Increased serum levels of the brain damage marker S100B after apnea in trained breath-hold divers: a study including respiratory and cardiovascular observations

2009 ◽  
Vol 107 (3) ◽  
pp. 809-815 ◽  
Author(s):  
Johan P. A. Andersson ◽  
Mats H. Linér ◽  
Henrik Jönsson
Keyword(s):  
Brain Damage ◽  
Serum Levels ◽  
Breath Hold ◽  
Long Term Effects ◽  
Arterial Blood ◽  
The Central Nervous System ◽  
Serious Injury ◽  
Protein S100b ◽  
The Brain ◽  
Damage Marker

The concentration of the protein S100B in serum is used as a brain damage marker in various conditions. We wanted to investigate whether a voluntary, prolonged apnea in trained breath-hold divers resulted in an increase of S100B in serum. Nine trained breath-hold divers performed a protocol mimicking the procedures they use during breath-hold training and competition, including extensive preapneic hyperventilation and glossopharyngeal insufflation, in order to perform a maximum-duration apnea, i.e., “static apnea” (average: 335 s, range: 281–403 s). Arterial blood samples were collected and cardiovascular variables recorded. Arterial partial pressures of O2 and CO2 (PaO2 and PaCO2) were 128 Torr and 20 Torr, respectively, at the start of apnea. The degree of asphyxia at the end of apnea was considerable, with PaO2 and PaCO2 reaching 28 Torr and 45 Torr, respectively. The concentration of S100B in serum transiently increased from 0.066 μg/l at the start of apnea to 0.083 μg/l after the apnea ( P < 0.05). The increase in S100B is attributed to the asphyxia or to other physiological responses to apnea, for example, increased blood pressure, and probably indicates a temporary opening of the blood-brain barrier. It is not possible to conclude that the observed increase in S100B levels in serum after a maximal-duration apnea reflects a serious injury to the brain, although the results raise concerns considering negative long-term effects. At the least, the results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system and do not preclude cumulative effects.

scholarly journals The Use of Botulinum Toxin for the Treatment of Chronic Joint Pain: Clinical and Experimental Evidence

Toxins ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 314 ◽  
Author(s):  
Nicole Blanshan ◽  
Hollis Krug
Keyword(s):  
Pain Relief ◽  
Joint Pain ◽  
Peripheral Sensitization ◽  
Long Term Effects ◽  
Neuropeptide Release ◽  
Osteoarthritis Pain ◽  
Catalytically Active ◽  
The Central Nervous System ◽  
The Brain

Chronic osteoarthritis pain is an increasing worldwide problem. Treatment for osteoarthritis pain is generally inadequate or fraught with potential toxicities. Botulinum toxins (BoNTs) are potent inhibitors of neuropeptide release. Paralytic toxicity is due to inhibition at the neuromuscular junction, and this effect has been utilized for treatments of painful dystonias. Pain relief following BoNT muscle injection has been noted to be more significant than muscle weakness and hypothesized to occur because of the inhibition of peripheral neuropeptide release and reduction of peripheral sensitization. Because of this observation, BoNT has been studied as an intra-articular (IA) analgesic for chronic joint pain. In clinical trials, BoNT appears to be effective for nociceptive joint pain. No toxicity has been reported. In preclinical models of joint pain, BoNT is similarly effective. Examination of the dorsal root ganglion (DRG) and the central nervous system has shown that catalytically active BoNT is retrogradely transported by neurons and then transcytosed to afferent synapses in the brain. This suggests that pain relief may also be due to the central effects of the drug. In summary, BoNT appears to be safe and effective for the treatment of chronic joint pain. The long-term effects of IA BoNT are still being determined.

