PubMed · 15259177
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
Michael O'Leary, Bazian Ltd. 2002. Erectile dysfunction.. https://pubmed.ncbi.nlm.nih.gov/15259177/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
STUDY DESIGN: Vasodilatation was studied in a model of experimental chronic cauda equina compression using measurements of vessel diameter on video recordings. OBJECTIVE: The vasodilative effect was compared between a prostaglandin E2 receptor (EP) subtype agonists (EP4 agonist) and a prostaglandin E1 (PGE1) derivate. SUMMARY AND BACKGROUND DATA: Reduction of blood flow is one important pathogenic factor of neurogenic intermittent claudication (NIC) for lumbar spinal canal stenosis. It is known that PGE1 improves the mean walking distance in patients with cauda equina compression type of NIC. There are four subtypes of EP: EP1, EP2, EP3, and EP4. EP4 is located in vessels of pigs and rabbits. A highly selective EP4 agonist, which has effects on dilatation of pig and rabbit vessels, has recently been developed. One may therefore assume that this agonist may improve blood flow in the chronically compressed cauda equina. METHODS: A total of 25 dogs were used. A plastic balloon inflated to 10 mm Hg was placed under the lamina of the seventh lumbar vertebra for 1 week. OP-1206 cyclodextrin clathrate (OP-1206 CD: prostaglandin E1 derivate) and ONO-4819 CD (a highly selective EP4 agonist) were intravenously administrated. The following 5 experimental groups were assigned: animals in group OP (3) (n = 5) and Group OP (10) (n = 5) received 3 eta g/kg per minute and 10 eta g/kg per minute of OP-1206 CD, respectively; those in Group EP (3) (n = 5) and Group EP (10) (n = 5) received 3 eta g/kg per minute and 10 eta g/kg per minute of ONO-4819 CD, respectively; and those in the control group (n = 5) received saline. After 7 days, the cauda equina was exposed and blood vessels of the second or third sacral nerve root were identified using a specially designed operation microscope equipped with a video camera. The diameters of the observed blood vessels were measured on video-recordings every 10 minutes until 60 minutes after administrating OP-1206 CD or ONO-4819CD. RESULTS: In the Groups OP (3), OP (10), and EP (10), the blood vessels were dilated and blood flow increased after injection of the agents. In the Group EP (10), the vessel diameter and blood flow increased significantly compared with that in the other four groups. In contrast, the blood vessels contracted and the blood flow was reduced in the Group EP (3). CONCLUSIONS: Our results suggested that the EP4 agonist at high concentrations might be a potential therapeutic agent since it is expected to increase blood flow in nerve roots in patients with spinal canal stenosis.
Myasthenic symptoms and the echocardiographic findings of dilated cardiomyopathy are very rare in primary AL amyloidosis. We report a 59-year-old man with dyspnea on effort and weakness after exercise. His electrocardiogram showed ischemic heart disease and echocardiography indicated dilated cardiomyopathy. Muscle biopsy revealed amyloidosis with deposits of lambda light chain-derived amyloid within the vessel wall. Treatment with PGE1 resulted in improvement of the myasthenic symptoms. This patient indicates that myasthenic symptoms and dilated cardiomyopathy would be a unique syndrome associated with systemic AL amyloidosis involving mainly the small vessels, i.e., AL amyloid angiopathy, in the skeletal muscles and myocardium vessels.
OBJECTIVE: The influences of groin incision, duration of ischemia, and the effects of prostaglandin E1 (PGE1) on ischemia-reperfusion (I/R) injury of the hind limb in rabbits were evaluated. DESIGN: A prospective study. SETTING: Laboratory. PARTICIPANTS: In 64 rabbits, bilateral hind limb ischemia was induced by occlusion of the abdominal aorta. Volume changes, neuromuscular function of the hind limb, and creatine kinase (CK) release were measured as variables of tissue injury. INTERVENTIONS: Eight rabbits served as untreated controls (CON). In 2 groups (each n = 14), 3 hours of ischemia were followed by 3 hours of reperfusion (I/R). In 2 different groups (each n = 14), 45 minutes of ischemia were followed by 2 hours of reperfusion. To determine effects of PGE1, 1 I/R group of each ischemia duration was treated intravenously with 80 ng/kg/min of PGE1 starting 30 minutes after the onset of ischemia (I/R-PGE1). To determine effects of groin incision on edema formation, volume changes were determined in the "operated" right (CON-R, 3h-R, 3h-PGE1-R and 45 min-R, 45 min-PGE1-R) or in the "nonoperated" left hind limb (CON-L, 3h-L, 3h-PGE1-L and 45 min-L, 45 min-PGE1-L), representing a subgroup analysis. MEASUREMENTS AND MAIN RESULTS: Volume changes after I/R occurred only in operated legs after ischemia (3h-R: 2.3 +/- 0.3 mL, p < 0.0001 v CON-R and 3h-L; 45 min-R: 0.8 +/- 0.2 mL, p < 0.01 v 45 min-L). PGE1 reduced edema formation in the operated legs (3h-PGE1-R: 1.0 +/- 0.4 mL, p < 0.0001 v 3h-R; 45 min-PGE1-R: 0.5 +/- 0.3 mL, p = 1.0 v 45 min-R). Groin incision without I/R had no effect on edema formation (CON-R: -0.13 +/- 0.17 mL of baseline). The increase of CK release from 616 +/- 584 U/L in controls to 5,921 +/- 2,156 U/L after 3 hours of ischemia (p < 0.001) was attenuated by treatment with PGE1 (3,732 +/- 2,653, p < 0.05 v I/R). Forty-five minutes of ischemia did not lead to cellular damage as measured by CK release (I/R: 606 +/- 364 U/L). Recovery of neuromuscular function was not affected by PGE1. CONCLUSION: Development of edema during I/R depends on groin incision of the hind limb and on the duration of ischemia. The I/R injury is attenuated by PGE1 treatment, in terms of reduced edema formation and CK release, but not in terms of neuromuscular function.