Stikkordarkiv: Blodsirkulasjon

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The underlying mechanisms for development of hypertension in the metabolic syndrome

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Studie som nevner «alt» om insulinresistens og hva det gjør i kroppen: magefett, symatisk overstimulering, oksidativt stress og blodkardysfunksjon, renin-angiotensin, betennelser og søvnapne.

http://www.nutritionj.com/content/7/1/10

«Visceral obesity, insulin resistance, oxidative stress, endothelial dysfunction, activated renin-angiotensin system, increased inflammatory mediators, and obstructive sleep apnea have been proposed to be possible factors to develop hypertension in the metabolic syndrome. These factors may induce sympathetic overactivity, vasoconstriction, increased intravascular fluid, and decreased vasodilatation, leading to development of hypertension in the metabolic syndrome.»

«As shown in Figure 1, accumulated visceral adipose tissue produce and secrete a number of adipocytokines, such as leptin, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), angiotensinogen, and non-esterified fatty acids (NEFA), which induce development of hypertension [11]. «

«Insulin resistance is the main pathophysiologic feature of the metabolic syndrome. Several mechanisms connect insulin resistance with hypertension in the metabolic syndrome. An anti-natriuretic effect of insulin has been established by accumulating data indicating that insulin stimulates renal sodium re-absorption [12–14]. This anti-natriuretic effect is preserved, and may be increased in individuals with insulin resistance, and this effect may play an important role for development of hypertension in the metabolic syndrome [15].»

«NEFA has been reported to raise blood pressure, heart rate, and α1-adrenoceptor vasoreactivity, while reducing baroreflex sensitivity, endothelium-dependent vasodilatation, and vascular compliance[28]. Insulin resistance increases plasma leptin levels, and leptin has been reported to elevate sympathetic nervous activity, suggesting that leptin-dependent sympathetic nervous activation may contribute to an obesity-associated hypertension [29]. Accumulating data suggest that metabolic syndrome is associated with markers of adrenergic overdrive [30].»

«In rats with the metabolic syndrome, induced by chronic consumption of a high fat, high refined sugar [31], hypertension is associated with oxidative stress [32], avid nitric oxide (NO) inactivation, and down-regulation of NO synthase (NOS) isoforms and endothelial NOS activator[32], suggesting that oxidative stress and endothelial dysfunction may be strongly associated with development of hypertension in the metabolic syndrome. Further, recent evidences suggest that oxidative stress, which is elevated in the metabolic syndrome [33], is associated with sodium retention and salt sensitivity [34].»

«The renin-angiotensin system (RAS) plays a crucial role in blood pressure regulation, by affecting renal function and by modulating vascular tone. The activity of the RAS appears to be regulated by food intake, and overfeeding of rodents has been reported to lead to increased formation of angiotensin II in adipocytes [38]. «

«Recent cohort studies have demonstrated that high-sensitivity C-reactive protein (hsCRP) independently presents additive prognostic values at all levels of metabolic syndrome [45]. Ridker PM, et al. suggest a consideration of adding hsCRP as a clinical criterion for metabolic syndrome[45]. Abnormalities in inflammatory mediators have been also reported to be implicated with development of hypertension.»

«TNF-α is involved in the pathophysiology of hypertension in the metabolic syndrome. TNF-α stimulates the production of endothelin-1 and angiotensinogen [48,49].»

«IL-6 stimulates the central nervous system and sympathetic nervous system, which may result in hypertension [54,55]. The administration of IL-6 leads to elevation in heart rate and serum norepinephrine levels in women [56]. Further, IL-6 induces an increase in plasma angiotensinogen and angiotensin II [57], leading to development of hypertension.»