Effects of insulin-like growth factor-I and LR3IGF-I on regional blood flow in normal rats

1997 ◽  
Vol 155 (2) ◽  
pp. 351-358 ◽  
Author(s):  
CM Gillespie ◽  
AL Merkel ◽  
AA Martin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Arterial Blood ◽  
Cardiovascular Side Effects ◽  
Igf I ◽  
The Central Nervous System ◽  
The Brain ◽  
Infusion Period

Two studies were conducted to investigate the haemodynamic effects of IGF-I and its analogue LR3IGF-I in normal anaesthetised rats. Infusion of IGF-I intravenously, at a dose of 125 micrograms/kg/h, for 20 min in the first study resulted in renal blood flow being significantly elevated by 35% above baseline. Mean arterial blood pressure (MABP) at this IGF-I dose fell by 18% of baseline, with LR3IGF-I also causing a significant decline in MABP (by 15%) at the dose of 125 micrograms/kg/h. In the second study the intravenous administration of IGF-I or LR3IGF-I, at a dose of 125 micrograms/kg/h, over a period of 60 min, resulted in MABP being significantly lowered by 25% of baseline values. Regional blood flow rates were determined using radioactive microspheres, 15 microns in diameter, injected systemically at the end of the peptide infusion period. The gastrocnemius, a representative skeletal muscle, was the only vascular region to show a significant increase in blood flow after IGF-I (by 58%) or LR3IGF-1 (by 308%) infusion. Vascular resistance in the brain was significantly reduced after infusion of IGF-I (by 60%) or LR3IGF-I (by 48%) as compared with vehicle. Skeletal muscle vascular resistance was also reduced by IGF-I (by 41%) and more particularly by LR3IGF-I (by 77%) in comparison to vehicle. These alterations to vascular tone produced by IGF infusion may be related to the central nervous system and systemic cardiovascular side-effects that have been reported during IGF-I administration in humans.

On the invasion of the central nervous system by nematodes: II. Invasion of the nervous system in ascariasis

Parasitology ◽  
1955 ◽  
Vol 45 (1-2) ◽  
pp. 41-55 ◽  
Author(s):  
J. F. A. Sprent
Keyword(s):  
Nervous System ◽  
Toxocara Canis ◽  
Blood Stream ◽  
Experimental Infections ◽  
Large Size ◽  
Arterial Blood ◽  
The Central Nervous System ◽  
The Brain ◽  
Traumatic Damage ◽  
Toxascaris Leonina

1. Experimental infections in mice showed that the larvae of Toxocara canis, T. mystax, Ascaris devosi, A. columnaris and Toxascaris transfuga reached the brain of mice; the larvae of Ascaris lumbricoides, A. suum, Parascaris equorum and Toxascaris leonina were not recovered from the brain. The larvae of T. canis, T. mystax, T. transfuga and A. columnaris remained hi the brain of mice for several months.2. Larvae reaching the brain produced characteristic haemorrhages on the surface of the cerebral hemispheres in the early stages of infection. It was concluded that the larvae reach the brain via the arterial blood stream, leave the arteries at the point where their diameter approximates that of the larvae, i.e. mostly on the surface of the brain, and penetrate into the brain from the subarachnoid space and chorioidal tissues.3. The larvae of T. canis were found to occur in the brain of mice in relatively greater numbers than the larvae of other species, but only very rarely caused nervous symptoms. The larvae of T. canis and T. mystax showed no growth in the brain.4. The larvae of A. columnaris (skunk) frequently caused nervous symptoms in mice, the effect appeared to result from traumatic damage due to the relatively large size attained by these larvae about 3 weeks after infection.5. The brain of infected mice showed very slight changes consequent upon infection with larvae of T. canis. These larvae moved actively through the tissues; they incited little or no cellular reaction, but left haemorrhagic tracks. The larvae of A. columnaris also moved actively; when in the extended state they were usually found in normal tissue; when coiled, they were often associated with a necrotic focus infiltrated with leucocytes.6. After experimental infections of dogs with larvae of T. canis, two out of twelve infected animals harboured larvae in the brain. No natural infections with these larvae were found in the brains of dogs and cats. After experimental infection, larvae of T. canis were found in the brain of mice, rats and guinea-pigs, but not of rabbits.7. Larvae of A. suum were recovered from the cerebrum of one pig suffering from posterior paralysis, but not in an experimentally infected pig.8. No larvae of P. equorum were found in the brain of foals in natural and experimental infections.

