Kategoriarkiv: Forskning og artikler

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Supplementary oxygen for nonhypoxemic patients: O2 much of a good thing?

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Nevner alt om hvordan oksygen er skadelig i høye mengder, både i klinisk sammenheng og eller. Bl.a. fordi med høy O2 går CO2 ned og da trekker blodårene seg sammen.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3218982/

Abstract

Supplementary oxygen is routinely administered to patients, even those with adequate oxygen saturations, in the belief that it increases oxygen delivery. But oxygen delivery depends not just on arterial oxygen content but also on perfusion. It is not widely recognized that hyperoxia causes vasoconstriction, either directly or through hyperoxia-induced hypocapnia. If perfusion decreases more than arterial oxygen content increases during hyperoxia, then regional oxygen delivery decreases. This mechanism, and not (just) that attributed to reactive oxygen species, is likely to contribute to the worse outcomes in patients given high-concentration oxygen in the treatment of myocardial infarction, in postcardiac arrest, in stroke, in neonatal resuscitation and in the critically ill. The mechanism may also contribute to the increased risk of mortality in acute exacerbations of chronic obstructive pulmonary disease, in which worsening respiratory failure plays a predominant role. To avoid these effects, hyperoxia and hypocapnia should be avoided, with oxygen administered only to patients with evidence of hypoxemia and at a dose that relieves hypoxemia without causing hyperoxia.

… the aim of oxygen therapy should be to increase the delivery of oxygen rather than to reach any arbitrary concentration in the arterial blood.

Hyperoxia marginally increases the arterial blood oxygen content (CaO2), theoretically increasing tissue oxygen delivery (DO2) assuming no reduction in tissue blood flow. However, oxygen causes constriction of the coronary, cerebral, renal and other key vasculatures – and if regional perfusion decreases concomitantly with blood hyperoxygenation, one would have a seemingly paradoxical situation in which the administration of oxygen may place tissues at increased risk of hypoxic stress. Any tissue damage in the course of oxygen administration would plausibly be attributed to the underlying disease process.

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Neurobiologic basis of craving for carbohydrates.

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Denne studen nevner 5 systemer som bidrar til at vi føler behov for karbohydrater. Den viktigste er at serotonin øker i hjernen, noe som over tid kan gi en avhengighet. De nevner også at evnen til å skille sult fra andre interne følelser kan bli dårligere, og at det gir behov for mat når andre ting i kropp og sinn er i ulage.

http://www.ncbi.nlm.nih.gov/pubmed/24139726

Serotonergic:  Increased brain serotonin improves mood. Brain serotonin levels depend on the availability of its Trp precursor. Dietary carbohydrates increase the passage of Trp through the blood–brain barrier, unlike proteins, which alter LNAA.  Faced with anxiety, an individual eats carbohydrates, which increase brain serotonin, thus improving mood.

Palatability and hedonic response: The pleasurable experience of eating food with high palatability immediately improves mood. This occurs in individuals with greater genetic sensitivity to sweet taste through the activation of the endogenous opioid system. Faced with anxiety, an individual eats a food with high palatability, activating the hedonic mechanism, which improvesmood.

Motivational system:  Carbohydrates act in the motivational system in the same manner as abused substances. This increases dopamine and endogenous opioids, which are associated with a known pleasurable effect, improving mood. If this behavior is repeated over time, structural changes in the brain are produced that generate dependence on highly palatable foods.

Stress response: Faced with anxiety associated with stress, the HPA axis activates. Highly palatable foods activate the motivational system and reduce the HPA axis, thus regulating the stress system. Therefore, when faced with anxiety, highly palatable food produces a hedonic reward as well as reducing the state of anxiety.

Gene–environment:  Eating is a coping tool to relieve negative emotions. The behavior is learned through inadequate parenting and environment. It also stems from an inability to distinguish hunger from other aversive internal states. There is greater susceptibility in carriers of the A1 allele of the DRD2 dopamine receptor and carriers of the short allele of the serotonin transporter gene.

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Respiratory dysregulation in anxiety, functional cardiac, and pain disorders. Assessment, phenomenology, and treatment.

