title: Partial prevention of calcium paradox in isolated perfused rat hearts by diltiazem.
abstract: It is well known that excessive calcium entry into the myocardial cells may contribute considerably to damage of the heart caused by postischemic reperfusion. The effect of increased calcium entry on hemodynamics, energy metabolism and histochemically estimated enzyme activities in isolated, perfused (Langendorff) rat heart preparation was investigated using calcium paradox (CaPX) as a model. After a 15 min period of stabilized perfusion of the heart, CaPX was induced at 37 degrees C by 2.5 min lasting calcium depletion (calcium-free perfusion) and subsequent calcium repletion (10 min). Changes induced by CaPX concerned loss of electrical and mechanical activities of the heart, significant decreases in coronary flow and ATP, ADP and the total content of adenine nucleotides in tissue as well as considerable depression in ATPases, SDH, beta-HBDH, LDH and glycogen phosphorylase activities in the myocardium. Diltiazem in concentration of 4.0 mumol.l-1 applied prior to calcium depletion and during calcium repletion prevented partially the deterioration of cardiac function by improving contractility and electrical activity of the heart as well as the coronary flow. The effect of diltiazem in concentration of 0.4 mumol.l-1 was less expressed. After both concentrations of diltiazem used, a better preserved ultrastructure, higher activities of the enzymes investigated, significantly higher ATP and total adenine nucleotide levels were seen in the myocardium as compared to the untreated controls.
authors.affiliation: Institute of Experimental Surgery, Slovak Academy of Sciences, Bratislava, Czechoslovakia.
authors.forename: A
authors.initials: A
authors.lastname: Ziegelhöffer
authors.forename: T
authors.initials: T
authors.lastname: Ravingerová
authors.forename: N
authors.initials: N
authors.lastname: Tribulová
authors.forename: J
authors.initials: J
authors.lastname: Slezák
authors.forename: J
authors.initials: J
authors.lastname: Okolicány
authors.forename: V
authors.initials: V
authors.lastname: Trégerová
authors.forename: E G
authors.initials: EG
authors.lastname: Krause
authors.forename: S
authors.initials: S
authors.lastname: Bartel
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002118:Calcium / Q000502:physiology*; D004110:Diltiazem / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects; D066298:In Vitro Techniques; D009200:Myocardial Contraction / Q000187:drug effects; D015425:Myocardial Reperfusion; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D000251:Adenosine Triphosphatases; D004110:Diltiazem; D002118:Calcium