure accompanied by profound heart rate reduction) during the longer balloon inflation period. It should be noted that spinal cord transection at the same level did not cause neurogenic pulmonary edema., J. Šedý ... [et al.]., and Obsahuje seznam literatury