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Biomedical subjects

O Appenzeller

Publications and source records attributed to O Appenzeller.

At least 37 records · Page 2Linked to original sources
PubMed1997

Immunohistochemical localisation of neuropeptides and nitric oxide synthase in sural nerves from Egyptian mummies.

Paleopathology is a well established science with numerous papers and books on the subject but, in contrast, paleoneurobiology is almost non-existent. We examined sections of sural nerves obtained from seven embalmed Egyptian mummies and one naturally desiccated Peruvian mummy, immunohistochemically stained for several neurochemicals. Immunoreactivity for type I nitric oxide synthase (NOS), protein gene-product 9.5, galanin, and calcitonin gene-related peptide immunoreactivity was observed in the nervi nervorum. No immunoreactivity was seen using antibodies directed against substance P, vasoactive intestinal polypeptide or neuropeptide Y. NOS-immunoreactivity was also observed in biopsied samples of contemporaneous human sural nerves. Thus, using a standard immunohistochemical technique it was possible to detect neurochemicals in ancient sural nerves that had been preserved by mummification. Furthermore, the finding of NOS in the ancient nerves led to its detection in contemporaneous sural nerves.

Egypt↗
PubMed1997

Acute and persistent effects of a 46-kilometer wilderness trail run at altitude: cardiovascular autonomic modulation and baroreflexes.

OBJECTIVE: To test the hypothesis that prolonged physical exercise induces long-lasting effects on blood pressure and heart rate we studied 17 endurance runners before and after the 1995 Sandia Wilderness Crossing Research Run (46 km of rocky trails, average altitude 2500 m). METHODS: We evaluated the response of the cardiovascular system to sympathetic stimulation by orthostatism and to sympathetic and parasympathetic carotid baroreceptor stimulations by sinusoidal neck suction at different frequencies (sympathetic activity on blood pressure by low-frequency stimulation, parasympathetic activity on RR interval by high-frequency stimulation). We used power spectral analysis of beat-to-beat RR interval, systolic and diastolic non-invasive blood pressure, in order to quantify the respiratory fluctuations (depending on vagal activity on the RR interval) and the slower non-respiratory fluctuations, depending on sympathetic activity on the blood pressure. Recordings were performed 24 h before, and 30 min, 24 h and 48 h after the run. RESULTS: Thirty minutes after the race we found reduced blood pressure, signs of relative sympathetic predominance (increased RR interval low-frequency/high-frequency ratio from 0.65 +/- 0.15 to 1.63 +/- 0.37, P < 0.05), reduced effect of parasympathetic baroreceptor stimulation (decrease in RR interval high-frequency neck-suction synchronous oscillations, from 5.33 +/- 0.34 to 3.55 +/- 0.37 ln-ms2, P < 0.005), unchanged blood pressure responses to sympathetic stimulations; 24 h after the race, the response to parasympathetic stimulation was increased (to 6.44 +/- 0.32 ln-ms2, P < 0.0005) compared to baseline (24 h before the race), whereas sympathetic stimulation by neck suction had no longer an effect on blood pressure. CONCLUSION: The acute effects of prolonged exertion are associated with a relative increase in sympathetic activity. Twenty-four hours after this race an increased sensitivity to vagal and reduced sensitivity to sympathetic baroreflex stimulation was found. In this field study at altitude we found long-lasting effects on cardiovascular autonomic modulation after physical exertion.

Adult↗
PubMed1996

Autonomic regulation of heart rate and peripheral circulation: comparison of high altitude and sea level residents.

1. To evaluate the activity of the autonomic nervous system on the heart and peripheral circulation in native high-altitude residents, during a Himalayan expedition we studied 12 men (age: 48 +/- 4, mean +/- SEM), life-long resident in a village at 4800 m (Sumdo village, Zanskar, India) and 7 healthy sea-level residents (age: 37 +/- 4) after 7 days of acclimatization (acclimatized lowlanders) at the same altitude. Furthermore 25 sea level residents (age: 46 +/- 2) underwent the same protocol at sea level. 2. R-R interval (RR), respiratory signal, non-invasive blood pressure, and skin arteriolar blood flow were evaluated in three different conditions: during free breathing in supine position and during controlled breathing (at 0.15 Hz), in supine and upright position, and analysed by autoregressive spectral analysis [low- (around 0.1 Hz) and high-frequency (respiratory) fluctuations, LF and HF, markers of sympathetic and vagal activity, respectively]. 3. High-altitude residents showed in supine position a higher RR than acclimatized lowlanders, similar to sea-level residents. RR variability was reduced in acclimatized lowlanders compared to both high-altitude residents and sea level residents. Systolic blood pressure (SBP) did not show significant differences between the three groups. High altitude residents showed in supine lower LF in RR signal compared to sea-level residents, and, compared to acclimatized lowlanders, higher HF and lower LF/HF ratio; high-altitude residents showed a reduction in skin microcirculation variability compared to sea-level residents, but this was eight fold greater than in acclimatized lowlander, thus indicating a much greater vasoconstriction in acclimatized lowlanders than in high-altitude residents. 4. In upright position, high-altitude residents showed the same behaviour as sea-level residents, with increase in LF-RR, and decrease in HF and LF-SBP. Acclimatized lowlanders showed similar directional trends though not significant changes for RR-LF. 5. After one week of acclimatization, lowlanders still manifested sympathetic activation and skin vasoconstriction; high-altitude residents did not show reduced vagal tone compared to sea-level residents, but a mild vasoconstriction appeared to be present. In conclusion, normal or enhanced vagal tone and preserved vasomotion are probably evidence of adaptation at high altitude hypoxia.

