PubMed · 6606291
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
G B Azzena. [Vestibular compensation: experimental data].. https://pubmed.ncbi.nlm.nih.gov/6606291/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Carotid sinus hypersensitivity (CSH) is recognised in up to 45% of elderly patients with syncope, falls, and dizziness that may not be attributed to specific myocardial sinus node dysfunction, various diseases that affect pacemaker activity, cardiac output and blood supply to the brain. The pathophysiology of CSH is unclear but it is associated with ageing, hypertension, and ischaemic heart disease. CSH is potentially treatable with dual chamber pacing for prolonged sinus arrest (cardio-inhibitory CSH) but therapy for the more prevalent hypotension (vasodepressor CSH) is unsatisfactory. However, hypersensitivity of the carotid sinus is not consistent with the known blunting effects of senescence and hypertension on baroreflex sensitivity. The present hypothesis proposes that CSH in elderly patients results from up-regulation of brainstem postsynaptic alpha-2 adrenoceptors. Reduced carotid sinus compliance in elderly arteriosclerotic hypertensive patients will reduce afferent impulse traffic in the baroreflex pathway. Such relative deafferentation may be expected to cause baroreflex postsynaptic hypersensitivity, mediated by up-regulation of the dominant postsynaptic receptor population in the baroreflex pathway, ie, alpha-2 adrenoceptors. Vigorous carotid sinus stimulation, eg, massage, could thus cause an overshoot baroreflex efferent response, resulting in profound hypotension and bradycardia. Hypotension and bradycardia are compounded by the effects of age, hypertension, ischaemic heart disease and arteriosclerosis on rapid cardiovascular compensation, resulting in cerebral hypoperfusion and syncope. Thus CSH in elderly patients should be considered as a clinical marker of widespread arteriosclerotic disease, rather than as a distinct disease entity. If correct, this hypothesis has potentially important implications for the pharmacotherapy of hypotension-related symptoms in elderly arteriosclerotic patients.
We have investigated the time course and extent to which peripheral nerve lesions cause a morphological reorganization of the central terminals of choleragenoid-horseradish peroxidase (B-HRP)-labelled primary afferent fibers in the mammalian dorsal horn. Choleragenoid-horseradish peroxidase is retrogradely transported by myelinated (A) sensory axons to laminae I, III, IV and V of the normal dorsal horn of the spinal cord, leaving lamina II unlabelled. We previously showed that peripheral axotomy results in the sprouting of numerous B-HRP-labelled large myelinated sensory axons into lamina II. We show here that this spread of B-HRP-labelled axons into lamina II is detectable at 1 week, maximal by 2 weeks and persists for over 6 months postlesion. By 9 months, however, B-HRP fibers no longer appear in lamina II. The sprouting into lamina II occurs whether regeneration is allowed (crush) or prevented (section with ligation), and does not reverse at times when peripheral fibers reinnervate the periphery. We also show that 15 times more synaptic terminals in lamina II are labelled by B-HRP 2 weeks after axotomy than in the normal. We interpret this as indicating that the sprouting fibers are making synaptic contacts with postsynaptic targets. This implies that A-fiber terminal reorganization is a prominent and long-lasting but not permanent feature of peripheral axotomy. We also provide evidence that this sprouting is the consequence of a combination of an atrophic loss of central synaptic terminals and the conditioning of the sensory neurons by peripheral axotomy. The sprouting of large sensory fibers into the spinal territory where postsynaptic targets usually receive only small afferent fiber input may bear on the intractable touch-evoked pain that can follow nerve injury.
Severe micturition dysfunction can occur following spinal cord injury (SCI) due to abnormal contractions of the urethral sphincter during bladder contractions (bladder/sphincter dyssynergia). This causes urinary retention, bladder overdistension, and increases the workload of the bladder leading to hypertrophy of the bladder muscle. Bladder hypertrophy induced by urethral outlet ligation in rats is accompanied by enlargement of both the afferent and efferent neurons innervating the bladder. The primary aim of this study was to test whether SCI-induced bladder hypertrophy produces a similar enlargement of bladder afferent neurons in the dorsal root ganglia (DRG) or efferent neurons in the major pelvic ganglia (MPG). Following SCI in female Wistar rats, there was a four-fold increase in bladder weight. The mean cross-sectional area of bladder DRG cell profiles increased approx. 50% after SCI; however, the mean area of MPG cell profiles did not change significantly. Urinary diversion (disconnecting the ureters from the bladder) prevented both the bladder hypertrophy and the DRG cell hypertrophy after SCI, suggesting that bladder hypertrophy drives DRG cell enlargement. On the other hand, since the size of MPG cells did not change significantly after SCI, bladder hypertrophy does not mandate MPG cell enlargement. However, preliminary results indicate that the mean cross-sectional area of MPG cells did increase (2-3 times) in SCI rats when the neural input to the MPG was eliminated by transecting the pelvic and hypogastric nerves; this suggests that the lack of change in size of MPG cells after SCI may be due to an inhibitory influence from the spinal cord.