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Biomedical subjects

O Appenzeller

Publications and source records attributed to O Appenzeller.

At least 19 recordsLinked to original sources
PubMed1992

Chronic neurodegenerative disease associated with HTLV-II infection.

Although human T-cell leukemia virus (HTLV) type I is known to cause a number of diseases, there has been no convincing evidence of pathological changes after infection with the related virus, HTLV-II. We have found an endemic focus of HTLV-II infection among members of an American Indian population in New Mexico, USA. We set out to determine the pathological consequences of HTLV-II infection in this population and identified two sisters (aged 59 and 46 years) with a disease superficially resembling the myeloneuropathy induced by HTLV-I. These women had a syndrome similar to the olivopontocerebellar atrophy variant of multiple system atrophy, and HTLV-II infection was confirmed by western blot and the polymerase chain reaction. Thus, HTLV-II may, like HTLV-I, cause a progressive neurodegenerative disease.

Ataxia↗
PubMed1992

Differential vulnerability of neuropeptides in nerves of the vasa nervorum to streptozotocin-induced diabetes.

Neuropeptides in perivascular nerves of vasa nervorum supplying blood to rat optic, sciatic, vagus and sympathetic chain nerve trunks are differentially vulnerable to streptozotocin (STZ)-induced diabetes. Immunohistochemical analysis of epineurial/perineurial nerve sheaths showed that 8 weeks after induction of diabetes, the density of neuropeptide Y (NPY)-immunoreactive nerve fibres in optic nerve sheaths was increased, while it was decreased in sciatic, vagus and sympathetic nerve sheaths. Vasoactive intestinal polypeptide (VIP)-immunoreactivity was increased in vasa and nervi nervorum of optic, sciatic, vagus and sympathetic chain nerve sheaths. Immunoassay of NPY confirmed increased levels in optic nerve sheaths and showed that substance P and calcitonin gene-related peptide levels increased in sciatic but not optic nerve sheaths. Neuropeptide levels in the intrafascicular nerve fibres were unaffected. This provides further evidence for a disturbance in the autonomic control of blood flow to peripheral and cranial nerve trunks via vasa nervorum in STZ-induced diabetes, which may lead to ischaemic changes, alter local axon reflexes and contribute to the pathogenesis of the disease.

Animals↗
PubMed1992

Peptides and exercise at high and low altitudes.

Some peptides are released with stress. We therefore examined effects of different exercise stress at low and moderate altitudes and after heat stress on beta-endorphin and endothelin in the human circulation. We also assessed longitudinally the effects of chronic exertion on beta-endorphin and the relationship to melatonin secretion in well-trained athletes. All peptides and melatonin increased after exercise, but the magnitude of this increase was age-dependent. Chronic exertion is associated with a decrease in exercise induced opioid release and in such individuals melatonin secretion is not beta-endorphin related. Long term high altitude exposure is associated with high-beta-endorphin levels at rest. Atrial natriuretic factor and vasopressin is also released with exercise at moderate altitude. Endothelin, a powerful vasoconstrictor, is increased independent of type of exercise, duration and moderate hypoxia.

Adult↗
PubMed1992

Aging and the autonomic nervous system.

Most studies show a decline in autonomic nervous system (ANS) function with advancing age. The occasional heterogenous responses of ANS to aging, however, suggest that psychosocial and physiologic factors alter aging of ANS function.

Adult↗
PubMed1991

Pathogenesis of migraine.

Endothelial cells are not just a semipermeable membrane that forms a barrier between the blood and the vascular smooth muscles. This cell system is a highly active metabolic endocrine organ. It not only produces a number of important substances in vascular and neural homeostasis but also inactivates vasoactive substances such as serotonin and bradykinin. In addition, it produces endothelin-1 and angiotensin II; more importantly in the context of migraine, endothelial cells produce the vasodilators prostacyclin and EDRF-NO, both of which are local (paracrine) hormones. The physiologic function of endothelial cells is affected by aspirin, which prevents prostacyclin formation but has little effect on normal blood pressure. From this information, one can infer that endothelial cell production of prostacyclin does not play an important part in normal cardiovascular control. On the other hand, the administration of Ng-monomethyl-L-arginine causes immediate increases in blood pressure. Because the administration of this substance inhibits the release of EDRF-NO, it appears that this paracrine endothelial hormone actively dilates the normal circulation. It is of cardinal importance that damage or flow perturbations of cell membranes of the endothelial lining of blood vessels cause an increased production of prostaglandins. However, smooth muscle cells underlying the endothelial lining also synthesize prostacyclin. This mechanism is thought to be held in reserve to reinforce local production of prostacyclin and vasodilatation when cell damage to the endothelial lining occurs and EDRF-No is not produced. Many theories for the causation of migraine have been proposed, and some have been reviewed. Those holding sway tend to ignore inconsistencies and cite supporting evidence in favor of their pet explanation only. I therefore have no hesitation to show that the best explanation at present, based on the most recent cellular evidence, explains all features of migraine and the response of migraineurs to therapy. The endothelial cell is the most likely site of the primary abnormality (Fig. 1). Although under physiologic circumstances perivascular innervation and endothelial systems closely interact in the control of vascular tone during pathologic conditions such as ischemia, the dominant role in protecting the circulation is endothelium-mediated. The biology of headache is so diverse and our ignorance sufficiently pervasive that the investigation of endothelial cell function may solve the mystery of migraine. To match the postulated crucial role of the endothelial cell in the pathogenesis of migraine, another cell would have to be ubiquitously present throughout the vasculature and not just confined to the central nervous system.(ABSTRACT TRUNCATED AT 400 WORDS)