Adaptation, Physiological↗
PubMed1995

Heart rate and respiratory rhythm dynamics on ascent to high altitude.

OBJECTIVE: To investigate the alterations in autonomic control of heart rate at high altitude and to test the hypothesis that hypoxaemic stress during exposure to high altitude induces non-linear, periodic heart rate oscillations, similar to those seen in heart failure and the sleep apnoea syndrome. SUBJECTS: 11 healthy subjects aged 24-64. MAIN OUTCOME MEASURES: 24 hour ambulatory electrocardiogram records obtained at baseline (1524 m) and at 4700 m. Simultaneous heart rate and respiratory dynamics during 2.5 hours of sleep by fast Fourier transform analysis of beat to beat heart rate and of an electrocardiographically derived respiration signal. RESULTS: All subjects had resting hypoxaemia at high altitude, with an average oxyhaemoglobin saturation of 81% (5%). There was no significant change in mean heart rate, but low frequency (0.01-0.05 Hz) spectral power was increased (P < 0.01) at high altitude. Time series analysis showed a complex range of non-linear sinus rhythm dynamics. Striking low frequency (0.04-0.06 Hz) heart rate oscillations were observed during sleep in eight subjects at high altitude. Analysis of the electrocardiographically derived respiration signal indicated that these heart rate oscillations correlated with low frequency respiratory oscillations. CONCLUSIONS: These data suggest (a) that increased low frequency power during high altitude exposure is not simply attributable to increased sympathetic modulation of heart rate, but relates to distinctive cardiopulmonary oscillations at approximately 0.05 Hz and (b) that the emergence of periodic heart rate oscillations at high altitude is consistent with an unstable cardiopulmonary control system that may develop on acute exposure to hypoxaemic stress.

Adult↗
PubMed1993

Innervation of normal human sural and optic nerves by noradrenaline- and peptide-containing nervi vasorum and nervorum: effect of diabetes and alcoholism.

Histochemical, immunohistochemical and neurochemical techniques were used to examine the innervation of epineurial nerve sheaths and fascicular nerve bundles of human sural and optic nerves from controls and patients with peripheral neuropathy due to diabetes or alcoholism. The normal distribution of autonomic nerves in both nerve trunk sheaths consisted of a dense innervation by noradrenaline (NA)-containing nerves of the vasa nervorum, together with some fibres in the nervi nervorum. Intrafascicular NA-containing nerves were only present in the sural nerve. Vasoactive intestinal polypeptide (VIP)- and neuropeptide Y (NPY)-containing nerves also innervated the vasa nervorum and nervi nervorum of the nerve sheaths, although their density was considerably less. Substance P (SP)-containing nerves were sparse and primarily intrafascicular. Neurochemical assays for NA, VIP, NPY and SP in fascicular and epineurial preparations from the sural and optic nerves confirmed the light microscopical observations. Post mortem delay significantly affected the NA levels in the sural nerve but not in the optic nerve while the NA fascicular/epineurial ratio for the sural nerve was independent of this factor. Age, sex and the presence of alcohol at time of death had no effect on transmitter levels in normal sural nerves. In the optic nerve fascicles NA levels were higher in females than in males. In patients with peripheral neuropathy there was a significant reduction in the SP fascicular/epineurial ratio in both the optic nerve, which was histologically normal, and in the sural nerve, where there was evidence of neuropathy. The NA fascicular/epineurial ratio was also significantly reduced in the sural nerve from patients with peripheral neuropathy with a possible greater effect in diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Increased endothelin and creatine kinase after electrical stimulation of paraplegic muscle.

The purpose of this study was to assess changes in creatine kinase (CK) and endothelin (ET) in individuals with spinal cord injury (SCI) after computerized functional electrical stimulation leg ergometry (CFES LE). Eight subjects (7 male and 1 female) with complete spinal cord lesions (C7 to L1) completed zero-loaded CFES LE tests at baseline, after 3, 6, and 12 wk of CFES LE training (30 min, 3 times/wk), and also after detraining (DT) (n = 5). Venous blood samples were drawn 24, 48, and 72 h after CFES LE for measurement of ET and CK. The CK response was largest (peak CK) 72 h after baseline tests (28.2 +/- 6.0 to 895.7 +/- 345.9 ktals/l) and was no different from baseline by weeks 3, 6, and 12. After DT, CK was similar before and after CFES LE (153.8 +/- 19.0 and 189.7 +/- 34.5 ktals/l, respectively). CFES LE also significantly increased peak ET after baseline (from 11.7 +/- 1.5 to 18.0 +/- 2.5 pg/ml). During the subsequent training, peak ET remained significantly higher than the baseline value at weeks 3, 6, and 12 (20.2 +/- 1.8, 18.0 +/- 1.1, and 16.9 +/- 2.2 pg/ml, respectively). After DT, peak ET increased significant relationship (r = 0.44) existed between ln peak CK activity and peak ET. In summary, the increase in circulating ET in spinal cord-injured individuals may have implications for baroreceptor function and therefore blood pressure control in SCI. Further research into CFES LE, ET, and baroreceptor function in SCI is warranted.

Adult↗
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↗