Home About us Contact
|
Home About us Contact | ||
|
|
||
Nerve Blood Flow (nerve + blood_flow)
Selected AbstractsReduced Nerve Blood Flow In Diabetic Rats Is A Reflection Of Hindlimb Muscle WastingJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Dr Tomlinson We examined the influence of muscle wasting, as a result of streptozotocin-induced diabetes, on sciatic nerve laser Doppler flux (SNLDF), as an index of nerve blood flow, and conduction velocity (NCV). We compared dietary-restricted weight-reduced non-diabetic rats with controls and with diabetic rats and we studied the effects of clenbuterol, an anabolic ,-adrenoceptor agonist, in control and diabetic rats. Dietary restriction reduced the weights of hindlimb muscles,extensor digitorum longus, soleus and gastrocnemius,half as much as did streptozotocin-diabetes and clenbuterol increased muscle weights in control and diabetic rats. This gave a hierarchy of muscle weights in the order,clenbuterol-controls, untreated controls, weight-reduced non-diabetics, clenbuterol-diabetics and untreated diabetics. Diabetes without treatment reduced SNLDF by 51% (p < 0.01); dietary restriction by 25% (p < 0.01) and there were proportional increases associated with clenbuterol treatment. Combined muscle weights regressed closely with SNLDF (r2=0.69; p < 0.001) and, when the latter was expressed relative to muscle weights, a similar value was obtained for all five groups,there were no significant differences. Thus, sciatic nerve blood flow is closely related to hindlimb muscle weight and the effect of diabetes on nerve blood flow may be secondary to muscle wasting. Sciatic/tibialis motor and sensory conduction velocities were also reduced by muscle wasting in the dietary restricted group of non-diabetic rats, but, unlike nerve Doppler flux, it was unaffected by clenbuterol. [source] Microcirculatory Responses To Electrical Spinal Cord Stimulation In Painful Diabetic Neuropathy And Other Painful ConditionsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Nd Harris Electrical spinal cord stimulation (ESCS) has been used to provide pain relief in a number of conditions, including painful diabetic neuropathy (PDN). ESCS has also been shown to increase microvascular blood flow in peripheral vascular disease. If nerve hypoxia contributes to pain in PDN, ESCS may relieve this by increasing nerve blood flow. We have therefore investigated skin and sural nerve microvascular responses to ESCS. We studied subjects implanted with ESCS for pain relief, 4 had PDN and 7 were controls with other painful conditions. Blood flow, before and during stimulation, was assessed using Laser Doppler flowmetry. Only one (PDN) subject showed a statistically significant increase in skin blood flow during stimulation. The three remaining PDN subjects showed significant reductions in skin blood flow, as did 3/7 of controls. Sural nerve blood flow was measured on a separate occasion. During stimulation nerve blood flow increased in 1 (control) subject, decreased in 1 (PDN) subject and did not change in the other 5 tested (3 PDN and 2 control). In summary, ESCS did not produce any consistent increase in skin or nerve microvascular blood flow. ESCS reduces pain in a variety of different conditions, however this does not appear to be mediated by changes in blood flow. Until a thorough understanding of the pathogenic mechanisms causing PDN is achieved, therapy will be limited to providing symptomatic relief. [source] Reduced Nerve Blood Flow In Diabetic Rats Is A Reflection Of Hindlimb Muscle WastingJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Dr Tomlinson We examined the influence of muscle wasting, as a result of streptozotocin-induced diabetes, on sciatic nerve laser Doppler flux (SNLDF), as an index of nerve blood flow, and conduction velocity (NCV). We compared dietary-restricted weight-reduced non-diabetic rats with controls and with diabetic rats and we studied the effects of clenbuterol, an anabolic ,-adrenoceptor agonist, in control and diabetic rats. Dietary restriction reduced the weights of hindlimb muscles,extensor digitorum longus, soleus and gastrocnemius,half as much as did streptozotocin-diabetes and clenbuterol increased muscle weights in control and diabetic rats. This gave a hierarchy of muscle weights in the order,clenbuterol-controls, untreated controls, weight-reduced non-diabetics, clenbuterol-diabetics and untreated diabetics. Diabetes without treatment reduced SNLDF by 51% (p < 0.01); dietary restriction by 25% (p < 0.01) and there were proportional increases associated with clenbuterol treatment. Combined muscle weights regressed closely with SNLDF (r2=0.69; p < 