Humans↗
PubMed1991

Effects of endurance training and long distance running on blood viscosity.

The effect of endurance training on blood viscosity was studied by comparing blood rheological properties in control subjects (untrained) and endurance trained subjects. The effect of running on blood viscosity was studied in the 33 endurance trained subjects before and after a 48-km mountain race (Sandia Wilderness Crossing Research Run). Runners started at an altitude of 1700 m, ran 26 km to 3300 m, then descended 22 km to finish at 1900 m. Venous blood viscosity (eta b) and plasma viscosity (eta p) were measured at 37 degrees C at shear rates of 11.25, 22.5, 45, 90, and 225.s-1, using a cone-plate viscometer. Endurance trained subjects had significantly higher pre-race blood viscosity at 11.25 and 22.5.s-1 than control subjects but similar plasma viscosity and hematocrits. Following the race, there was no significant change in mean hematocrit, but eta b increased significantly at all shear rates except 225.s-1. Plasma viscosity at 225.s-1 increased significantly from 1.44 to 1.53 cP following the run. Since eta b did not increase, an increase in red cell deformability is inferred. The mechanism of the increase in eta b at lower shear rates in runners is due in part to the higher plasma viscosity. An additional mechanism at lower shear rates is in an increase in red cell aggregation. Increased plasma fibrinogen was measured in six of six resting subjects taken from 1600 m to 3300 m and is speculated to be the mechanism of enhanced aggregation and deformability in the runners.

Adult↗
PubMed1990

Studies of vasoactive intestinal polypeptide expression in injured peripheral neurons using capsaicin, sympathectomy and mf mutant rats.

The increased expression of vasoactive intestinal polypeptide (VIP) in injured peripheral neurons was studied. In contrast to substance P, there was a marked increase, and maintained fast axonal transport, of VIP in rat sciatic nerve after peripheral axotomy. Local capsaicin application to the nerve trunk failed to inhibit the injury-induced VIP increase, and capsaicin even increased VIP levels when applied locally to uninjured nerves. Pharmacological sympathectomy showed that some of the peripheral VIP increase may occur in post-ganglionic sympathetic fibres. The VIP increase after injury appeared unaffected in the mf mutant rat, in spite of its loss of lumbar dorsal root ganglion cells. VIP-staining fibres in the epi- and peri-neurium and perivascular plexuses of sciatic nerve showed an increase in number in parallel with the changes of the nerve VIP content. These findings suggest that sensory and sympathetic nerve fibres expressing VIP after injury play a role in the regulation of blood flow to nerves, and in the pathophysiological processes in nerve and dorsal spinal cord which follow peripheral nerve injury.

Animals↗
PubMed1989

Increase in plasma melatonin, beta-endorphin, and cortisol after a 28.5-mile mountain race: relationship to performance and lack of effect of naltrexone.

Strenuous exercise increases plasma melatonin, cortisol, and beta-endorphin concentrations. Furthermore, a relationship between endogenous opioids and melatonin has been proposed. We measured plasma melatonin, cortisol, and beta-endorphin in 46 subjects before and after a 28.5-mile high altitude race. Thirteen of the subjects received the orally active opioid antagonist naltrexone immediately before the race. The mean plasma melatonin, cortisol, and beta-endorphin levels were higher after the race than before it; the melatonin results were confirmed by gas chromatography-mass spectrometry assay of 12 subjects. Naltrexone had no effect on the increase in any of the three hormones. The run-induced increases in plasma melatonin, beta-endorphin, and cortisol were negatively correlated with finishing time, but only the plasma beta-endorphin and cortisol rises correlated with each other. We conclude that prolonged exercise in trained athletes can increase plasma melatonin and that this rise is not due to the concomitant opioid release.

