2 edition of effect of calcium antagonists on the normoxic and the ischaemic myocardium found in the catalog.
effect of calcium antagonists on the normoxic and the ischaemic myocardium
Jacqueline Geertruida Hugtenburg
Published
1989
by [s.n.] in Amsterdam
.
Written in English
Edition Notes
| Statement | Jacqueline Geertruida Hugtenburg. |
| Classifications | |
|---|---|
| LC Classifications | QP113.2 .H84 1989 |
| The Physical Object | |
| Pagination | 159 p. : |
| Number of Pages | 159 |
| ID Numbers | |
| Open Library | OL14930707M |
| ISBN 10 | 9051700180 |
Protective Effect of Pretreatment with the Calcium Antagonist Anipamil on the Ischemic-Reperfused Rat Myocardium: A Phosphorus Nuclear Magnetic Resonance Study Article Jun The cardioprotective effect of hypoxic adaptation most likely results from oxygen deprivation because normoxic perfusion before the study did not increase tolerance to subsequent ischemia. Our study is the first to suggest a role for the K ATP channel in long-term adaptation to hypoxic stress.
Abstract. We have investigated whether Ca 2+ antagonists reduce the amount of noradrenaline (NA) lost from the myocardium during periods of ischaemia and reperfusion. Hearts obtained from adult, male, normotensive Sprague-Dawley rats were perfused at 37°C before being made globally ischaemic for 15 or 60 min and assayed for catecholamines. As a class of therapeutic agents calcium antagonists have attracted increasing attention in recent years. Their major indications have been in the treatment of ischaemic myocardial syndromes, certain cardiac arrhythmias, hypertension, obstructive cardiomyopathies, and a number of lesser clinical disorders in which their role is less clearly defined.
Get this from a library! Adrenergic Mechanisms in Myocardial Ischemia. [Gerd Heusch; John Ross] -- Stress-induced myocardial ischemia is a frequent manifestation of coronary heart disease, and sympathetic activation is an important precipitating and aggravating factor in such stress induced. Twenty-four hearts were perfused with ANP at , , and 1 μmol/L or without ANP (n = 6 each) in normoxic conditions. Because μmol/L ANP induced a threefold increase in cyclic guanosine monophosphate release into the coronary effluent without any effect on cardiac function, we used the μmol/L ANP dose for ischemia-reperfusion studies.
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To assess whether pretreatment with the calcium antagonist anipamil protects the heart against ischemic and reperfusion damage and to establish how long the protection persists after cessation of the therapy, rabbits were injected subcutaneously twice daily for 5 days with 2 mg/kg body weight of this drug.
The heart was then isolated 2, 6, or 12 hours after the last injection and was Cited by: function ("stunned myocardium") (9). Because ischemia-reperfusion damage in myocardial cells is associated with the accumulation of calcium (ea2+) ions in the cytoplasm and mitochondrial matrix (6,10,11), calcium antagonists have been used to protect the myocardium during ischemia (2,12,13) and subsequent reperfusion (14,15).
Protective effect of pretreatment with the calcium antagonist anipamil on the ischemic-reperfused rat myocardium: a phosphorus nuclear magnetic resonance study.
Kirkels JH(1), Ruigrok TJ, Van Echteld CJ, Meijler FL. Author information: (1)Interuniversity Cardiology Cited by: The negative inotropic effects of calcium channel antagonists on the myocardium were used as a standard for the definition and determination of potency of this group of drugs.
2 The effects of six calcium channel antagonists (verapamil, methoxyverapamil (D), nifedipine, lidoflazine, perhexiline and diltiazem) were compared on cultured chick Cited by: Calcium Antagonists and Cardiac Noradrenaline Release in Ischemia.
Journal of Molecular and Cellular Cardiology () 23, The effects of the calcium antagonists verapamil, gallopamil, nifedipine, felodipine and diltiazem on noradrenaline release during ischemia were studied in isolated perfused rat by: To assess whether the prophylactic administration of anipamil, a new calcium antagonist, protects the heart against the effects of ischemia and reperfusion, rats were injected intraperitoneally twice daily for 5 days with 5 mg/kg body weight of this drug.
Calcium channel blockers (CCB), calcium channel antagonists or calcium antagonists are a group of medications that disrupt the movement of calcium (Ca 2+) through calcium channels. Calcium channel blockers are used as antihypertensive drugs, i.e., as medications to decrease blood pressure in patients with are particularly effective against large vessel stiffness, one of the.