Brain Damage in Diabetes Mellitus

1973 ◽  
Vol 122 (568) ◽  
pp. 337-341 ◽  
Author(s):  
R. N. Bale
Keyword(s):  
Diabetes Mellitus ◽  
Central Nervous System ◽  
Brain Damage ◽  
Cerebrovascular Accident ◽  
Diabetic Encephalopathy ◽  
Autopsy Study ◽  
The Central Nervous System ◽  
Permanent Brain Damage ◽  
The Brain

Several previous studies have demonstrated involvement of the central nervous system in diabetes mellitus. Reske-Nielsen and Lundbaek (1963) gave a description of cerebral changes seen in an autopsy study of three cases of long term diabetes and considered these to contribute a diabetic encephalopathy. Lawrence et al. (1942) demonstrated lesions in the brain following fatal hypoglycaemia, and Fineberg and Altschul (1952) described cases in which permanent brain damage followed non-fatal hypoglycaemia. Grunnet (1963) found cerebral atherosclerosis to develop at an earlier age and more severely in the diabetic than the non-diabetic, and a higher incidence of cerebrovascular accident was found in diabetic than non-diabetic subjects by Alex et al. (1962).

scholarly journals The influence of occupational environment and professional factors on the risk of cardiovascular disease

Medicina ◽  
2006 ◽  
Vol 43 (2) ◽  
pp. 96 ◽  
Author(s):  
Vytautas Obelenis ◽  
Vilija Malinauskienė
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Circulatory System ◽  
Electrolyte Imbalance ◽  
Vascular Lesions ◽  
Cholesterol Concentration ◽  
Long Term Effects ◽  
Arterial Blood ◽  
The Central Nervous System

The article reviews the recent scientific literature and the authors’ studies on this topic. Occupational conditions and psychological factors have been shown to play an important role in the etiopathogenesis of cardiovascular diseases. Their effect is often indirect, through damage to the central nervous, respiratory, and neuroendocrine systems. Hot climate in the workplace and intense infrared radiation cause the water and electrolyte imbalance and chronic hyperthermia and manifests as neurovegetative dystonia. The long-term effects of low temperatures condition ischemic lesions in circulatory system, trophic organ destruction. The influence of ultrahigh-frequency electromagnetic radiation on the cardiovascular system is directly related to the central nervous system and neurohumoral lesions. “Microwave disease” often manifests as polymorphic dystonia. Exposure to occupational vibration causes “white finger” syndrome or Raynaud’s phenomenon together with cerebral vascular lesions. Recent studies have confirmed that noise as a chronic stressor causes the imbalance in the central and vegetative nervous systems and changes in homeostasis. Noise increases catecholamine and cholesterol concentration in blood, has an effect on plasma lipoprotein levels, increases heart rate, arterial blood pressure, and risk of myocardial infarction. Psychophysiological changes caused by long-term stress influence constant pathological changes in the central nervous system, endocrine and cardiovascular systems. The long-term effect of psychogenic stressors is very important in the etiopathogenesis of psychosomatic diseases.

scholarly journals Advances in Fetal Neurophysiology

2008 ◽  
Vol 2 (3) ◽  
pp. 19-34 ◽  
Author(s):  
Maja Predojevic ◽  
Aida Salihagic Kadic
Keyword(s):  
Brain Function ◽  
State Of The Art ◽  
Sensory System ◽  
Nerve Cells ◽  
Long Term Effects ◽  
Intrauterine Life ◽  
Period 2 ◽  
The Central Nervous System ◽  
The Brain

Abstract The human brain function is certainly one of the most amazing phenomena known. All behavior is the result of the brain function. The 100 billion nerve cells are the home to our centers of feelings and senses, pleasure and satisfaction; it is where the centers for learning, memory and creative work are located; where laughing and crying areas and the centers of our mind are. Our cognitive functions, such as thinking, speaking or creating works of art and science, all reside within the cerebral cortex. One of the tasks of the neural science is to explain how the brain marshals its millions of individual nerve cells to produce behavior and how these cells are affected by the environment.1 The brain function still remains shrouded in a veil of mystery. But what is known is that over 99 percent of the human neocortex is produced during the fetal period.2 Owing to the employment of state-of-the-art methods and techniques in prenatal investigations, a growing pool of information on the development of the central nervous system (CNS) and behavioral patterns during intrauterine life has been made available. This review outlines these events, along with the development of the fetal sensory system and circadian rhythms, the senses of vision and hearing, fetal learning and memory, and long-term effects of fetal stress on behavior. In brief, this review offers a glimpse of the fascinating world of the intrauterine life.

