The effect of alpha and beta adrenergic blockade on Ni induced coronary spasm in scalded rats.
After 20% total body surface scalding inducing 3d degree burn in rats the following parameters were studied in ebb and flow phases, as well as in burn disease, 2 hours, 2 and 7 days postburn: atomic absorption spectrophotometric study of the serum and myocardial Ni levels; the effect of Ni ions (10(-8)-10(-4) M/l) in vitro on total coronary resistance in the isolated perfused rat heart; the effect of alpha and beta adrenergic blocking agents (phenoxibenzamine, oxprenolol) on Ni-induced coronary vasoconstriction; electron cytochemical study of the ultrastructural changes of the myocardium 7 days after scalding. It was found that: During the first 2-3 hours after scalding or bleeding there was a significant elevation of serum Ni level which levelled off by the end of the first week. Total coronary resistance (TCR) increasing effect of Ni ions was significantly augmented during the first 2-3 hours after burn and bleeding (ebb phase). In the scalded group it decreased to the control value by the 2-3d day (flow phase) and increased again a week later (burn disease). In the scalded groups in vivo pretreatment with oxprenolol (10(-4) g/kg) completely inhibited the Ni induced coronary spasm. PBZ treatment in vitro (10(-5) M/l) had similar effect in the three postburn periods tested. Ultrastructural changes and intracellular Ni-dimetilglyoxim complexes could be detected. Oxprenolol treatment continuously applied from the 4th day postburn (2 X 0.5 mg/kg) prevented the development of myocardial damage, while the electron dense complexes containing Ni were still detectable. In view of our previous data we assume that the endogenous Ni increase in the serum after burn may be cardiopathogenic. The phasic changes of the sensitivity of the coronary vessels to Ni ion and the similarity of the effects of alpha and beta adrenergic blocking agents may be explained by the alterations in the neuroendocrine system and metabolic disturbances.
D000818:Animals; D002056:Burns / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D003329:Coronary Vasospasm / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D009532:Nickel / Q000378:metabolism / Q000494:pharmacology*; D010096:Oxprenolol / Q000494:pharmacology; D010643:Phenoxybenzamine / Q000494:pharmacology; D051381:Rats; D013565:Sympatholytics / Q000494:pharmacology*; D014655:Vascular Resistance / Q000187:drug effects
D013565:Sympatholytics; D010643:Phenoxybenzamine; D010096:Oxprenolol; D009532:Nickel