Interaction between non-ionic contrast medium and prostaglandin E1 incorporated in lipid microspheres: in-vitro comparative study of direct and non-direct mixing.

H Hayashi; N Uchiyama; H Kawamata; R Takagi; Y Abe; T Kumazaki

PubMed · 11246996

Interaction between non-ionic contrast medium and prostaglandin E1 incorporated in lipid microspheres: in-vitro comparative study of direct and non-direct mixing.

H Hayashi·N Uchiyama·H Kawamata·R Takagi·Y Abe·T Kumazaki

Abstract

PURPOSE: To examine whether there is any interaction between non-ionic contrast medium and prostaglandin E1 incorporated in lipid microspheres (Lipo-PGE1) in direct and non-direct mixing. MATERIALS AND METHODS: Iopamidol 300 and 370 mgI/ml, iohexol 300 and 350 mgI/ml, and iopromide 300 and 370 mgI/ml were mixed with Lipo-PGE1. In the direct mixing test, both agents were mixed directly in a tube. The appearance of the mixture, average size of the Lipo-PGE1 particles, and changes in pH were observed. In the non-direct mixing test, both agents were poured one after the other into a narrow luminal glass tube. The appearance of the mixture was observed. Lipo-PGE1 and the contrast agent were discharged sequentially via a catheter placed in 5 L of physiological saline. The appearance of the physiological saline was observed. RESULTS: In the direct mixing test, no interaction was observed between iopamidol, iohexol, or iopromide 300 mgI/ml and Lipo-PGE1. Aggregation and creaming were observed in the mixture of iopromide 370 mgI/ml and Lipo-PGE1, and average particle size increased over time. However, there was no apparent change in pH. In the non-direct mixing test, none of the test contrast agents interacted with Lipo-PGE1. CONCLUSION: The test non-ionic contrast media, even if they interacted with Lipo-PGE1 when mixed directly, did not appear to interact with Lipo-PGE1 when mixed in a non-direct manner, which represents the clinically used prescription in pharmacoangiography.

Explore related subjects

Alprostadil Contrast Media Drug Interactions Humans In Vitro Techniques Iohexol Iopamidol Microspheres Vasodilator Agents Comparative Study Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

H Hayashi, N Uchiyama, H Kawamata, R Takagi, Y Abe, T Kumazaki. Interaction between non-ionic contrast medium and prostaglandin E1 incorporated in lipid microspheres: in-vitro comparative study of direct and non-direct mixing.. https://pubmed.ncbi.nlm.nih.gov/11246996/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Intravenously administered vasodilatory prostaglandins increase retinal and choroidal blood flow in rats.

We established an experimental system for measuring blood flow in the rat fundus and examined whether intravenously administered vasodilatory prostaglandins (PGE(1), PGE(2), and PGI(2)), 8-(4-chlorophenylthio)-cAMP (a cAMP analogue), and nicardipine (a Ca(2+)-channel blocker) increase fundus blood flow (FBF). Under artificial ventilation, rats were injected with tetrodotoxin (50 microg/kg, i.v.) to eliminate any nerve activity and prevent movement of the eye. After tetrodotoxin, the rats were infused with norepinephrine (0.3 - 0.5 microg . kg(-1) . min(-1)) and epinephrine (2.7 - 4.5 microg . kg(-1) . min(-1)) simultaneously to maintain adequate systemic circulation. We found that intravenous infusion of PGE(1) (2 - 10 microg . kg(-1) . min(-1)), PGE(2) (3 - 30 microg . kg(-1) . min(-1)), and PGI(2) (1 - 10 microg . kg(-1) . min(-1)) increased the FBF in a dose-dependent manner. The vasodilatory PGs decreased arterial pressure, whereas they did not affect heart rate. Like vasodilatory PGs, 8-(4-chlorophenylthio)-cAMP (30 micromol/kg, i.v.) increased FBF and decreased arterial pressure. While infusion of nicardipine (0.3 - 3 microg . kg(-1) . min(-1)) produced comparable depressor responses with those to vasodilatory PGs and the cAMP analogue, it did not increase FBF. These results suggest that vasodilatory PGs and cAMP act more selectively than Ca(2+)-channel blockers on retinal/choroidal blood vessels. Therefore, the vasodilatory PGs might be considered to be possible candidates for the therapeutics to treat disorders of retinal/choroidal circulation.

Alprostadil↗

PubMed2007

Limaprost.

Limaprost, an alprostadil (prostaglandin E1) analogue, is a vasodilator that increases blood flow and inhibits platelet aggregation. The efficacy of oral limaprost was evaluated in adult Japanese patients in three randomised, double-blind, 6-week trials. One study included patients with thromboangiitis obliterans and two trials included patients with lumbar spinal canal stenosis. Limaprost was generally well tolerated and serious adverse events were uncommon. THROMBOANGIITIS OBLITERANS: In a randomised, double-blind trial in Japanese patients primarily with thromboangiitis obliterans (n=136), there was no significant difference between patients receiving limaprost 30 microg/day and those receiving oral ticlopidine 500 microg/day in the improvement of ischaemic symptoms. LUMBAR SPINAL CANAL STENOSIS: Limaprost 15 microg/day was superior to limaprost 3 microg/day for overall drug usefulness and overall improvement from baseline to study end in a phase III trial in 146 patients with lumbar spinal canal stenosis. Assessment of overall improvement considered various objective symptoms (e.g. muscle strength, walking ability) and subjective symptoms (e.g. pain or numbness in extremities), while overall usefulness also considered safety issues. The efficacy of limaprost 15 microg/day was not significantly different from that of 30 microg/day, but tended to be better than that of 6 microg/day in a phase II trial in patients with lumbar spinal canal stenosis and normal straight leg raise test results. The optimal dosage of limaprost for this indication was therefore deemed to be 15 microg/day.

Alprostadil↗

PubMed2006

The effect of intraportal prostaglandin E1 on adhesion molecule expression, inflammatory modulator function, and histology in canine hepatic ischemia/reperfusion injury.

BACKGROUND: Prostaglandin E1 (PGE1) is known to protect the liver from I/R, however, the mechanism of cytoprotection is not well understood. This study investigates the effect of intraportal infusion of PGE1 in a warm liver ischemia/reperfusion (I/R) model on cytokines, adhesion molecules and liver structure. MATERIALS AND METHODS: Twenty dogs underwent laparotomy under general anesthesia. PGE1 (0.02 microg\kg\min) was perfused through the portal vein in the PGE1 group (n = 10), or a similar volume of Ringer's solution in the control group (n = 10) for 15 min. Liver ischemia was induced by hepatic artery and portal vein occlusion and PGE1 was infused via the portal vein for 60 min. The occlusion was released and PGE1 infusion recommenced for 30 min. Blood and liver biopsies were sampled at baseline, 60 min ischemia, and 30 min reperfusion and assessed for transaminases, cytokines, adhesion molecules, and electron microscopy. RESULTS: PGE1 infusion significantly reduced transaminases TNF-alpha, sICAM-1, sP-selectin, and sE-selectin on ischemia and reperfusion. PGE1 reduced hepatocytic degeneration, portal and central ICAM-1 expression, central and sinusoidal VCAM-1 expression, portal and central P-selectin expression, and portal and sinusoidal E-selectin expression on reperfusion. CONCLUSION: Intraportal PGE1 infusion reduced I/R injury and was associated with down-regulation of ICAM-1, VCAM-1, P-selectin, and E-selectin on reperfusion.

Alprostadil↗