Reduction of hyperthermic ischemic acidosis by a conditioning event in cats.

Abstract

We investigated the effects of multiple episodes of cerebral ischemia on intracellular brain pH using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy. Four cats were subjected to two 16-minute episodes of complete global cerebral ischemia 6 hours apart; the second episode occurred under hyperthermic conditions (mean +/- SD body temperature 40.8 +/- 0.4 degrees C). Intracellular pH in these four cats was compared with that in nine cats subjected to a single 16-minute episode of complete global cerebral ischemia under hyperthermic conditions (mean +/- SD body temperature 40.6 +/- 0.2 degrees C). Intracellular pH during hyperthermic recirculation was significantly (p less than 0.03) greater in cats subjected to a previous ischemic event than that in cats subjected to only a single hyperthermic ischemic event. We speculate that the induction of heat shock proteins by an initial ischemic event may protect brain tissue from further ischemic insult.

The temporal profile of 72-kDa heat-shock protein expression following global ischemia

“…Our data present essentially the opposite picture. Nonetheless, these findings do not exclude the possibility that induction of HSP72 prior to ischemia will reduce subsequent cell injury (Chopp et al, 1989).…”

Altered epithelial density and expansion of bulbar projections of a discrete HSP70 immunoreactive subpopulation of rat olfactory receptor neurons in reconstituting olfactory epithelium following exposure to methyl bromide

“…In contrast to possible stress‐induced de novo HSP70 expression, the possibility of HSP70‐enhanced 2A4(+)ORN survival is strongly supported by the impact of elevated stress protein levels on cell death (e.g., Li and Werb, 1982; Li and Laszlo, 1985; Johnson and Kucey, 1988; Riabowol et al, 1988; Rordorf et al, 1991; Beckmann et al, 1992; Sato et al, 1996; Bellmann et al, 1996). Reduction of stress‐induced cell death by prior stress exposure, whether of the same or a different type of physiological stress, is well documented (see, e.g., Barbe et al, 1988; Chopp et al, 1989; Lowenstein et al, 1991; Feder et al, 1996; Wagstaff et al, 1998). Importantly, the reduced mortality is related to enhanced HSP70 levels induced by the initial stress.…”

Retinal Ganglion Cell Protection with Geranylgeranylacetone, a Heat Shock Protein Inducer, in a Rat Glaucoma Model

“…These proteins function under normal, developmental, and stressful conditions. 4 The induction of HSP72 in the mammalian central nervous system by hyperthermia has been associated with the neuronal tolerance to ischemic insults 7,8 and neuroprotective effects against light-induced injury in the rat retina. 9 Intracellular expression of HSP72 has been demonstrated to protect cerebral neurons against heat shock, 10 oxidative stress, apoptotic stimuli, 11 excitotoxic insults, [12][13][14] and ischemia-like conditions.…”