0.001) and, when the latter was expressed relative to muscle weights, a similar value was obtained for all five groups,there were no significant differences. Thus, sciatic nerve blood flow is closely related to hindlimb muscle weight and the effect of diabetes on nerve blood flow may be secondary to muscle wasting. Sciatic/tibialis motor and sensory conduction velocities were also reduced by muscle wasting in the dietary restricted group of non-diabetic rats, but, unlike nerve Doppler flux, it was unaffected by clenbuterol. [source] A double masked placebo controlled study on the effect of nifedipine on optic nerve blood flow and visual field function in patients with open angle glaucomaBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 2 2001Georg Rainer Aims, To investigate whether nifedipine affects ocular perfusion or visual fields in open angle glaucoma patients. Methods, In a parallel group study nifedipine or placebo was administered for 3 months (n = 30). Ocular fundus pulsation amplitude (FPA), cup blood flow (Flowcup) and visual field mean deviation (MD) were measured. Results, Five patients receiving nifedipine discontinued due to adverse events. Nifedipine did not affect FPA [difference: 0.3 µm (95% CI ,0.3,0.9); P = 0.70], Flowcup: [difference: ,9 rel.units (95% CI ,133,114); P = 0.99], or MD [difference: 0.2dB (95% CI ,2.2,2.7); P = 0.51]vs placebo. Conclusions, Systemic nifedipine is not well tolerated in glaucoma patients and exerts no effect on visual fields or ocular perfusion. [source] 2151: Interaction of vascular and biomechanical aspects of glaucomaACTA OPHTHALMOLOGICA, Issue 2010M LESK Purpose In an attempt to understand some of the reasons why some optic nerves appear to be sensitive to IOP and others not, I will review studies describing the interaction between vascular and biomechanical factors in open angle glaucoma. Methods Studies using biomechanical modelling, epidemiologic data, measurements of ocular or systemic blood flow, measurment of peripheral vasospasticity, and measurement of ocular biomechanical parameters will be reviewed. Hypotheses will be presented regarding the interpretation of these data. Results Studies suggest that the optic nerves of vasospasctic patients may be more IOP-sensitive than those of non-vasospastic patients. Non-invasive measurements of ocular blood flow suggest that this pressure-sensitivity may be related to IOP-sensitive optic nerve blood flow. Biomechanical modelling suggests that scleral and lamina cribrosa elasticity, axial length, and eye wall thickness contribute to optic nerve head stress and strain. Cross-sectional clinical data supports the role of increased ocular elasticity in the susceptibilty of the optic nerve to glaucoma damage, especially in vasospastic patients. Some promising new avenues for research in this area will be presented. Conclusion There is increasing evidence that biomechanical and vascular ocular factors interact leading to an elevated susceptibilty of the optic nerve to glaucomatous optic nerve damage. Commercial interest [source] Optic nerve blood flow in glaucomaCLINICAL AND EXPERIMENTAL OPTOMETRY, Issue 3 2000Renuka Bathija FRACO FRACS Background: Glaucomatous optic neuropathy often occurs in the absence of elevated intraocular pressure and, conversely, elevated intraocular pressure may occur without associated damage of the optic nerve. These findings challenge the simple explanation of intraocular pressure being the sole cause of neural loss and have led to theories of ischaemic causes of the morbidity. This paper reviews the vascular anatomy of the optic disc, the factors that control its blood flow and the existing techniques for measurement of the blood flow. It also briefly discusses the possible role of apoptosis in glaucomatous visual loss. Method: Literature review. Conclusions: The posterior ciliary artery circulation is the main source of the blood supply to the optic nerve head with additional lesser supply via the central retinal artery and the choroidal circulation. There is considerable individual variation in the distribution of this circulation and complex regulatory systems govern its function. It is likely that microcirculatory changes in the vascular supply of the optic disc play a role in glaucoma, either as the primary abnormality or as a co-factor that increases susceptibility to damage from increased intraocular pressure through impaired auto-regulation. Clinical trials are currently in progress for the treatment of glaucoma with systemically administered agents that are antagonists of the receptors that mediate glutamine toxicity, a factor in the process of apoptosis. [source] | ||||||||||