Commentary. Postoperative cerebral hyperperfusion associated with impaired cognitive function in patients undergoing carotid endarterectomy.
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Biomedical subjects
Robert G Atnip
Publications and source records attributed to Robert G Atnip.
Opioid growth factor inhibits intimal hyperplasia in balloon-injured rat carotid artery.
OBJECTIVE: The endogenous opioid [Met(5)]-enkephalin (opioid growth factor [OGF]) is a tonically active, receptor-mediated inhibitory growth peptide in developing and adult vasculature. This study was designed to determine the role of OGF in neointimal hyperplasia. METHODS: The carotid artery in adult male Sprague-Dawley rats was denuded with balloon catheterization. OGF (10 mg/kg), the opioid antagonist naltrexone (NTX; 30 mg/kg), or saline solution (0.2 mL) was injected intraperitoneally daily for 28 days into the rats, and restenosis of the carotid artery was examined with morphometric analysis using Optimas software. Proliferation of the neointima and media was measured by radioactive thymidine incorporation over 3 hours. The presence of OGF and its receptor, OGFr, were examined with immunofluorescence microscopy. RESULTS: OGF depressed DNA synthesis in the intima and media from 16% to 78% of control levels in the first 2 weeks after deendothelialization, whereas NTX exposure elevated DNA synthesis by 21% to 89%. OGF action was receptor-mediated. In the month after injury the thickness of the intima in OGF-treated rats was decreased by 18% to 31% from control values, whereas intimal thickness was increased in the NTX group by 10% to 31%. Luminal area was almost 25% greater than control values in the OGF group, but was reduced 17% by NTX. OGF and the OGF receptor were detected in the carotid artery with immunohistochemistry. CONCLUSIONS: These results demonstrate for the first time that a native opioid system modulates repair of vascular injury. OGF is a constitutively active peptide that has a receptor-mediated action in the negative regulation of neointimal growth, a major cause of restenosis.
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Contrast enhanced duplex ultrasound imaging of the mesenteric arteries.
Duplex ultrasound of the visceral arteries is a technically challenging procedure. We examined the clinical usefulness of perflutren intravenous ultrasound contrast to improve the diagnostic accuracy of such studies. Seventeen patients were prospectively studied. A color duplex imaging study of the visceral vasculature was performed with and without the contrast agent. Vessels were imaged and peak systolic velocity and Doppler waveforms of the aorta, celiac artery, superior mesenteric artery, and the inferior mesenteric artery were examined. These results were independently compared to those of contrast angiography. From this analysis we concluded contrast-enhanced duplex imaging of the mesenteric arteries is safe but not routinely required when performed by an experienced sonographer. Ultrasound contrast may be helpful in difficult patients when the vessels are not initially successfully visualized.
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Differential effects of vascular growth factors on arterial and venous angiogenesis.
OBJECTIVE: Angiogenesis, the development of new blood vessels, has become an area of increased interest for both scientific and clinical application purposes. Proangiogenic agents, such as vascular endothelial growth factor (VEGF) and naltrexone, have been shown to effectively induce new blood vessel growth. Other growth factors, such as the endogenous opioid growth factor (OGF; [Met(5)]-enkephalin) and retinoic acid, are inhibitors of angiogenesis. The differential effects on veins and arteries, however, by any vascular growth factor, have not previously been investigated. METHODS: The chick chorioallantoic membrane (CAM) assay was used for the in vivo quantitation of angiogenesis. After 3 days of incubation, fertilized chick embryos were explanted, and a 3.2-mm methylcellulose disk containing either the known angiogenic stimulators VEGF (0.2 microg, 1.0 microg) or naltrexone (0.1 microg, 5.0 microg), or the angiogenic inhibitors OGF (1.0 microg, 5.0 microg) or retinoic acid (1.0 microg) was placed onto the CAM surface. An equal volume of distilled water served as a control. After 2 days of growth, the CAM arteries and veins were identified, and images were obtained with a digital camera. Quantitative analysis of angiogenesis was performed on a 100-mm(2) area surrounding the applied disk, and the number and length of the veins and arteries were measured. RESULTS: The angiogenic stimulators VEGF and naltrexone markedly increased both the total number and length of all blood vessels as compared with control values. The mean length of blood vessels decreased, suggesting the induction of new vessel growth. VEGF and naltrexone proportionately increased vein and arterial angiogenesis, maintaining artery/vein ratios for vessel number and length that were unchanged compared with controls. The angiogenic inhibitors, OGF and retinoic acid, notably decreased the total number and length of blood vessels in the CAM preparations. However, these compounds had a disproportionately greater inhibitory effect on arterial angiogenesis as reflected in decreased artery/vein ratios for vessel number and length. CONCLUSIONS: The angiogenic stimulators VEGF and naltrexone induce development of veins and arteries in a proportional manner. In contrast, the angiogenic inhibitors OGF and retinoic acid demonstrated a greater inhibitory effect on arterial as compared with venous angiogenesis. Such differential effects on angiogenesis may be important in both defining mechanisms of action and designing therapeutic interventions.
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