Partial saturation and regional variation in the blood-to-brain transport of leptin in normal weight mice

2000 ◽  
Vol 278 (6) ◽  
pp. E1158-E1165 ◽  
Author(s):  
William A. Banks ◽  
Cecilia M. Clever ◽  
Catherine L. Farrell
Keyword(s):  
Arcuate Nucleus ◽  
Maximum Velocity ◽  
Brain Perfusion ◽  
Serum Levels ◽  
Brain Regions ◽  
Normal Weight ◽  
Normal Serum ◽  
Optimal Function ◽  
The Central Nervous System ◽  
The Brain

Impaired blood-brain barrier transport of leptin into the arcuate nucleus has been suggested to underlie obesity in humans and outbred aging mice. Here, we used a brain perfusion method in mice to measure transport rates and kinetic parameters for leptin at vascular concentrations between 0.15 and 130 ng/ml. Transport into whole brain was partially saturated at all concentrations, not only those seen in obesity. Leptin entered all regions of the brain, not only the hypothalamus, with entry and saturation rates differing among the brain regions. The value of the Michaelis-Menten constant of the transporter approximates normal serum levels and the maximum velocity value varies significantly among brain regions. These results suggest an important role for low serum levels signaling starvation status to the brain and show that the levels of leptin seen in obesity greatly saturate the transporter. Differences in regional uptake and saturation provide a mechanism by which leptin can control events mediated at the arcuate nucleus and other regions of the central nervous system with different regional thresholds for optimal function.

scholarly journals Motor Adaptation Impairment in Chronic Cannabis Users Assessed by a Visuomotor Rotation Task

2019 ◽  
Vol 8 (7) ◽  
pp. 1049 ◽  
Author(s):  
Ivan Herreros ◽  
Laia Miquel ◽  
Chrysanthi Blithikioti ◽  
Laura Nuño ◽  
Belen Rubio Ballester ◽  
...  
Keyword(s):  
Prolonged Exposure ◽  
Motor Adaptation ◽  
Brain Structures ◽  
Healthy Controls ◽  
Long Term Effects ◽  
Visuomotor Rotation ◽  
Important Player ◽  
The Central Nervous System ◽  
Implicit Motor ◽  
The Brain

Background—The cerebellum has been recently suggested as an important player in the addiction brain circuit. Cannabis is one of the most used drugs worldwide, and its long-term effects on the central nervous system are not fully understood. No valid clinical evaluations of cannabis impact on the brain are available today. The cerebellum is expected to be one of the brain structures that are highly affected by prolonged exposure to cannabis, due to its high density in endocannabinoid receptors. We aim to use a motor adaptation paradigm to indirectly assess cerebellar function in chronic cannabis users (CCUs). Methods—We used a visuomotor rotation (VMR) task that probes a putatively-cerebellar implicit motor adaptation process together with the learning and execution of an explicit aiming rule. We conducted a case-control study, recruiting 18 CCUs and 18 age-matched healthy controls. Our main measure was the angular aiming error. Results—Our results show that CCUs have impaired implicit motor adaptation, as they showed a smaller rate of adaptation compared with healthy controls (drift rate: 19.3 +/− 6.8° vs. 27.4 +/− 11.6°; t(26) = −2.1, p = 0.048, Cohen’s d = −0.8, 95% CI = (−1.7, −0.15)). Conclusions—We suggest that a visuomotor rotation task might be the first step towards developing a useful tool for the detection of alterations in implicit learning among cannabis users.

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