«Patients with OSA are often considered to be obese, however, Kono M et al. reported that OSA was associated with hypertension, dyslipidemia, and hyperglycemia, independent of visceral obesity [59]. «

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Vascular insulin abnormalities, hypertension, and accelerated atherosclerosis

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Studie som bekrefter at insulin resistens (ikke høyt insulinnivå alene) gjør at blodkar trekker seg sammen og hemmer blodsirkulasjon. Pluss at de mister sin sensitivitet for sammentreking og utvidelse, de blir med andre ord stive.

http://www.ncbi.nlm.nih.gov/pubmed/8503434

«However, recent data from our laboratory suggest that cellular insulin resistance rather than hyperinsulinemia per se may lead to hypertension. The basic tenet proposed in this article is that a deficiency of insulin at the cellular level represents a common mechanism that is involved in the development of hypertension in both type I and type II diabetes mellitus»

«For example, recently reported studies from our laboratory demonstrate that insulin attenuates the vascular contractile response to phenylephrine, serotonin, and potassium chloride. Thus, it appears that insulin normally modulates (attenuates) vascular smooth muscle contractile responses to vasoactive factors, and insulin resistance should accordingly be associated with enhanced vascular reactivity.»

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Carbon dioxide influence on nitric oxide production in endothelial cells and astrocytes: Cellular mechanisms

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Viktig studie som nevner hvordan CO2 forholder seg til NO og vasodilasjon. Nevner mekanismene bak eNOS og nNOS og hva som faktisk skjer i cellene. Denne studien er på celler, men beskriver mye av det som skjer in vivo og refererer til andre viktige studier.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073030/

«Cerebral vessels may regulate cerebral blood flow by responding to changes in carbon dioxide (CO2) through nitric oxide (NO) production. »

«NO levels in endothelial cells increased during hypercapnia by 36% in 8 hours and remained 25% above baseline. NO increase in astrocytes was 30% after 1 hour but returned to baseline at 8 hours. NLA blocked NO increase in endothelial cells under hypercapnia.»

«This study suggests that cerebral endothelial cells and astrocytes release NO under normocapnic conditions and NO production is increased during hypercapnia and decreased during hypocapnia independent of pH. Further, this demonstrates that endothelial cells may play a pivotal role in chemoregulation by modulating NOS activity.»

«Modulation of cerebral vascular tone in response to changes in the arterial partial pressure of carbon dioxide (pCO2) is defined as chemoregulation. In humans hypocapnia produces vasoconstriction resulting in decreased cerebral blood flow (CBF), whereas hypercapnia produces vasodilation and increased CBF (Lavi et al., 2003). »

«Using nitric oxide synthase (NOS) inhibitors, several in vivo studies have suggested that vasodilation in response to increased pCO2may be mediated by NO (Lavi et al., 2006). »

«Under hypercapnic conditions (pCO2 56.3±8.7 mmHg), NO concentration increased from baseline levels to a mean of 10±0.6×10-10M during the first 4 hours (Figure 1A). NO concentration peaked at 36% (10.2±0.5×10-10M) above baseline at 8 hours and stabilized 25% (9.4±0.5×10-10M) above baseline until completion of the experiment.»

«By plotting NO changes as a function of pCO2, we could disregard time as a variable in NO production (Figure 3) to establish that changes in NO levels correlate with changes in pCO2 (R=0.99).»

CO2 og NO

«Under hypercapnic conditions (pCO2 56.3±8.7 mmHg), human fetal astrocytes increased NO production by 30% over baseline values to a mean level of 2.5±1.2×10-10M in the first hour of hypercapnia (Figure 2). NO production then gradually decreased to control levels after 8 hours and remained at control levels for the remainder of the experiments.»

CO2 og NO i astrocytt

«The pH values were kept stable within a neutral gap under normocapnic (7.39±0.01), hypercapnic (7.36±0.02) and hypocapnic (7.40±0.01) conditions.»

» Stimulation of NOS in the endothelial cells is consistent with the NO-dependent vasodilation and increased CBF that occur in vivo during hypercapnia, as has been shown in rats (Iadecola, 1992) and in primates (Thompson et al., 1996). Decreased NO production by endothelial cells also correlates with the in vivo vasoconstrictive response to hypocapnia shown previously (Lavi et al., 2003;Thompson et al., 1996).»

