Decreased viscosity of human erythrocyte suspension induced by chlorpromazine and isoxsuprine

Suda, Takeo; Shimizu, Daizaburo; Maeda, Nobuji; Shiga, Tohru

doi:10.1016/0006-2952(81)90223-9

Cited by 32 publications

(14 citation statements)

References 19 publications

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“…It is noteworthy that equivalent concentrations of mepacrine did not modify the first phase of aggregation to ADP, indicating the difference between ADP and PGAP actions at the platelet membrane. The phenothiazine neuroleptics, of which chlorpromazine is the prototype, are lipophilic and also have a variety of effects on membranes (Suda, Schimizu, Maeda & Shiga, 1981). Chlorpromazine, though less potent than mepacrine, inhibited both PGAP-induced biphasic aggregation and release and, at higher concentrations, inhibited first phase aggregation.…”

Section: Discussionmentioning

confidence: 99%

Acetal phosphatidic acids: novel platelet aggregating agents

Brammer

Maguire

Walaszek

et al. 1983

British J Pharmacology

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1 Pahmitaldehyde, olealdehyde and linolealdehyde acetal phosphatidic acids induced rapid shape change and dose-dependent biphasic aggregation of human platelets in platelet-rich plasma; aggregation was reversible at low doses and irreversible at high doses of the acetal phosphatidic acids. The palmitaldehyde congener elicited monophasic dose-dependent aggregation of sheep platelets in platelet-rich plasma. 4 The adenosine diphosphate (ADP) antagonist, 2-methylthio-AMP, and the cyclo-oxygenase inhibitor, aspirin, abolished PGAP-induced second phase aggregation and release in human platelets but did not affect the first, reversible, phase of aggregation. Both the first and second phases of PGAP-induced aggregation were abolished by chlorpromazine, by the phospholipase A2 inhibitor, mepacrine, and by nmolar concentrations of prostaglandin E1 (PGEI); these agents abolished the second, but not the first phase of ADP-induced aggregation.5 The related phospholipids, lecithin, lysolecithin and phosphatidic acid, at < 100 tM, neither induced aggregation of human platelets in platelet-rich plasma, nor modified PGAP-induced aggregation; 1-palmityl lysophosphatidic acid elicited aggregation of human platelets at a threshold concentration of 100 jIM. 6 It is concluded that the acetal phosphatidic acids induce platelet aggregation per se by direct action at the platelet membrane, and that the acetal function is of primary importance in their potent platelet-stimulating activity. Moreover, as the acetal phosphatidic acids are the major components of the smooth muscle-contracting acidic phospholipid tissue extract 'Darmstoff' (Vogt, 1949), their potent platelet-aggregating properties may be of physiological or pathological significance.

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Section: Discussionmentioning

confidence: 99%

Acetal phosphatidic acids: novel platelet aggregating agents

Brammer

Maguire

Walaszek

et al. 1983

British J Pharmacology

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“…Chlorpromazine also inhibited C. krusei, C. parapsilosis, C. tropicalis, and Torulopsis glabrata. We conclude that phenothiazines have direct anti-Candida activity and that these drugs appear to have a broad antimicrobial spectrum.Phenothiazines are widely used antipsychotic drugs which have multiple cellular effects, including modification of membranes, alteration of cyclic nucleotide metabolism, and intercalation into DNA (7,8,15 …”

mentioning

confidence: 99%

“…Phenothiazines are widely used antipsychotic drugs which have multiple cellular effects, including modification of membranes, alteration of cyclic nucleotide metabolism, and intercalation into DNA (7,8,15 …”

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confidence: 99%

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Inhibitory effects of chlorpromazine on Candida species

Wood¹,

Nugent²

1985

Antimicrob Agents Chemother

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Chlorpromazine was tested for antifungal activity by using Candida albicans and standard assays. The MIC of chlorpromazine was 35 pi/ml; the minimal fungicidal concentration was also 35 Fig/ml. The minimal effective concentration was 2.2 to 3.5 ptg/ml (using assays based on quantitative cultures and growth). There was a slight positive interaction between chlorpromazine and amphotericin B but no interaction between chlorpromazine and rifampin. Chlorpromazine also inhibited C. krusei, C. parapsilosis, C. tropicalis, and Torulopsis glabrata. We conclude that phenothiazines have direct anti-Candida activity and that these drugs appear to have a broad antimicrobial spectrum.Phenothiazines are widely used antipsychotic drugs which have multiple cellular effects, including modification of membranes, alteration of cyclic nucleotide metabolism, and intercalation into DNA (7,8,15

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“…The viscosity of echinocytes in suspension is higher than that of discocytes (Meiselman, 1978;Suda, Shimizu, Maeda & Shiga, 1981;Kon, Maeda, Suda, Sekiya & Shiga, 1983;Suda, Maeda, Shimizu, Kamitsubo & Shiga, 1982). In order to examine the relation between the deoxygenation rate and the theological behaviour, the change of viscosity following echinocytic transformation was also measured.…”

Section: Suspension Viscosity Of the Transformed Erythrocytesmentioning

confidence: 99%

The influence of deformation of transformed erythrocytes during flow on the rate of oxygen release.

Kon¹,

Maeda²,

Shiga³

1983

The Journal of Physiology

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SUMMARY1. The deoxygenation rates of transformed erythrocytes were compared with those ofnormal discocytes by both stopped-flow and continuous-flow methods. Echinocytic and spherostomatocytic transformations were induced by various anionic and cationic drugs, respectively, without altering the oxygen affinity of haemoglobin, the cell volume or the membrane fluidity.2. The echinocytic transformation reduced the deoxygenation rate at slow-flow velocities (50 cm/sec), as detected by the continuous-flow method. However, at higher flow velocities (150 cm/sec) the rate was similar to that seen in normal discocytes. A close correlation between the degree of echinocytosis, the retardation of deoxygenation rate and the increase of suspension viscosity were observed.3. Microscopic observation of flowing erythrocytes revealed that the echinocytes scarcely deformed at the slower flow velocity, but clearly deformed at the higher flow velocity to various shapes resembling the flowing discocytes.4. Transformation to spherostomatocytes had no effect on the deoxygenation rate, which was comparable with that of the discocytes, and even the higher flow force did not induce any deformation.5. The retarded deoxygenation and the increased viscosity of echinocytes was probably due to an augmented stagnant layer around the cells (i.e. an increase of the hydrodynamic effective volume); this layer was reduced when the echinocytes were deformed with increasing flow force.

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Decreased viscosity of human erythrocyte suspension induced by chlorpromazine and isoxsuprine

Cited by 32 publications

References 19 publications

Acetal phosphatidic acids: novel platelet aggregating agents

Acetal phosphatidic acids: novel platelet aggregating agents

Inhibitory effects of chlorpromazine on Candida species

The influence of deformation of transformed erythrocytes during flow on the rate of oxygen release.

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