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Nevner at hypokapni (lav CO2) er vanlig hos panikkpasienter, de med hjerte/kar problemer og de med smerteproblemer.

http://www.ncbi.nlm.nih.gov/pubmed/11530714

Klikk for å få tilgang til FH%20Wilhelm%20et%20al%20-%20Respiratory%20dysregulation%20review.pdf

Abstract

Respiration is a complex physiological system affecting a variety of physical processes that can act as a critical link between mind and body. This review discusses the evidence for dysregulated breathing playing a role in three clinical syndromes: panic disorder, functional cardiac disorder, and chronic pain. Recent technological advances allowing the ambulatory assessment of endtidal partial pressure of CO2 (PCO2) and respiratory patterns have opened up new avenues for investigation and treatment of these disorders. The latest evidence from laboratories indicates that subtle disturbances of breathing, such as tidal volume instability and sighing, contribute to the chronic hypocapnia often found in panic patients. Hypocapnia is also common in functional cardiac and chronic pain disorders, and studies indicate that it mediates some of their symptomatology. Consistent with the role of respiratory dysregulation in these disorders, initial evidence indicates efficacy of respiration-focused treatment.

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Effect of short-term practice of breathing exercises on autonomic functions in normal human volunteers

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Nevner hvordan sakte pust bedrer tilstanden i det autonome nervesystem. De bruker 6 sek inn og 6 sek ut i denne studien, som stimulerer vagusnerven best.

Klikk for å få tilgang til 0807.pdf

Background & objectives: Practice of breathing exercises like pranayama is known to improve autonomic function by changing sympathetic or parasympathetic activity. Therefore, in the present study the effect of breathing exercises on autonomic functions was performed in young volunteers in the age group of 17-19 yr.

Methods: A total of 60 male undergraduate medical students were randomly divided into two groups: slow breathing group (that practiced slow breathing exercise) and the fast breathing group (that practiced fast breathing exercise). The breathing exercises were practiced for a period of three months. Autonomic function tests were performed before and after the practice of breathing exercises.

Results: The increased parasympathetic activity and decreased sympathetic activity were observed in slow breathing group, whereas no significant change in autonomic functions was observed in the fast breathing group.

Interpretation & conclusion: The findings of the present study show that regular practice of slow breathing exercise for three months improves autonomic functions, while practice of fast breathing exercise for the same duration does not affect the autonomic functions.

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One molecule, many derivatives: a never-ending interaction of melatonin with reactive oxygen and nitrogen species?

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Alt om hvordan melatonin virker som en antioksidant. Jo større ROS utfordring vi har, jo mer spiser det av melatoninlagrene våre. Når vi får mindre ROS, feks gjennom kostholdsendringer og stressreduksjon, så økes melatonin igjen.

http://www.ncbi.nlm.nih.gov/pubmed/17198536

Melatonin is a highly conserved molecule. Its presence can be traced back to ancient photosynthetic prokaryotes. A primitive and primary function of melatonin is that it acts as a receptor-independent free radical scavenger and a broad-spectrum antioxidant. The receptor-dependent functions of melatonin were subsequently acquired during evolution. In the current review, we focus on melatonin metabolism which includes the synthetic rate-limiting enzymes, synthetic sites, potential regulatory mechanisms, bioavailability in humans, mechanisms of breakdown and functions of its metabolites. Recent evidence indicates that the original melatonin metabolite may be N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) rather than its commonly measured urinary excretory product 6-hydroxymelatonin sulfate. Numerous pathways for AFMK formation have been identified both in vitro and in vivo. These include enzymatic and pseudo-enzymatic pathways, interactions with reactive oxygen species (ROS)/reactive nitrogen species (RNS) and with ultraviolet irradiation. AFMK is present in mammals including humans, and is the only detectable melatonin metabolite in unicellular organisms and metazoans. 6-hydroxymelatonin sulfate has not been observed in these low evolutionary-ranked organisms. This implies that AFMK evolved earlier in evolution than 6-hydroxymelatonin sulfate as a melatonin metabolite. Via the AFMK pathway, a single melatonin molecule is reported to scavenge up to 10 ROS/RNS. That the free radical scavenging capacity of melatonin extends to its secondary, tertiary and quaternary metabolites is now documented. It appears that melatonin’s interaction with ROS/RNS is a prolonged process that involves many of its derivatives. The process by which melatonin and its metabolites successively scavenge ROS/RNS is referred as the free radical scavenging cascade. This cascade reaction is a novel property of melatonin and explains how it differs from other conventional antioxidants. This cascade reaction makes melatonin highly effective, even at low concentrations, in protecting organisms from oxidative stress. In accordance with its protective function, substantial amounts of melatonin are found in tissues and organs which are frequently exposed to the hostile environmental insults such as the gut and skin or organs which have high oxygen consumption such as the brain. In addition, melatonin production may be upregulated by low intensity stressors such as dietary restriction in rats and exercise in humans.