«Thus, it is unlikely that eNOS is responsible for the early or fast phase response during chemoregulation in vivo. There are several explanations for this phenomenon. First, nitrite (NO2), being a storage pool of NO, can be reduced to NO under acidic and hypoxic conditions in vivo (Cosby et al., 2003). Under these conditions nitrite releases NO in the presence of deoxygenated hemoglobin in blood (Cosby et al., 2003;Nagababu et al., 2003) or neuroglobin (Burmester et al., 2000) in neurons acting as a nitrite reductase (Petersen et al., 2008). »

«The chemoregulatory response to CO2 changes in vivo is rapid, occurring on the order of milliseconds; our results did not demonstrate this component of the chemoregulatory response.»

«Cerebrovascular reactivity in response to CO2 is impaired in diabetic or hypertensive patients with endothelial dysfunction (Lavi et al., 2006), suggesting an important role for endothelial cells in modulating CBF response to CO2. »

«It has been reported that the ATP-sensitive K+ channels play a pivotal role in microvessel vasodilation of the cerebral cortex in response to decreased pH corresponding to mild hypercapnia and that a NOS inhibitor could not alter this vasodilation (Nakahata et al., 2003).»

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The role of corticosteroids in the regulation of vascular tone

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Viser til mekanismene for hvordan kortisol (og stress) hemmer blodsirkulasjon og over tid kan gi høyt blodtrykk og mange medfølgende sykdommer. Kortisols effekt på blodkar sammentrekning er først og fremst ved å øke reaksjonen og blodkarcellenes sensitivitet til adrenalin. Men også øke nyrenes tilbakeholdelse av salt.

http://cardiovascres.oxfordjournals.org/content/41/1/55.full

«In addition, corticosteroids in lesser amounts are essential for the maintenance of peripheral vascular resistance in healthy persons. This review details the proposed mechanisms by which corticosteroids maintain and, in excess, enhance vascular tone.»

«Disease states resulting from excesses of circulating (adreno)corticosteroids include primary hyperaldosteronism, renal artery stenosis, ACTH-secreting tumors, and administration of glucocorticoids for treatment of other diseases. Hypertension is commonly associated with these diseases. »

«Potent vasoconstrictor hormones that have been investigated include α-adrenergic agonists (norepinephrine), angiotensin II, arginine vasopressin, endothelin and thromboxanes.»

«Results from other studies have suggested that corticosteroids act directly on blood vessels in potentiating norepinephrine vasoconstrictor actions. »

«Corticosteroids enhance contractile responses to norepinephrine in humans. For example, Kurland and Freedberg [20]administered increasing doses of norepinephrine intravenously to three patients before and 24 h after initiation of glucocorticoid therapy and observed much greater pressor responses in the presence of corticosteroid than in the absence of corticosteroid. »

«For the most part, glucocorticoids and mineralocorticoids have been reported to enhance the vasoconstrictor actions of angiotensin II.»

Viser til at forskjellige steder i kroppen har forskjellig sensitivitet for kortisol:
«It is possible that differences in responses to corticosteroids in vascular beds in different parts of the body may explain the above-mentioned discrepancies. »

«From the above review, one can see that corticosteroids foster hypertension not only by enhancing renal sodium reabsorption but also by augmenting vascular tone. «

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Endothelial dysfunction as a possible link between C-reactive protein levels and cardiovascular disease

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Nevner at lavgrads betennelse er utgangspunktet for arterosklerose. Og at det hemmer endotelfunksjonen, altså blodkar cellenes evne til å trekke seg sammen og utvide seg.

http://www.clinsci.org/cs/098/0531/cs0980531.htm

«Low-grade chronic inflammation, characterized by elevated plasma concentrations of C-reactive protein (CRP), is associated with an increased risk of atherosclerotic cardiovascular disease.»

