Characteristics of the protective action of ethacizine on the ischemic myocardium

1984 ◽  
Vol 98 (3) ◽  
pp. 1220-1222
Author(s):  
N. V. Kaverina ◽  
S. V. Gatsura ◽  
A. I. Turilova
Keyword(s):  
Protective Action ◽  
Ischemic Myocardium

Protective action of phosphocreatine of ischemic myocardium

1984 ◽  
Vol 16 ◽  
pp. 44-44 ◽  
Author(s):  
V SAKS ◽  
V SHAROV ◽  
V KUPRIYANOV ◽  
V SMIRNOV ◽  
M SEMENOVSKY
Keyword(s):  
Protective Action ◽  
Ischemic Myocardium

scholarly journals Cardioprotection of Ischemic Myocardium

2018 ◽  
Vol 16 (2) ◽  
pp. 13-17 ◽  
Author(s):  
Valentina V Bulion ◽  
Irina B Krylova ◽  
Elena N Selina
Keyword(s):  
Protective Action ◽  
Pulmonary Ventilation ◽  
Creatine Phosphate ◽  
Ischemic Myocardium ◽  
Cardioprotective Effect ◽  
Lipid Hydroperoxides ◽  
Sod Activity ◽  
Male Wistar Rats ◽  
Selective Blocker ◽  
Mitokatp Channels

Aim. Cardioprotective effect of precursors in the synthesis of the uridine-5ʼ-diphosphate (UDP) - the mitochondrial ATP-dependent potassium channels (mitoKATP channels) endogenous activator - uridine and uridine-5ʼ-monophosphate (UMP) and the relation between there mechanism of action and activity of mitoKATP channels were studied. Methods. The experiments were performed on the male Wistar rats weighing 300-350 g. Acute myocardial ischemia (MI) lasting 60 min was produced by occlusion of the descending branch of the left coronary artery (LCA) under artificial pulmonary ventilation. Animals were anesthetized with sodium ethaminal (50 mg/kg). Uridine or UMP in the dose of 30 mg/kg was injected intravenously 5 min prior to LCA occlusion. A selective blocker of these channels 5-hydroxydecanoate (5-HD, 5 mg/kg intravenously 5 min prior to injection of uridine or UMP) was used to detect the involvement of mitoKATP channels in the effects of drugs. ATP and creatine phosphate (CP) was determined in the heart homogenates. The intensity of lipid peroxidation (LPO) was estimated by the content of lipid hydroperoxides (LHP) and the state of the antioxidant system (AOS) by superoxidedismutase (SOD) activity and the reduced glutathione (GH) content. Results. Occlusion of the LCA during 60 min led to the decrease of ATP and CP content in the myocardium by 35% and 59% respectively. At the same time changes in LPO and AOS were observed. The amount of LHP increased by 97%, the activity of SOD was reduced by 28% and the content of GH decreased by 30%. Uridine and UMP given 5 minutes prior to LCA occlusion prevented the development of these metabolic disorders in the ischemic myocardium. Selective blocker of mitoKATP channels 5-HD eliminated the protective effect of both drugs. Conclusion. Uridin and UMP have the evident cardioprotective effect in the acute MI, stabilizing the miocardium energy metabolism, preventing the AOS function depression and excessive activation of LPO. The mechanism of protective action of the drugs is associated with the activation of mitoKATP channels. (For citation: Bulion VV, Krylova IB, Selina EN. Cardioprotection of ischemic myocardium. Reviews on Clinical Pharmacology and Drug Therapy. 2018;16(2):13-17. doi: 10.17816/RCF16213-17).

Protective Action of Purinergic and Cholinergic Agonists on the Ischemic Myocardium in the Rat

1998 ◽  
Vol 28 (7) ◽  
pp. 1141
Author(s):  
Jae Ha Kim ◽  
Sang-Duck Park ◽  
Jeong-Min Ju ◽  
Hyun Kook ◽  
Jeong-Gwan Cho ◽  
...  
Keyword(s):  
Protective Action ◽  
Ischemic Myocardium ◽  
Cholinergic Agonists

Protective action of lithium hydroxybutyrate on the ischemic myocardium

1988 ◽  
Vol 105 (1) ◽  
pp. 56-58
Author(s):  
G. G. Chichkanov ◽  
I. B. Tsorin ◽  
G. Yu. Kirsanova ◽  
D. M. Lomtadze
Keyword(s):  
Protective Action ◽  
Ischemic Myocardium ◽  
Lithium Hydroxybutyrate

Lack of a direct metabolic effect of fructose, 1,6-diphosphate in ischemic myocardium

1981 ◽  
Vol 241 (4) ◽  
pp. H576-H582
Author(s):  
L. J. Eddy ◽  
D. Chambers ◽  
S. Honig ◽  
J. M. Downey
Keyword(s):  
Direct Action ◽  
Protective Action ◽  
Canine Model ◽  
High Energy ◽  
Metabolic Effect ◽  
Ischemic Myocardium ◽  
The Other ◽  
High Energy Phosphate ◽  
Ischemic Tissue ◽  
Lactate Levels

