Single injection of a sustained-release prostacyclin analog improves pulmonary hypertension in rats

Am J Respir Crit Care Med. 2008 Jan 15;177(2):195-201. doi: 10.1164/rccm.200703-349OC. Epub 2007 Nov 1.

Abstract

Rationale: Although prostacyclin is recognized as a therapeutic breakthrough for pulmonary hypertension, it needs continuous infusion because of its short action. Therefore, we developed a new drug delivery system for prostacyclin. We prepared ONO-1301MS, a novel sustained-release prostacyclin analog polymerized with poly(d,l-lactic-co-glycolic acid) (PLGA) microspheres.

Objectives: We examined whether ONO-1301MS attenuates monocrotaline (MCT)-induced pulmonary hypertension in rats, and attempted to elucidate the underlying mechanisms responsible for the beneficial effects of ONO-1301MS.

Methods: After MCT injection, rats were randomized to receive a single subcutaneous injection of 100 mg/kg ONO-1301MS or vehicle.

Measurements and main results: We prepared ONO-1301MS, which was polymerized with PLGA to release ONO-1301 for 3 weeks. A single administration of ONO-1301MS achieved sustained elevation of its circulating level and plasma cyclic adenosine 3',5'-monophosphate level for 3 weeks, and attenuated an increase in a metabolite of thromboxane A(2) level. Rats had developed pulmonary hypertension 3 weeks after MCT injection; however, treatment with ONO-1301MS significantly attenuated the increases in right ventricular systolic pressure and right ventricular weight to body weight ratio. ONO-1301MS significantly inhibited hypertrophy of pulmonary arteries. Phosphorylation of extracellular signal-regulated protein kinase (ERK) in the lung was significantly increased in the control group, whereas this increase was markedly attenuated by treatment.

Conclusions: We developed a new drug delivery system for prostacyclin using PLGA and ONO-1301. A single injection of ONO-1301MS resulted in sustained activity for 3 weeks, and attenuated pulmonary hypertension, partly through its antiproliferative effect on vascular smooth muscle cells via inhibition of ERK phosphorylation.

MeSH terms

  • Animals
  • Antihypertensive Agents / administration & dosage*
  • Delayed-Action Preparations
  • Disease Models, Animal
  • Drug Compounding
  • Epoprostenol / agonists*
  • Extracellular Signal-Regulated MAP Kinases / drug effects
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Hemodynamics / drug effects
  • Hypertension, Pulmonary / chemically induced
  • Hypertension, Pulmonary / drug therapy*
  • Hypertension, Pulmonary / physiopathology
  • Injections, Subcutaneous
  • Male
  • Microspheres
  • Monocrotaline
  • Pyridines / administration & dosage*
  • Pyridines / chemistry
  • Pyridines / pharmacokinetics
  • Rats
  • Rats, Wistar
  • Thromboxane-A Synthase / antagonists & inhibitors

Substances

  • Antihypertensive Agents
  • Delayed-Action Preparations
  • Pyridines
  • ONO 1301
  • Monocrotaline
  • Epoprostenol
  • Extracellular Signal-Regulated MAP Kinases
  • Thromboxane-A Synthase