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Calvin B. Early, Richard C. Dewey, Heinz P. Pieper and William E. Hunt

O ne major problem in defining pressure-flow characteristics in living vascular beds is that autoregulation can alter bed characteristics during the period of observation. In fact, the flat part of the Lassen 7 curve is the net result of these vasomotor responses to changes in pressure. Flow remains constant between 50 and 150 mm Hg arterial pressure only as long as normal vasomotor responses occur. Not only the properties of flow and pressure but also the property of vasomotor tone must be identified before the flow characteristics of the vascular bed are

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Experimental cerebral hemodynamics

Vasomotor tone, critical closing pressure, and vascular bed resistance

Richard C. Dewey, Heinz P. Pieper and William E. Hunt

T he response of the cerebral circulation to changes in mean arterial pressure is well known. Flow is maintained constant at pressures between 50 and 150 mm Hg by adjustments of vasomotor tone; this is due to autoregulation. It has long been presumed that the vasomotor responses maintain constant flow by adjusting the caliber of the resistance vessel. No previous work has demonstrated the mechanism whereby changes in vasomotor tone produce changes in cerebral blood flow (CBF). This report presents evidence that changes in vasomotor tone per se may affect

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Harold D. Portnoy, Michael Chopp, Craig Branch and Michael B. Shannon

Laplace, T = P TM × R. At Ro, only T A balances P TM and any decrease in pressure below this point will cause the vessel to collapse. 5–7, 25 Thus, an instability point (IP) is defined where T A of the smooth muscle just balances P TM . § Any increase in P TM above the IP results in a stable condition with stretch of the vessel wall, and any decrease in P TM results in collapse of the vessel. The arteriolar wall is thus maintained, whenever possible, under the least tension without collapse. At the IP, vasomotor tone is thus equivalent to a pressure defined by T

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Marek Czosnyka, Hugh K. Richards, Zofia Czosnyka, Stefan Piechnik and John D. Pickard

related to phenomena that underlay benign intracranial hypertension. 42 We investigated an animal model of CSF compensation during constant-rate subarachnoid infusion to study changes in CSF compensation with variations in vasomotor tone produced by different concentrations of arterial CO 2 , at different levels of ABP, and immediately after death. We studied all the CSF compensatory parameters with particular attention paid to the resistance to CSF outflow, the brain elastance coefficient, and the pulse amplitude of ICP. The practical aim of this study was to

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Masakazu Takayasu and Ralph G. Dacey Jr.

mechanisms all contribute to the maintenance of cerebral vasomotor tone. Metabolic mechanisms have been implicated in the autoregulatory response to cerebral oligemia. For example, post-reperfusion cerebral hyperemia occurs immediately after restoration of the circulation following temporary ischemia. 10, 14, 21, 27 In this phenomenon, cerebral blood flow increases temporarily above resting level after a period of circulatory arrest. This increased flow has been explained by the accumulation of metabolic vasodilator products such as hydrogen ion, potassium ion, or

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Samuel J. Hassenbusch, Michael Stanton-Hicks, Derek Schoppa, James G. Walsh and Edward C. Covington

allodynia and spontaneous deep pain; 2) moderately effective in improving vasomotor tone changes; 3) mildly effective in improving motor deficits; and 4) most effective in patients with symptoms and findings entirely in the distribution of one major peripheral nerve. Patient Eligibility All patients in this study had a diagnosis of RSD based on the following symptoms: 1) light touch—induced allodynia that spreads beyond the area of stimulation and persists after the stimulus; 2) deep burning pain; 3) clinical evidence of vasomotor tone changes; 4) at least some

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Richard E. Clatterbuck, Philippe Gailloud, Travis Tierney, Victoria M. Clatterbuck, Kieran J. Murphy and Rafael J. Tamargo

increased in aneurysmal SAH 34, 53 and NO is depleted at the same time. 24, 46 This combination of molecular events alters the equilibrium of vasomotor tone toward constriction. Given that NO directly affects smooth-muscle relaxation, its application in the treatment of vasospasm is attractive. Furthermore, NO appears to be a specific inhibitor of ICAM-1 expression and thus of leukocyte—endothelial cell interaction. 8, 39 Results from a series of experiments in various animals indicate NO's potential clinical utility in the treatment of delayed cerebral vasospasm. 1

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B. Gregory Thompson, Ryszard M. Pluta, Mary E. Girton and Edward H. Oldfield

, chemoregulation, or autoregulation in primates. Thus, these models provide limited information about the role of NO in the graded physiological response to hypercapnia or hypotension and leave unanswered the question of what role NO plays in the regulation of CBF in primates. We developed a primate model to assess in vivo regulation of cerebral vasoregulation by NO and used it to establish the role of NO in the regulation of CBF in primates. We sought to answer: 1) whether maintenance of resting (basal) vasomotor tone requires NO; 2) whether NO mediates chemoregulation of

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Shin-Han Tsai, Chun-Jen Shih, Thung-Tai Shyy and Jiang-Chuan Liu

✓ Vasomotor responses of the skin of the thumb and the big toe were measured in normal subjects and patients with spinal transection at a neutral ambient temperature of 22.0 ± 0.5°C, and in a cool (12.0 ± 0.5°C) and warm (32.0 ± 0.5°C) environment. The vasomotor response of the hand and foot to the cooling and warming of part of the opposite upper or lower extremity was also recorded. Spinal transection at T5–11 abolishes acutely all vasomotor responses in the paraplegic lower extremities, but does not alter the responses in the upper extremities. By 4 months, the vasomotor tone in the lower extremities at a neutral ambient temperature returned to normal values as did the response to a cool and warm environment. The crossed vasomotor reflex to cooling and warming one lower extremity recovers more slowly, requiring a period of 18 months for complete recovery. The slower recovery of the vasomotor reflex in spinally transected man than in similarly treated dogs is thought to be due to the greater spinal shock in the former. The recovery of vasomotor responses in the paraplegic limbs to cooling and warming after thoracic transections suggests that these responses are primitive and powerful thermoregulatory mechanisms.

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correct. The sentence reads: “Rounding of both the CSFPW [CSF pulse wave] and SSPW [sagittal sinus pulse wave] and an increase in Pss [sagittal sinus pressure] indicate a loss of autoregulation.” This is true only when autoregulation is impaired due to a primary loss of vasomotor tone such as seen during hypercapnia. When due to intracranial hypertension the CSFPW is rounded, but the SSPW is decreased in amplitude and is less rounded, and Pss decreases or does not change. The important point is that impairment of autoregulation is associated with rounding of the CSFPW