The Experts below are selected from a list of 24 Experts worldwide ranked by ideXlab platform
George B Stefano - One of the best experts on this subject based on the ideXlab platform.
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endomorphin 1 and 2 inhibit human Vascular sympathetic norepinephrine release lack of interaction with mu 3 opiate receptor subtype
Acta Pharmacologica Sinica, 1998Co-Authors: Christos M Rialas, Caterina Fimiani, Thomas V Bilfinger, Michel Salzet, George B StefanoAbstract:AIM: To determine if endomorphin-1 (End-1) and -2 (End-2) interact with mu 3 opiate receptor subtype and in this way cause Vascular hypotension. METHODS: Amperometric nitric oxide (NO) determinations associated with opiate binding displacement analysis and preloaded [3H]norepinephrine KCl stimulated release in human Vascular tissues from sympathetic nerve fibers in vitro. RESULTS: The endomorphins did not release NO from human monocytes, granulocytes, saphenous vein, and internal thoracic artery endothelium and did not displace opiate alkaloid binding to mu 3 receptor. However, they did inhibit KCl-stimulated [3H]norpinephrine release from Vascular Nerves. CONCLUSION: The data strongly suggested that End-1 and -2 caused hypotension by blocking sympathetic Vascular sympathetic activity.
Keyvan Hajirayat - One of the best experts on this subject based on the ideXlab platform.
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Minimizing thermal damage to Vascular Nerves while drilling of calcified plaque.
BMC Research Notes, 2019Co-Authors: Seifollah Gholampour, Keyvan HajirayatAbstract:Drilling of calcified plaque (DCP) inside the artery is a method for removing calcified plaques. This study investigated the effect of drill. To validate the maximum temperature calculated by computer simulation, this value was also measured by an experimental on a phantom model. Increasing drill bit diameter during drilling would increase the temperature in Vascular Nerves. In a drill bit with a diameter of 4 mm, the risk of thermal necrosis in Vascular Nerves of the artery wall decreased by 8.57% by changing the drill from WC to NT. The same value for a drill bit with a diameter of 6 mm was 10.17%. However, the trend of the generated temperature in the Vascular Nerves did not change significantly with change of the material and diameter of the drill bit. The results showed that for DCP with the least risk of thermal necrosis in Vascular Nerves and subsequently the lowest risk of restenosis, coagulation and thermal stroke of the patient, the best option is to use a drill bit with a diameter of 4 mm and NT material for drilling.
Christos M Rialas - One of the best experts on this subject based on the ideXlab platform.
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endomorphin 1 and 2 inhibit human Vascular sympathetic norepinephrine release lack of interaction with mu 3 opiate receptor subtype
Acta Pharmacologica Sinica, 1998Co-Authors: Christos M Rialas, Caterina Fimiani, Thomas V Bilfinger, Michel Salzet, George B StefanoAbstract:AIM: To determine if endomorphin-1 (End-1) and -2 (End-2) interact with mu 3 opiate receptor subtype and in this way cause Vascular hypotension. METHODS: Amperometric nitric oxide (NO) determinations associated with opiate binding displacement analysis and preloaded [3H]norepinephrine KCl stimulated release in human Vascular tissues from sympathetic nerve fibers in vitro. RESULTS: The endomorphins did not release NO from human monocytes, granulocytes, saphenous vein, and internal thoracic artery endothelium and did not displace opiate alkaloid binding to mu 3 receptor. However, they did inhibit KCl-stimulated [3H]norpinephrine release from Vascular Nerves. CONCLUSION: The data strongly suggested that End-1 and -2 caused hypotension by blocking sympathetic Vascular sympathetic activity.
Seifollah Gholampour - One of the best experts on this subject based on the ideXlab platform.
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Minimizing thermal damage to Vascular Nerves while drilling of calcified plaque.
BMC Research Notes, 2019Co-Authors: Seifollah Gholampour, Keyvan HajirayatAbstract:Drilling of calcified plaque (DCP) inside the artery is a method for removing calcified plaques. This study investigated the effect of drill. To validate the maximum temperature calculated by computer simulation, this value was also measured by an experimental on a phantom model. Increasing drill bit diameter during drilling would increase the temperature in Vascular Nerves. In a drill bit with a diameter of 4 mm, the risk of thermal necrosis in Vascular Nerves of the artery wall decreased by 8.57% by changing the drill from WC to NT. The same value for a drill bit with a diameter of 6 mm was 10.17%. However, the trend of the generated temperature in the Vascular Nerves did not change significantly with change of the material and diameter of the drill bit. The results showed that for DCP with the least risk of thermal necrosis in Vascular Nerves and subsequently the lowest risk of restenosis, coagulation and thermal stroke of the patient, the best option is to use a drill bit with a diameter of 4 mm and NT material for drilling.
James Orourke - One of the best experts on this subject based on the ideXlab platform.
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functional and morphologic evidence of the presence of tissue plasminogen activator in Vascular Nerves implications for a neurologic control of vessel wall fibrinolysis and rigidity
Journal of Neuroscience Research, 1998Co-Authors: Yafei Wang, Arthur R Hand, Yuhsiung Wang, Mina Mina, Concettina Gillies, Tao Peng, Robert E Cone, James OrourkeAbstract:Tissue plasminogen activator (t-PA) is expressed by hypothalamic and peripheral sympathetic neurons. The sympathetic axons that permeate artery walls have not been investigated as possible sources of intramural t-PA. The plasmin produced by such a system would locally activate both fibrinolysis and matrix metalloproteinases that regulate arterial collagen turnover. To assess this neural t-PA production, we investigated the capacity of rat cervical sympathetic ganglion neurons to synthesize and release t-PA, and the expression of the enzyme in carotid artery and the iris-choroid microVascular tissues that receive the ganglion axon distribution. Functional studies confirmed that (i) the ganglion neuron cell bodies synthesize t-PA mRNA, (ii) cultured ganglion carotid artery and iris-choroid microVascular explants predominantly release t-PA rather than urokinase, (iii) microVascular tissues release ∼20 times more t-PA per milligram than carotid explants (which accords with the higher innervation density of small vessels), and (iv) removal of the endothelium did not cause major reductions in the t-PA release from carotid and microVascular explants. Immunolocalization studies then confirmed a strong expression of the enzyme within the ganglion axons, the carotid adventitia that receives these axons, and the predominantly sympathetic axon terminals in the iris-choroid microvasculature. These data indicate the existence of a previously undescribed system for the delivery of neural t-PA to vessel walls. The intramural production of plasmin induced by this system represents a novel principle for the regulation of arterial matrix flexibility, especially in the media of densely innervated small arteries and resistance arterioles involved in the pathogenesis of stroke, hypertension, and Vascular aging. Thus, the data suggest an important new interface between neuroscience and Vascular biology that merits further exploration. J. Neurosci. Res. 53:443–453, 1998. © 1998 Wiley-Liss, Inc.
