Effect of lysolecithin and lecithin of blood serum on the sensitivity of heart to acetylcholine

Zvezdina, N. D.; Prokasova, Nina V.; Vaver, V. A.; Bergel'son, L. D.; Turpaev, T. M.

doi:10.1016/0006-2952(78)90192-2

Cited by 3 publications

(2 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…injection of different LPCs over the same concentration range as that used in our experiments. Possible influences of haemolysis, heart rate, cholinolytic effectivity [7] and other regulatory factors have to be ruled out in order to clearly explain this Potentiation of PA at low concentrations and inhibition of PA at high concentrations of LPC and tetradecyl-PC, respectively.…”

Section: Influence Of Lpc On Blood Vessel Reactivitymentioning

confidence: 99%

“…While studying the response of rat platelets to a homologous PAF obtained from peritoneal macrophages we observed that they were irresponsive to a synthetic PAF fully active upon rabbit platelets [7]. These findings prompted us to characterize the direct vascular actions of the compound, once the activation of rat platelets could be ruled out by in vitro experiments.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of lysolecithin on blood vessel reactivity and of some ethers and esters of glycerophosphocholine and phosphocholine, respectively, on aggregation of rat platelets

et al. 1981

View full text Add to dashboard Cite

Infusion of lysolecithin (LPC; e.g. 88 microgram/ml for 0.5-1.0 min) did not significantly impair the vasopressor action of norepinephrine (NE), prostaglandin F2 alpha (PGF2 alpha) and extract of posterior pituitary (EPP) in the isolated perfused hind legs of rats. In other words, vascular smooth muscle behaves differently from the smooth muscle of the guinea-pig small intestine, since, in the latter, contractions evoked by acetylcholine, prostaglandins etc., are inhibited by LPC. Triton X 100 which, by comparison, was used as a detergent effective on the guinea-pig small intestine, depressed the vasopressor effect of NE, PGF2 alpha and EPP. LPC, at low concentrations (40 mumol/l), potentiated (15% max.) ADP-induced platelet aggregation (PA) in rat PRP but, at high concentrations, inhibited PA (IC50 = 390 mumol/l). 2-Hexadecylglycerophosphocholine and its short-chain 1-alkyl ethers, which are structurally related to platelet-activating factor, as well as some long-chain alkanol phosphocholine esters, were somewhat more active than LPC. Dipalmitoyllecithin (4-700 mumol/l) was without any effect.

show abstract

Section: Influence Of Lpc On Blood Vessel Reactivitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of lysolecithin on blood vessel reactivity and of some ethers and esters of glycerophosphocholine and phosphocholine, respectively, on aggregation of rat platelets

et al. 1981

View full text Add to dashboard Cite

show abstract

Protective effects of phosphatidylcholine against mechanisms of ischemia and reperfusion-induced arrhythmias in isolated guinea pig ventricular tissues

Duan

Moffat

1990

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

The effects of exogenous phosphatidylcholine (PC) on some potential mechanisms of ischemia and reperfusion-induced arrhythmias were tested using the superfused right ventricular free wall of the guinea pig. Exposure of the preparation to simulated "ischemia" (hypoxia, acidosis, glucose deprivation and hyperkalemia) resulted in several electrophysiological derangements, including a marked depolarization of the maximum diastolic potential (MDP) in both endocardium and epicardium, shortening of the action potential duration (APD), and prolongation of the transmural conduction time followed by transmural conduction block. In a few preparations, coupled beats were also observed. Reperfusion was associated with arrhythmic activity in all preparations. Both the characteristics and the severity of reperfusion-associated arrhythmias were dependent upon the duration of the preceding "ischemia". In hearts exposed to ischemic conditions for 40 min, transmural conduction block persisted until 45 min of reperfusion and no electrical activity was present in the epicardium during this time. However, both coupled beats as well as abnormal automaticity were observed in the endocardium. When the period of "ischemia" was reduced to 20 min, recovery from transmural conduction block occurred sooner and coupled beats and abnormal automaticity were detected in both epicardial and endocardial layers. Superfusion with PC during both "ischemia" and reperfusion (PC1 group), or during reperfusion only (PC2 group), significantly altered the response of the preparations to reperfusion. Following 40 min "ischemia", preparations treated with PC recovered from transmural conduction block more rapidly (PC1 group, 4 min, P less than 0.05; PC2 group, 23 min, ns), compared to control.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Phospholipids in mitochondrial dysfunction during hemorrhagic shock

Leskova

2016

J Bioenerg Biomembr

View full text Add to dashboard Cite

Energy deficiency plays a key role in the development of irreversible shock conditions. Therefore, identifying mitochondrial functional disturbances during hemorrhagic shock should be considered a prospective direction for studying its pathogenesis. Phospholipid (PL)-dependent mechanisms of mitochondrial dysfunction in the brain (i.e., in the frontal lobes of the cerebral hemispheres and medulla oblongata) and liver, which, when damaged, leads to an encephalopathy, are examined in this review. These mechanisms show strong regional specificity. Analyzing the data presented in this review suggests that the basis for mitochondrial functional disturbances is cholinergic hyperactivation, accompanied by a choline deficiency and membrane phosphatidylcholine (PC) depletion. Stabilization of the PL composition in mitochondrial membranes using "empty" PC liposomes could be one of the most important methods for eliminating energy deficiency during massive blood loss.

show abstract

Effect of lysolecithin and lecithin of blood serum on the sensitivity of heart to acetylcholine

Cited by 3 publications

References 25 publications

Effect of lysolecithin on blood vessel reactivity and of some ethers and esters of glycerophosphocholine and phosphocholine, respectively, on aggregation of rat platelets

Effect of lysolecithin on blood vessel reactivity and of some ethers and esters of glycerophosphocholine and phosphocholine, respectively, on aggregation of rat platelets

Protective effects of phosphatidylcholine against mechanisms of ischemia and reperfusion-induced arrhythmias in isolated guinea pig ventricular tissues

Phospholipids in mitochondrial dysfunction during hemorrhagic shock

Contact Info

Product

Resources

About