Inactivation of kallikrein and kininases and stabilization of whole rat brain kinin levels following focused microwave irradiation.

Focused microwave irradiation was employed to stabilize endogenous whole rat brain bradykinin levels prior to a simple extraction procedure. Skull microwave exposure (2450 MHz, 3.8 kW., 2.45 sec) resulted in inactivation to less than 5% of control of whole brain kallikrein and kininase activity. Using this adequate exposure duration whole rat brain kinin levels as measured by a sensitive radioimmunoassay were approximately 0.6 pmol/g (wet weight). Further purification of irradiated brain extracts using HPLC revealed that immunoreactive kinin eluted as a single peak that co-chromatographed with authentic bradykinin. Microwave fixation duration of 1.25 sec yielded greatly increased levels of immunoreactive kinin which following HPLC purification eluted in two peaks, corresponding to authentic bradykinin and T-kinin, respectively. The tissue injury resulting from incomplete microwave fixation resulted in the release of kinins. This excess immunoreactive kinin may be derived from cerebral blood, since the predominant form of kinin-generating protein in plasma is T-kininogen.

The level of blood kinins, their creation and inactivation after one exposure to intense ultraviolet radiation in rabbits.

Experimental rabbits were exposed to ultraviolet radiation once for 45 minutes, and blood samples were obtained from the carotid artery in these animals 45 min and 3, 6 and 24 hours after the end of this exposure. In the group of control rabbits blood samples were obtained in the same way without previous exposure to radiation. The hairs on the back were cut closely at the skin and this skin area was exposed to ultraviolet rays from a Hanau Q 400 burner at 405--289 nm wavelengths and at an intensity of 134 000 erg/sec/cm2, using an UG 2 T Schott filtre and an absorber of long-wave radiation. Blood samples were taken under thiopental anaesthesia. In the samples the level of free kinins was determined in the blood, and the level of kininogen and the activity of kallikreins and kininases were determined in the plasma. In the irradiated animals a rise of the kinin level was observed, with a fall in the kininogen level most pronounced after 3 hours, while the activity of kallikreins was raised and that of kininases was decreased particularly after 6 hours.

Effect of long-term exposure of rabbits to ultraviolet radiation on the level, creation and inactivation of kinins in blood.

Experimental rabbits were exposed to ultraviolet radiation during 6 weeks once daily for 10 minutes (from a high-pressure. Hanau Q 400 mercury lamp with a Schott UG 2 T filtre and absorber of long-wave radiation using ultraviolet rays of 405--289 nm wavelength and 134 000 erg/sec/cm2 power, directed onto skin with cropped hair of the back). Under general anaesthesia with pentothal blood samples were obtained from the carotid artery in 4 groups of 8 rabbits in each group. The blood samples were taken from non-exposed control rabbits and from the experimental groups after 2, 4 and 6 weeks of exposure. In the samples the levels of free kinins in the blood, and kininogen, and the activity of kallikreins and kininases in the plasma were determined. In the irradiated animals a progressive rise of free kinins most pronounced after 6 weeks was observed, and other findings included: a fall of kininogen level particularly steep after 2 weeks, very small rise in the activity of kallikreins, and progressing reduction of the activity of kininase, particularly steep after 2 weeks.

The effect of dianabol on the postirradiation disturbances of kininogenesis in rats.

The effect of Dianabol on the irradiation-induced disturbances in kininogenesis in rats was studied. It was found that Dianabol inhibits the postradiation increase of the kininforming activity in tissues of rats and decreases the level of kinins in irradiated animals. A probable role of these properties of Dianabol in its radioprotective activity is discussed.