Impulse flow in sympathetic efferents of the abdominal aortic nerve after intrathecal administration of the substrate and inhibitor of nitric oxide synthase.

Experiments were performed on rats anesthetized with urethane and nembutal. Intrathecal administration of a nitric oxide inhibitor L-NAME (60 mg) into the cerebrospinal fluid of the thoracic spinal cord was followed by a 40-45% decrease in tonic activity of efferent fibers of the abdominal aortic nerves. L-NAME reduced a reflex increase in the rate of efferent impulses, which was induced by tetanic stimulation of afferent C-fibers in the mesenteric nerve.

Intracerebroventricular administration of creatine protects against damage by global cerebral ischemia in rat.

Although a large body of evidence shows that pretreatment of brain tissue with creatine protects against anoxic injury in vitro, only a couple of papers have investigated creatine protection in vivo, and they yielded conflicting results. We attempted to clarify how creatine may be protective in an in vivo model of global cerebral ischemia (GCI). We administered creatine either before of after GCI.

Structural organization of astrocytes in the rat hippocampus in the post-ischemic period.

The aim of the present work was to study the location and structural organization of astrocytes in the rat hippocampus, which contain immunoreactive glial fibrillary acid protein (GFAP) after ischemic damage to the brain after intracerebroventricular administration of the neuroprotective agent creatine and without treatment. Light microscopy and immunocytochemical methods were used to study the brains of 26 adult male Sprague-Dawley (Koltushi) rats, some of which were subjected to total cerebral ischemia (12 min) under anesthesia with subsequent reperfusion (seven days). Creatine was given to 11 animals intracerebroventricularly using an osmotic pump (Alzet Osmotic Mini-Pump).

[Concentration of hydrochloric acid and pepsin in gastric juice in dogs after starvation and refeeding].

Feeding fogs with meat after a 3-day period of starvation increased hydrochloric acid concentration with subsequent return of the parameter to normal values. Under the same conditions, pepsin concentration decreased and raised up after re-feeding. Histamine administration following the starvation decreased hydrochloric acid concentration with subsequent normalising.