«These data demonstrate for the first time a relationship between low-grade chronic inflammation and basal endothelial NO synthesis (measured using an invasive method), and support the notion that endothelial dysfunction is a critical intermediate phenotype in the relationship between inflammation and cardiovascular disease.»

«Inflammation may increase cardiovascular risk via effects on known cardiovascular risk factors (e.g. lipid profiles), by altering other putative risk markers (e.g. fibrinogen, plasminogen activator inhibitor-1), or by impairing carbohydrate metabolism [2]. «

«In this clinical study we provide, to the best of our knowledge, the first direct evidence for an association between endothelial dysfunction and low-grade chronic inflammation. »

Viser til at blodkar får vansker med å slappe av når det er betennelsesfaktorer tilstedet:
«Our data also complement previous experiments by Bhagat et al. [6,7], who noted that infusion of endotoxin or pro-inflammatory cytokines [interleukin-1, tumour necrosis factor-a (TNF-a)] into superficial hand veins of healthy volunteers (provoking a local acute inflammatory response) caused a selective impairment of endothelium-dependent relaxation. «

«Correlation does not imply causality, but the relationship we have suggested between inflammation and endothelial dysfunction is biologically plausible. Low-grade chronic vascular inflammation may promote biochemical (e.g. peroxidative) and cellular changes in the vessel wall.»

Viser at NO produksjonen synker ved betennelse og gjør at blodet lettere levrer seg, som videre øker sjansen for sammentrekning, trombose og full avstengning av blodkar.
«A decrease in basal NO production secondary to low-grade chronic inflammation would favour increased expression of cell-surface adhesion molecules for leucocytes and platelets, promote interaction between these cells and the vascular endothelium, and induce procoagulant activity. Such effects, in turn, might increase the likelihood of vasospasm, thrombosis and vessel occlusion [1]. Thus endothelial dysfunction may be a critical factor in the relationship between low-grade chronic inflammation and cardiovascular disease.»

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Alteration of substance P-mediated vasodilatation and sympathetic vasoconstriction in the rat knee joint by adjuvant-induced inflammation

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Nevner at kronisk bentente ledd mister reaksjonsevnen på nerveimpulser og blodsirkulasjon. Kunne trengt å lese hele denne studien.

http://www.sciencedirect.com/science/article/pii/0304394094900027

«In control knees, nerve stimulation produced a frequency-dependent vasoconstruction»

«Chronically inflamed joints showed virtually no response to either nerve stimulation or SP application, suggesting a radical alteration in sympathetic and neuropeptidergic actions.»

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Positive Effect of an Autologous Platelet Concentrate in Lateral Epicondylitis in a Double-Blind Randomized Controlled Trial

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Viser at Platelet-Rich Plasma (PRP) gir betraktelig økning i regnerering av tennisalbue. Med apnea-trening pumper milten ut ny PRP, så denne studien kan bekrefte apnea som helbreldelse. Resultatene er langt bedre enn ved kortisoninjeksjoner.

http://ajs.sagepub.com/content/38/2/255.short

«Treatment of patients with chronic lateral epicondylitis with PRP reduces pain and significantly increases function, exceeding the effect of corticosteroid injection. »

«The results showed that, according to the visual analog scores, 24 of the 49 patients (49%) in the corticosteroid group and 37 of the 51 patients (73%) in the PRP group were successful, which was significantly different (P <.001).»

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THE EFFECT OF GUIDED IMAGERY IN A HYPNOTIC CONTEXT ON FOREARM BLOOD FLOW

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Nevner hvordan hypnose og visualisering kan øke blodgjennomstrømning i spesifikke deler av kroppen.

http://bscw.rediris.es/pub/bscw.cgi/d4434404/McGuirk-Effect_guided_imagery_forearm_blood_flow.pdf
«This study was conducted to determine in a non- ulcerated population, the potential of guided imagery in a hypnotic context to influence blood flow, which is a critical variable in the process of ulcer healing.»

