Paulo Roberto B ÉvoraI; Paul J PearsonII; Marilyn OeltjenII; Berent DiscigilII; Hartzell V SchaffII
DOI: 10.1590/S0102-76381996000200010
RESUMO
O presente ensaio experimental estudou o efeito da infusão de solução cardioplégica cristalóide a altas pressões sobre a função endotelial de artérias epicárdicas de cães. Não se encontraram alterações a nível de receptores (curvas dose-respostas à ACH e ADP; da transdução do sinal iniciado nos receptores/sitema de G-proteínas (fluoreto de sódio) e nos processos intracelulares da produção de EDRF/ NO (fosfolipase C e ionóforo do cálcio A23187). A função da musculatura lisa vascular não foi afetada quando se analisaram as respostas relaxantes (nitroprussiato de sódio e isoproterenol) e contrateis (KCI e prostaglandina 2alfa). Estes achados permitem as seguintes considerrações especulativas: a) O barotrauma produzido pela infusão da cardioplegia cristalóide a altas pressões ocorreria apenas em circulações coronarianas previamente doentes? b) Uma vez que as infusões duraram de 2 a 3 minutos, seria o barotrauma coronariano um fenômeno dependente do tempo de infusão? c) Para que ocorra o barotrauma seriam necessários níveis mais elevados de potássio? d) Questionar a existência do fenômeno do barotrauma coronariano produzido pela infusão de soluções cadioplégicas pelo menos nas condições experimentais utilizadas, e) A metodologia empregada estuda apenas as reatividades vasculares de artérias coronárias epicárdicas. Estas artérias seriam menos sensíveis aos efeitos da pressão de infusão da cardioplegia do que a microcirculação coronariana? f) Seria a circulação coronária do cão menos sensível a altas pressões do que do homem? Estas observações experimentais sugerem que a infusão de cardioplegia cristalóide, moderadamente hipocalêmica, a altas pressõe em um tempo de 2 a 3 minutos, não interfere com a produção de EDRF/NO pelo endotélio de coronárias epicárdicas do cão.ABSTRACT
Experiments were performed in "organ chambers" to investigate if high pressures infusions of crystalloid cardioplegia effect the endothelium function of epicardic canine coronary arteries. These experiments did not show any alterations at level of receptors (dose-response curves to ACH and ADP); signal transduction/G-proteins (dose-response curve to sodium fluoride); intracellular mechanisms of the EDRF/NO release (dose-response curves to phospholipase C and calcium ionophores A23187). The smooth muscular relaxant function (dose-response curves to sodium nitroprusside and isoproterenol) and contarctions (doseresponse curves to KCI and PGF2alpha) were also preserved. These experimental observations allow the following speculative considerations: a) Should barotrauma be a phenomenon present only in damaged coronary circulation? b) All infusion were performed in no more than two or three minutes. Is cardioplegia barotrauma a phenomenon time-dependente? c) High levels of potassium could be associated with barotrauma, d) Cardioplegia barotrauma is a fancy, at least in our experimental conditions? e) Experiments in "organ chambers" study only epicardic arteries. Could barotrauma damage the microcirculation? f) The canine coronary circulation is less affeccted by high pressure than human coronaries? These data are suggestive that crystalloid moderately hyperkalemic infusions at high pressures for two or three minutes, do not impair the endothelium release of EDRF/NO of canine epicardic coronary arteries.REFERÊNCIAS
1. Chiavarelli R, Macchiarelli G, Familiari G et al. - Ultrastructural changes of coronary artery endothelium induced by cardioplegic solutions. Thorac Cardiovasc Surgeon 1989; 37: 151-7.
2. Harjula A, Mattila S, Myllarniemi H et al. - Effects of synthetic blood and crystalloid cardioplegia solutions on coronary end lium: an experimental scanning electron microscopic study. J Surg Res 1985; 39: 405-12. [MedLine]
3. Molina J E, Galliani C A, Einzig S, Bianco R, Rasmussen T, Clack R - Physical and mechanical effects of cardioplegic injection on flow distribution and myocardial damage in hearts with normal coronary arteries. J Thorac Cardiovasc Surg 1989; 97: 870-7. [MedLine]
4. Kontos H A & Wei E P - Reversal of acetylcholineinduced cerebral vasodilation in acute hypertension Microvasc Res 1985; 29: 231-2.
5. Furchgott R F & Zawadski J V - The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature 1980; 228: 373-6.
6. Furchgott R F - Studies on relaxation of rabbit aorta by sodium nitrite: the basis for the proposal that the acid-activated inhibitory factor from bovine retractor penis is inorganic nitrite and the endothelium-derived relaxing factor is nitric oxide. In: Vanhoutte PM ed. Mechanisms of vasodilatation, New York, Raven Press 1988. Vol IV, p. 401-14.
7. Ignarro L J, Byrns R E, Wood K S - Biochemical and pharmacological properties of EDRF and its similarity to nitric oxide radical. In: Vanhoutte PM (ed.) Mechanisms of vasodilatation, New York, Raven Press 1988; Vol IV, p. 427-35.
8. Palmer R M J, Ashton D S, Moncada S - Vascular endothelial cells synthesize nitric oxide from L-arginine. Nature 1988; 333: 664-6. [MedLine]
9. Carpentier S, Murawsky M, Carpentier A - Cytotoxicity of cardioplegic solutions: evaluation by tissue culture. Circulation 1981; 64 (Supl 2): 90-5.
10. Solberg S, Larsen T, Lindal S, Prydz P, Jorgensen L, Sorlie D - The effects of two different crystalloid cardioplegic solutions on cultured human endothelial cells. J Cardiovasc Surg 1989; 30: 669-74.
11. Saldanha C & Hearse D J - Coronary vascular responsiveness to 5-hydroxytryptamine before and after infusion of hyperkalemic crystalloid cardioplegic solution in the rat heart. J Thorac Cardiovasc. Surg 1989; 98: 783-7. [MedLine]
12. Evora P R B, Pearson P J, Schaff H V - Crystaloid cardioplegia and hypothermia do not impair endothelium-dependent relaxation or damage vascular smooth muscle of epicardial coronary arteries. J Thorac Cardiovasc Surg. 1992; 104: 1365-74. [MedLine]
13. Evora P R B - O impacto científico da descoberta do óxido nítrico como vasodilatador e antitrombótico endógeno (Editorial). Arq Bras Cardiol 1993; 61: 3-5. [MedLine]
14. Evora P R B, Pearson P J, Schaff H V - Impaired endothelium-dependent relaxation to sodium fluoride following coronary reperfusion: evidence for G-protein dysfunction. Circulation 1991; 84 (Supl 2): 275. [MedLine]
15. Flavahan N A & Vanhoutte P M - Pertussis toxin inhibits endothelium-dependent relaxations evoked by fluoride. Eur J Pharmacol 1990; 178: 121-4. [MedLine]
16. De Nucci G, Gryglewski R J, Warner T D, Vane J R - Receptor-mediated release of endothelium-derived relaxing factor and prostacyclin from bovine aortic endothelial cells is coupled. Proc Natl Acad Sci (USA) 1988; 85: 2334-8.
Article receive on terça-feira, 2 de abril de 1996