Fructose 1,6-diphosphate (FdP) reportedly protects ischemic myocardium. To determine whether this is a direct action on the heart, we used a canine model in which two coronary arteries were perfused at identical but reduced rates. Into one artery we infused FdP (total doses of 400 mg or 1.8 g) while the other received 0.9% NaCl. After 1 h, biopsies were taken from a normal region and the two ischemic regions and were analyzed for ATP, phosphocreatine (PC), and lactate content. In the 0.9% NaCl-treated ischemic tissue, ATP and PC fell to half the nonischemic levels. The FdP-treated tissue exhibited high-energy phosphate levels similar to the 0.9% NaCl-treated tissue with no significant differences between the two ischemic areas. Lactate levels in both ischemic areas were elevated threefold above nonischemic levels. Contractility studies showed that infusion of FdP directly into the coronary artery depressed contractility in both nonischemic and ischemic conditions. Our data show that, if FdP does have a protective action in ischemia, it is not through a direct action on the heart.

Liquorice exaggerates protective action of Solanum xanthocarpum against cigarette smoke induced pulmonary inflammation

Planta Medica ◽  
2014 ◽  
Vol 80 (10) ◽  
Author(s):  
RA Manek ◽  
NR Sheth ◽  
JR Chavda ◽  
JD Vaghasiya ◽  
KP Modi ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Protective Action ◽  
Pulmonary Inflammation ◽  
Solanum Xanthocarpum

Heparin from Intestine and Lung Source Administered in Large Dose to Dogs with Acute Myocardial Ischemia

1978 ◽  
Vol 40 (02) ◽  
pp. 407-417
Author(s):  
Michael J Saliba ◽  
Richard J Pavalec
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischemia ◽  
Adenosine Triphosphate ◽  
Intestinal Mucosa ◽  
Large Dose ◽  
Acute Myocardial Ischemia ◽  
Ischemic Myocardium ◽  
Atp Levels ◽  
Initial Control ◽  
The Difference

SummaryIntestinal mucosa heparin (IMH) and beef lung heparin (BLH) were infused into dogs subjected to myocardial ischemia by intermittent coronary artery occlusions. The IMH was from a mixture of beef, sheep, and pig intestinal mucosa. Initial control occlusion and recovery was followed by a second occlusion with 60,000 units of IMH or BLH added. Electrocardiographic S-T segment elevations (ST) were measured acutely. There were no significant differences in ST in non-ischemic myocardium before occlusions or with occlusions. In ischemic myocardium, IMH significantly lowered control ST 84% in amount (t = 6.1 p <0.00005), and 76% in number (t = 11.6 p <0.00001). BLH lowered control ST a significant, lesser, 36% in amount (t = 3.6 p <0.008), and 35% in number (t = 3.2 p <0.01). The difference between IMH and BLH in ischemic myocardium was a significant 48% in amount (t = 4.0 p <0.0007), and 41% in number (t = 2.0 p <0.06). Myocardial adenosine triphosphate (ATP) levels were assayed after 90 min. ATP levels were 31% higher in both ischemic and non-ischemic myocardium in IMH-treated dogs than in BLH- treated. It was concluded that IMH and BLH are functionally different, and IMH was significantly more effective.

Action of Lysolecithin on Blood Platelets

1963 ◽  
Vol 09 (03) ◽  
pp. 512-524 ◽  
Author(s):  
Chava Kirschmann ◽  
Sara Aloof ◽  
Andre de Vries
Keyword(s):  
Blood Platelets ◽  
Protective Action ◽  
Platelet Surface ◽  
Washed Platelet ◽  
Sufficient Concentration ◽  
Saline Medium

SummaryLysolecithin is adsorbed to washed blood platelets and, at sufficient concentration, lyses them, inhibits their clot-retracting activity and promotes their thromboplastin-generating activity. Lysolecithin adsorption to the platelet was studied by using P32-labelled lysolecithin obtained from the liver of rats injected with labelled orthophosphate. The amount of lysolecithin adsorbed to the surface of the washed platelet in saline medium is dependent on the concentration of lysolecithin in solution and reaches saturation — 5 × 10-8 jig per platelet — at a concentration of 9—10 µg per ml. Platelet lysis in saline medium begins at a lysolecithin concentration higher than 18 jig per ml. Plasma and albumin prevent adsorption of lysolecithin to the platelet and protect the platelet from damage by lysolecithin. Albumin is able to remove previously adsorbed lysolecithin from the platelet surface. The protective action of plasma explains the lack of platelet damage in blood, the plasma lecithin of which has been converted to lysolecithin by the action of Vipera palestinae venom phosphatidase, in vitro and in vivo.

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