Intensive oxidative stress results in a rapid drop of circulating melatonin levels. This melatonin decline is not related to its reduced synthesis but to its rapid consumption, i.e. circulating melatonin is rapidly metabolized by interaction with ROS/RNS induced by stress. Rapid melatonin consumption during elevated stress may serve as a protective mechanism of organisms in which melatonin is used as a first-line defensive molecule against oxidative damage. The oxidative status of organisms modifies melatonin metabolism. It has been reported that the higher the oxidative state, the more AFMK is produced. The ratio of AFMK and another melatonin metabolite, cyclic 3-hydroxymelatonin, may serve as an indicator of the level of oxidative stress in organisms.

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Primitive, and protective, our cellular oxygenation status?

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Om hvordan oksygennivået i mitokondriene er nesten ingen ting, og har vært slik siden tidenes morgen for å beskytte oss mot svingende oksygennivåer i atmosfæren gjennom evlusjonen.

http://www.ncbi.nlm.nih.gov/pubmed/14499489/

The primitive atmosphere where aerobic life started on earth was hypoxic and hypercapnic. Remarkably, an adaptation strategy whereby O2 partial pressure, PO2, in the arterial blood is maintained within a low and narrow range of 1-3 kPa, largely independent of inspired PO2, has also been reported in modern water-breathers. In mammalian tissues, including brain, the most frequently measured PO2 is also in the same low range. Based on the postulate that basic cellular machinery has been established since the early stages of evolution, we propose that this similarity in oxygenation status is the consequence of an early adaptation strategy which, subsequently, throughout the course of evolution, maintained cellular oxygenation in the same low and primitive range independent of environmental changes. Specialized enzymes aimed at protecting cells against O2 toxicity are thought to have appeared very early in evolution but we suggest that preventing high PO2’s is also the simplest and most efficient tool for limiting reactive oxygen species (ROS) production. It could be a cue mechanism to widen our understanding of the ageing process.

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Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome.

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I denen studien ble deltakerene bedøvet og fikk mekanisk senket ventilasjon til ca 8 L/min. De viste at mild hyperkapni gir økt blodsirkulasjon. Nevner også at «oxygen off-loading» økte (bohr effect).

http://www.ncbi.nlm.nih.gov/pubmed/8727430

Minute ventilation was reduced from 13.5 +/- 6.1 to 8.2 +/- 4.1 l/min (mean +/- SD), PaCO2 increased (40.3 +/- 6.6 to 59.3 +/- 7.2 mmHg), pH decreased (7.40 +/- 0.05 to 7.26 +/- 0.05), and P50 increased (26.3 +/- 2.02 to 31.1 +/- 2.2 mmHg) (p < 0.05). Systemic vascular resistance decreased (865 +/- 454 to 648 +/- 265 dyne.s.cm-5, and cardiac index (CI) increased (4 +/- 2.4 to 4.7 +/- 2.4 l/min/m2) (p < 0.05).

These data indicate that acute hypercapnia increases DO2 and O2 off-loading capacity in ARDS patients with normal plasma lactate, without increasing O2 extraction. Whether this would be beneficial in patients with elevated lactate levels, indicating tissue hypoxia, remains to be determined.

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Effect of acute moderate changes in PaCO2 on global hemodynamics and gastric perfusion.

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Nevner at mild hyperkapni gir økt blodsirkulasjon.

http://www.ncbi.nlm.nih.gov/pubmed/10708167

Acute hypercapnia (Paco2 from 40+/-3 to 52+/-3 torr, p<.05) increased cardiac index (3.43+/-0.37 vs. 3.97+/-0.43 mL/min/m2, p<.05), heart rate (95+/-6 vs. 105+/-3 beats/min, p<.05), and mean pulmonary artery pressure (21+/-1 vs. 24+/-1 mm Hg, p<.05) and reduced systemic vascular resistance (992+/-98 vs. 813+/-93 dyne x sec/ cm5, p<.05) and oxygen extraction ratio (27+/-3% vs. 22+/-2%, p<.05).

In this small group of stable patients, moderate acute variations in Paco2 had a significant effect on global hemodynamics, but splanchnic perfusion, assessed by deltaPco2, did not change.

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High reliability of measure of diaphragmatic mobility by radiographic method in healthy individuals.

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Nevner bevegelsen i diafragma under en spirometri test (innpust og utpust) og at noen har observert 9cm bevegelighet.

http://www.ncbi.nlm.nih.gov/pubmed/23778774

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1413-35552013000200128&lng=en&nrm=iso&tlng=en

There were large ranges of variation (in mm) in the obtained minimum and maximum values, and such variations were also reported in other studies8,6,24. Simon et al.13 observed a diaphragmatic value range from 0 to 85 mm, Houston et al.25 observed a range from 23 to 97 mm, Kantarci et al.27 observed a range from 25 to 84 mm and Boussuges et al.8 observed a range from 36 to 92 mm.