Adult↗
PubMed1988

Amantadine, fatigue, and multiple sclerosis.

In a double-blind placebo-controlled crossover study of ten patients with multiple sclerosis, we found amantadine hydrochloride therapy to be effective in improving fatigability in six. Administration of the drug was associated with significantly higher levels of beta-endorphin-beta-lipotropin and responders had significantly higher levels than nonresponders. Lactate levels were significantly higher and pyruvate levels lower in nonresponders. Amantadine given for fatigue to patients with multiple sclerosis is associated with measurable changes in levels of metabolites and peptides in the circulation.

Amantadine↗
PubMed1986

Adrenergic innervation of vasa and nervi nervorum of optic, sciatic, vagus and sympathetic nerve trunks in normal and streptozotocin-diabetic rats.

Adrenergic nerves were studied in nervi nervorum and perivascular nerve plexus of vasa nervorum in whole-mount nerve sheath preparations of optic, sciatic and vagus nerves and in the paravertebral sympathetic chain in normal and streptozotocin-treated diabetic rats. A substantial or complete loss of fluorescent adrenergic fibres around blood vessels in the optic nerves was observed 8 weeks after induction of diabetes. This was in marked contrast to the increase in perivascular adrenergic fibres in the sciatic, vagus and sympathetic chain nerve trunks of the same animals at the same time. Assays of noradrenaline levels in whole nerve segments also showed that they were not biochemically detectable in the optic nerves but were significantly higher in the vagus of diabetic animals (P less than 0.05). There was also an increase in numbers of mast cells in the vicinity of vasa nervorum of diabetic nerves.

Adrenergic Fibers↗
PubMed1986

Neurofibromatosis xenografts. Contribution to pathogenesis.

We transplanted Schwann cells of 3 patients with neurofibromatosis from neurofibromas, sural nerve, and from a malignant schwannoma into sciatic nerves of immunoincompetent mice. Three and six months later, the grafts and distal nerve segments contained normal myelinated fibers. After rendering host animals immune competent again, neurofibroma and malignant schwannoma Schwann cells were rejected, but grafts retained normally myelinated fibers indicating that these were of mouse origin. Sural nerve Schwann cells from a neurofibromatosis patient were rejected also leaving naked axons in the grafted segments showing that human Schwann cells from the sural nerve of one patient had invested and myelinated the regenerating mouse axons. The nature of putative signals passing between axons and Schwann cells might be elucidated by the combination of human and animal cells in immunoincompetent host nerves. Hypothetical signals for myelination of mouse axons were normally received by sural nerve Schwann cells of a patient with neurofibromatosis, but not by Schwann cells from neurofibromas or malignant schwannomas.

Animals↗
PubMed1979

Experimental autonomic neuropathy: ultrastructure and immunohistochemical study of a disorder of reflex vasomotor function.

Vasomotor function in ear vessels of rabbits was tested in animals with experimental autonomic neuropathy (EAUN), experimental allergic neuritis (EAN), and controls. Reflex vasodilatation was impaired in animals with EAUN but not in EAN or control rabbits. Ultrastructural examination of paravertebral sympathetic chain, perivascular nerves, and perivascular tissue showed similar changes in all animals differing in degree only. Occasional lymphocytes were seen in paravertebral chains of controls but large numbers of lymphocytes and macrophages occurred in EAUN and EAN. No active destruction of myelinated or unmyelinated fibers could be seen. Perivascular nerves showed similar cellular infiltrates and basophils were found in perivascular spaces of ear vessels which were most abundant in animals with EAUN. Fibre-size spectra analysis of unmyelinated fibres in the paravertebral sympathetic chain showed a shift to the left suggesting regeneration of unmyelinated axons in both EAN and EAUN. No specific immunofluorescence against neuronal components could be demonstrated in sensitized animals. It is concluded that the functional disturbance of reflex vasomotion in EAUN is not accompanied by specific ultrastructural lesions nor could neuronal components be immunologically implicated in the disorder. Regeneration of unmyelinated axons and recovery of function after some weeks together with abundance of basophils in perivascular tissue of sensitized animals, suggests that a localized inflammation may have occurred, the basophils interfacing between foreign antigens, the serum cascade systems, and other inflammatory cells. The usefulness of EAUN as a model for acute pandysautonomia in man remains to be determined.

Animals↗