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Intracellular sodium during ischemia and calcium-free perfusion: A 23Na NMR study on isolated rat hearts
J Mol Cell Cardiol20
(Supplement
V) (1988)
FR-JINTRACELLULAR SODIUM DURING ISCHEMIA AND CALCIUM-FREE PERFUSION: A 23Na NMR STUDY ON C.J.A. van Echteld, J.H. Kirk&s, P. van der Mew, T.J.C. ISOLATED RAT HEARTS. Interuniversity Cardiology Institute of The Netherlands and Ruigrok, F.L. Meijler. Department of Cardiology, University Hospital, Utrecht, The Netherlands. Intracellular sodium (Nat) accumulation during both ischemia and calcium-free perfusion has been suggested t8 play an important role in reyerfusion damage and the calcium paradox through Na-Ca exchange. However, data on [Na 1. are scarce and show considerable variation. Therefore we have measured [Na+]. in ikolated, Langendorff perfused rat hearts (370Cp375 mmHg) during total ischemi.& (30 min) and calcium-free perfusion (30 min) using Na NMR spectros?opy. Na. was distinguished from extracellular Na+ by adding the shift reagent DyTTHA (10 mh) to the perfusion fluids. [Na+]. during control perfusion was difficult to assess and was estimated to be
time (mM)
(min)
5 5.9
10 11.9
On the other hand, no increase in [Na+]. perfUSiOn. Cellular calcium accumulatioft fore well be mediated by Na-Ca exchange, a minor role during the calcium paradox.
15 15.3
20 18.1
25 19.3
30 22.9
was observed during 30 min of calcium-free during post-ischemic reperfusion may therewhereas this exchange mechanism can only play
FR-~ENDXWELIUM =VAL IN ~F~NARY RESISTANCE VESSELS OF ISOI&I'ED GUINEA-PIG HEAKI?~: HIS'IOJA3.XCALANDFUNCYIONALRESLJLTS Research, Dr. Karl Thomae E. Wiest, J. Schaper*, V. Trach. Department of Biological QnbH, Biberach; Coax Planck Institut, Bad Nauheim, West Germany. Studies on the influence of the endothelium (E) on coronary resistance vessels are limited to blocking effects on EDRF. Therefore we treated isolated guinea-pig (GP) hearts with Saponin (S) to eliminate total endothelial cell function and examined E-mcdulatiq effects on coronary flow (CF) regulation after challenge with different vasoactive agents. The hearts were perfused according to the Langendorff mode. E was removed by S-treatment (50 *g/ml) over 2 min. Bolus-administration of histamine and serotonin resulted in a CF increase before treatment ard a decrease after treatment. CF response to angiotensin I was attenuated whereas angiotensin II and Na-nitroprusside response remained unchanged. Electron microscopic examination of the hearts revealed a disruption of E in the coronary arteries without affecting smooth muscle and myccardium. Thus, S treatmsnt of isolated perfused GP hearts leads to a functional change of CF regulation similar to that seen after rmval of E in isolated vessels and therefore suggests an interesting approach to study the influence of E on CF-regulation in the intact heart.
S.18
(Supplement
V) (1988)
FR-JINTRACELLULAR SODIUM DURING ISCHEMIA AND CALCIUM-FREE PERFUSION: A 23Na NMR STUDY ON C.J.A. van Echteld, J.H. Kirk&s, P. van der Mew, T.J.C. ISOLATED RAT HEARTS. Interuniversity Cardiology Institute of The Netherlands and Ruigrok, F.L. Meijler. Department of Cardiology, University Hospital, Utrecht, The Netherlands. Intracellular sodium (Nat) accumulation during both ischemia and calcium-free perfusion has been suggested t8 play an important role in reyerfusion damage and the calcium paradox through Na-Ca exchange. However, data on [Na 1. are scarce and show considerable variation. Therefore we have measured [Na+]. in ikolated, Langendorff perfused rat hearts (370Cp375 mmHg) during total ischemi.& (30 min) and calcium-free perfusion (30 min) using Na NMR spectros?opy. Na. was distinguished from extracellular Na+ by adding the shift reagent DyTTHA (10 mh) to the perfusion fluids. [Na+]. during control perfusion was difficult to assess and was estimated to be
time (mM)
(min)
5 5.9
10 11.9
On the other hand, no increase in [Na+]. perfUSiOn. Cellular calcium accumulatioft fore well be mediated by Na-Ca exchange, a minor role during the calcium paradox.
15 15.3
20 18.1
25 19.3
30 22.9
was observed during 30 min of calcium-free during post-ischemic reperfusion may therewhereas this exchange mechanism can only play
FR-~ENDXWELIUM =VAL IN ~F~NARY RESISTANCE VESSELS OF ISOI&I'ED GUINEA-PIG HEAKI?~: HIS'IOJA3.XCALANDFUNCYIONALRESLJLTS Research, Dr. Karl Thomae E. Wiest, J. Schaper*, V. Trach. Department of Biological QnbH, Biberach; Coax Planck Institut, Bad Nauheim, West Germany. Studies on the influence of the endothelium (E) on coronary resistance vessels are limited to blocking effects on EDRF. Therefore we treated isolated guinea-pig (GP) hearts with Saponin (S) to eliminate total endothelial cell function and examined E-mcdulatiq effects on coronary flow (CF) regulation after challenge with different vasoactive agents. The hearts were perfused according to the Langendorff mode. E was removed by S-treatment (50 *g/ml) over 2 min. Bolus-administration of histamine and serotonin resulted in a CF increase before treatment ard a decrease after treatment. CF response to angiotensin I was attenuated whereas angiotensin II and Na-nitroprusside response remained unchanged. Electron microscopic examination of the hearts revealed a disruption of E in the coronary arteries without affecting smooth muscle and myccardium. Thus, S treatmsnt of isolated perfused GP hearts leads to a functional change of CF regulation similar to that seen after rmval of E in isolated vessels and therefore suggests an interesting approach to study the influence of E on CF-regulation in the intact heart.
S.18