Summary. In order to get more insight into the utilization of calcium in the mammalian heart and the influence of calcium antagonists on this process we have evaluated the negative inotropic and vasodilator effect of nifedipine, diltiazem, verapamil, bepridil and lidoflazine as well as of the intracellularly acting calcium antagonists ryanodine and TMB-8 in the presence of and mmol/l.
The reduced level of mitochondrial calcium in normoxic hearts treated with calcium antagonists shows the usefulness of these drugs in the preven- tion of myocardial damage due to ischaemia (Fleckenstein, ; Nayler, ).
References Borgers, M., E Thon6 anti L. Vet Donck,Sarcolemm~- bound calcium. Levosimendan (10−7 to 10−6 M) has positive inotropic, chronotropic, and vasodilatory effects on normoxic perfused control hearts, as well as during reperfusion after 45 minutes of normothermic cardioplegic arrest.
Similar effects were elicited in the presence of the blockers. Leblanc N, Ruiz-Ceretti E, Chartier D. Potassium loss from hypoxic myocardium: influence of external K concentration. Can J Physiol Pharmacol. May; 65 (5)– Nakaya H, Takeda Y, Tohse N, Kanno M. Effects of ATP-sensitive K+ channel blockers on the action potential shortening in hypoxic and ischaemic myocardium.
Br J Pharmacol. To assess whether the prophylactic administration of anipamil, a new calcium antagonist, protects the heart against the effects of ischemia and reperfusion, rats were injected intraperitoneally twice daily for 5 days with 5 mg/kg body weight of this drug.
The heart was then isolated and perfused by the Langendorff technique. Phosphorus nuclear magnetic resonance spectroscopy was used to. In book: New perspectives on calcium antagonists, Chapter: Calcium-channel blockers: possible mechanisms of protective effect on the ischemic myocardium.
Calcium antagonists and the acutely ischemic heart: experimental effects on ventricular fibrillation and enzyme release L. Opie MRC-UCT Ischaemic Heart Disease Research Unit, Department of Medicine, Groote Schuur Hospital and University of Cape Town.
Abstract. Having established that the calcium antagonists, including vascular selective calcium antagonists such as amlodipine, have a favourable effect on renal haemodynamics and function (Chapter 10), and before considering their usefulness as blood pressure lowering agents — particularly with respect to their long term use in the management of patients with essential hypertension (Chapter.
With the aim of gaining more insight into the metabolism of adenine nucleotides in working normoxic guinea-pigs and in hearts subjected to 45 min of global ischaemia and subsequent reperfusion for 25 min, we evaluated the effect of nifedipine, verapamil, diltiazem, bepridil, CERMlidoflazine, mioflazine and dipyridamole on the adenine nucleotide catabolite levels in these hearts.
To assess whether the prophylactic administration of anipamil, a new calcium antagonist, protects the heart against the effects of ischemia and reperfusion, rats were injected intraperitoneally twice daily for 5 days with 5 mg/kg body weight of this drug. The heart was. Functional and metabolic effects of extracellular magnesium in normoxic and ischemic myocardium.
Headrick JP(1), McKirdy JC, Willis RJ. Author information: (1)Rotary Centre for Cardiovascular Research, School of Health Science, Griffith University Gold Coast Campus, Southport, QueenslandAustralia.
Pathophysiology of sodium‐induced calcium overload. In those situations in which late I Na increases (ischemia, heart failure, hypoxia), the intracellular concentration of sodium increases, which in turn runs the Na + /Ca ++ exchanger in reverse mode (ie, by sodium exit and calcium enter in the cardiac cell).
The result is an overload of calcium that contributes to the appearance of. The protective effect of calcium antagonists on ischemic heart has been attributed to decreased energy expenditure.
We administered one of the newer calcium antagonists, DL-bepridil ( microM), to Langendorff rat hearts 10 or 15 min before ischemia (flow reduction approximately 80%). Effect of hypoxic PM during repolarization of infarcted myocardium.
Infarcted myocardium treated with PM or MSCs was analyzed for calcium-(SERCA2a, green) and potassium-related protein (Na+/K+.Calcium antagonists, such as nifedipine or nicardipine, are used for oral use of slow-release preparations is considered an advantage over intravenous treatment schedules.
Several studies have demonstrated that these agents are well tolerated and effective compared with other tocolytics, such as β 2-sympathomimetics (HaasPapatsonis, El-SayedJannet ).Effects of Calcium Slow Channel Blockers on the Slow Action Potentials of Cardiac Muscle and Vascular Smooth Muscle.
Mechanisms of the Beneficial Effects of Some Ca2+ Antagonists on the Ca2+-Paradox in Myocardium. Pages Dhalla, N. S. (et al.) Calcium Antagonists Book .
