Applications
Over 550 papers have been published using Living System Instrumentation's cannulated blood vessel system. We have compiled a bibliography, which may be accessed by clicking Bibliography. Available in Adobe Acrobat for search use.
A Host of Applications using these tools are at the disposal of the research investigator interested in obtaining new insights into the mechanisms of vascular function in human health and disease.
Typical Examples -
Studies: hypertension, diabetes, aging, and pregnancy
Tissue Sources: humans, primates, swine, rats, dogs, and rabbits
Vascular Beds: cerebral, coronary, lung, skin, and kidney
Vasoactive Agents: NO, endothelin, estrogen, peptides, and oxygen
Simultaneous Measurements: Fluorescence & Vessel Diameter

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Changes in diameter of rat gracilis arterioles as a function of perfusate flow From: Koller A, Sun D, Huang A, Kaley G Co-release of nitric oxide and prostaglandins mediates flow-dependent dilation of gracilis muscle arterioles. Am J Physiol 1994; 267:H326-H33 |
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Depolarization and constriction of rat myogenic cerebral arteries with tone by the KCA channel inhibitor iberiotoxin From: Nelson MT , Cheng H, Rubart M, Santana LF, Bonev AD, Knot HJ, Lederer WJ Relaxation of arterial smooth muscle by calcium sparks. Science 1995;270:633-637 Pressure = 60 mmHg |
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Coronary microvessel responses of normal and atherosclerotic monkeys to acetylcholine Vessel diameters = 122 - 220 µm From: Sellke FW, Armstrong ML, Harrison DG Endothelium-dependent vascular relaxation is abnormal in the coronary microcirculation of atherosclerotic primates. Circ 1990;81:1586-1593 |
Spontaneous vasomotion of cerebral artery diameter as a function of temperature Pressure = 80 mmHg From: Osol G, Halpern W Spontaneous vasomotion in pressurized cerebral arteries from genetically hypertensive rats. Am J Physiol 1988;254 (Heart Circ Physiol 23):H28-H33 |
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Oxygen reactivity of an isolated rat cremaster muscle arteriole Pressure = 65 mmHg; ID = 77 µm From: Messina EJ, Sun D, Koller A, Wolin MS, Kaley G Increases in oxygen tension evoke arteriolar constriction by inhibiting endothelial prostaglandin synthesis. Microvasc Res 1994;48(2):151-160 |