DDAVP: Does the drug have a direct effect on the vessel wall?

Barnhart, Marion I.; Chen, Shan te; Lusher, Jeanne M.

doi:10.1016/0049-3848(83)90326-2

Cited by 78 publications

(26 citation statements)

References 16 publications

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“…Since we (Hashemi et al, 1990) and other investigators have shown that DDAVP alone does not have a direct effect in enhancing the release of vWf from ECs in vitro (Barnhardt et al, 1983;Moffat et al, 19841, it has been proposed that stimulation of other intermediary target cells leads to the secretion of some unknown intercellular messenger, which then stimulates the re-lease of vWf from ECs. In a previous report from this laboratory (Hashemi et al, 1990), we showed that one of the target cells for DDAVP were monocytes and that they secreted some factor or factors, which following addition t o EC cultures enhanced the release of vWf.…”

mentioning

confidence: 85%

Platelet‐activating factor secreted by DDAVP‐treated monocytes mediates von willebrand factor release from endothelial cells

Hashemi

Palmer

Aye

et al. 1993

Journal Cellular Physiology

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We have previously shown that although DDAVP (1-deamino-8-D-arginine vasopressin), a synthetic analogue of the natural hormone arginine vasopressin, does not directly promote release of vWf from human umbilical vein endothelial cells (ECs), enhanced release does occur when ECs were exposed to either monocytes or to supernatants recovered from DDAVP-treated monocytes. In the present study, we have found that exposure of monocytes to DDAVP did not increase secretion of interleukins (IL)-1 beta, IL-6, IL-8, tumor necrosis factor (TNF-alpha), growth factors G-CSF (granulocyte-), GM-CSF (granulocyte, monocyte-colony stimulating factor), prostaglandins (PG) E2, PGF2 alpha, or PGI2 or purine nucleotides such as ATP and ADP. However, increased levels of platelet-activating factor (PAF) were secreted by DDAVP-treated monocytes in a time- and dose-dependent manner that positively correlated with the enhancement in vWf release from ECs. Moreover, this effect could also be elicited when lipid extracts of these supernatants or purified PAF were added directly to ECs. This response could be inhibited with (+/-)-trans-2,5-Bis(3,4,5-trimethoxyphenyl)-1,3-dioxolane, a specific PAF receptor antagonist, when the ECs were exposed to supernatants from DDAVP-treated monocytes or to pure PAF. The present data indicate that enhanced secretion of PAF from monocytes is one mechanism whereby DDAVP can provoke release of vWf from ECs.

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mentioning

confidence: 85%

Platelet‐activating factor secreted by DDAVP‐treated monocytes mediates von willebrand factor release from endothelial cells

Hashemi

Palmer

Aye

et al. 1993

Journal Cellular Physiology

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“…The vasopressin analogue desmopressin has direct and local effects on the blood vessel wall and causes release of high molecular weight multimers of vWF resulting in a local increase in platelet adhesion and enhanced coagulation [51]. There have been reports of its effectiveness in the management of bleeding in patients with and without vWF deficiency [52].…”

Section: Gastrointestinal Involvementmentioning

confidence: 99%

Gastrointestinal and Hepatic Manifestations of Hereditary Hemorrhagic Telangiectasia

Sharma

Howden

1998

Dig Dis

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Hereditary hemorrhagic telangiectasia (HHT) or Osler-Rendu-Weber (ORW) disease is an autosomal-dominant disorder that frequently presents with gastrointestinal bleeding which may be a diagnostic and therapeutic challenge. Hepatic involvement in this disease is increasingly recognized and poses another therapeutic challenge. With advances in genetic screening and diagnostic procedures, and the increasing awareness of the condition by physicians and patients, this disease is being diagnosed more often. This article reviews the available literature on gastrointestinal and hepatic manifestations of HHT, and the various diagnostic and therapeutic modalities available for its management.

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“…This mecha nism may well be at least in part responsible for correction (or partial correction) of the BT [15]. There is also suggestive evidence for oth er mechanisms which may account for short ening of the BT [ 19,20].…”

Section: Mechanisms Of Actionmentioning

confidence: 99%

“…However, Mannucci and Lusher [37,42] cautioned that even though there was no clear-cut evidence of a causative association, close surveillance of persons receiving IV DDAVP seemed war ranted, especially in persons with clinical and/ or laboratory evidence of coronary or cerebral atherosclerosis. If there is an increased risk of arterial thrombosis in persons with underly ing coronary artery disease, possible mecha nisms might include high levels of tPA inhibi tor (preventing fibrinolytic responses) [43]; increased platelet adhesion at injury sites in the vessel wall, mediated by vWF release, or by a direct effect on the injured vascular endo thelium [19]. It should be noted that the pau city of reports of MI or cerebral thrombosis in persons receiving DDAVP makes a causal relationship uncertain.…”

Section: Potential Side Effectsmentioning

confidence: 99%

Response to 1-Deamino-8-<i>D</i>-Arginine Vasopressin in von Willebrand Disease

Lusher

1994

Pathophysiol Haemos Thromb

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The synthetic agent, l-deamino-8-D-arginine vasopressin (DDAVP), is generally regarded to be the treatment of choice for persons with type I von Willebrand disease (vWD), and may be useful in type IIA vWD as well. Several formulations of the drug are available, including a highly concentrated intranasal spray formulation which is ideal for home use. The degree of F VIII and vWF response to DDAVP varies among individuals, but is generally consistent in individual patients over time. Some have tachyphylaxis while others do not. While side effects are uncommon, DDAVP is a potent antidiuretic agent. Thus one should be aware of the possibility of hyponatremia and water intoxication if certain precautions are not observed.

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DDAVP: Does the drug have a direct effect on the vessel wall?

Cited by 78 publications

References 16 publications

Platelet‐activating factor secreted by DDAVP‐treated monocytes mediates von willebrand factor release from endothelial cells

Platelet‐activating factor secreted by DDAVP‐treated monocytes mediates von willebrand factor release from endothelial cells

Gastrointestinal and Hepatic Manifestations of Hereditary Hemorrhagic Telangiectasia

Response to 1-Deamino-8-<i>D</i>-Arginine Vasopressin in von Willebrand Disease

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