«It is known, however, that psychologi- cal factors are important in healing. Stress, for example, can affect the healing of experimental wounds (Kiecolt-Glaser et al., 1995) and there is contradictory evidence as to whether it affects healing of duodenal ulcers (Holtmann et al., 1992; Armstrong et al., 1993).»

«More specifically in the case of leg ulcers the pathological process is associated with disturbed blood flow and consequent tissue breakdown due to inade- quate oxygenation. Any psychological intervention that assisted in altering and cor- recting the blood flow in the affected limbs would be expected to facilitate healing.»

«Similarly Moore and Wiesner (1996) used suggestions of hand- warming in hypnosis, augmented by biofeedback, to create local vasodilation (as measured by objective increases in hand temperature) with a concomitant reduction in pain in patients with upper extremity repetitive strain injury. In earlier work from the same research group Moore and Kaplan (1983) reported acceleration of burn wound healing and pain reduction by hypnotically induced vasodilation in the targeted hand compared with the control hand.»

«The authors concluded that while the blood flow change is under central neurological control, and hence can be directly affected by hypnotic suggestion, ery- thema reflects local changes related to the release of inflammatory mediators.»

Subjective temperature (arbitrary units)

Target ‘hot’ arm 90·8 (18·6)
Target ‘cold’ arm 89·4 (21·7)
Before After

103·5 (18·6) 38·1 (21·8)

Change (%)
+12·7 (13·9) –51·3 (57·4)

*Means (and standard deviations)

«The subjective temperature change, however, was greater for ‘cold’ imagery. This may be because the subjects perceived their arms as already warmer than usual prior to the imagery suggestions, thereby creating a ceiling effect. An alternative explanation is that the cold script was the more powerful of the two or possibly that reducing perceived temperature in a limb is an inherently easier task. «

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Basilar Artery Response to Hyperventilation in Panic Disorder

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Nevner hvordan hyperventilering fjerner CO2 og gjør at blodkar trekker seg sammen. Nevner spesielt basilary artery inni hjernen.

http://ajp.psychiatryonline.org/data/journals/ajp/3682/1603.pdf

«Gibbs (2) reported that nine panic disorder patients in a neurology clinic experienced a significantly greater decrease in basilar artery blood flow during voluntary hyperventilation (mean decrease, 62%) than did nine normal comparison subjects (mean decrease, 36%). However, no respiratory measures were assessed dur- ing hyperventilation, and this omission is important, since changes in carbon dioxide levels are critical in regulating cerebral arterial flow (3).»

«For mean blood flow, the panic patients had a 55% reduction (mean change=–21.1 cm/sec, SD=7.1), which was sig- nificantly greater than the 42% reduction for the com- parison group (mean change=–15.8 cm/sec, SD=5.4)»

«The increases in the dizziness ratings were associated with the percent- ages of the decreases in both peak flow (r=–0.60, N=24, p<0.01) and mean flow (r=–0.57, N=24, p<0.01).»

«The pCO2 level of the panic disorder patients decreased 33% during hyperventilation (pCO2 level dur- ing hyperventilation: mean=24.80 mm Hg, SD=7.29), which did not differ significantly from the 37% decrease for the comparison subjects (pCO2 during hyperventila- tion: mean=24.55 mm Hg, SD=3.09) (t=–0.14, df=7, n.s.).»

«The ratio of blood flow changes to pCO2 changes is approximately 1.0 in normative studies (4), which is consistent with the values for our comparison group. The patients with panic disorder had a ratio of blood flow change to pCO2 change that was almost twice that of the normal subjects. This suggests that the sensitivity of the basilar artery in patients with anxiety disorders may not be due solely to changes in respiratory physiology.»

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Factors contributing to the variability in muscle ageing

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Nevner at aldring og muskelatrofi skjer mye på grunn av «low grade inflammation».

http://www.ncbi.nlm.nih.gov/m/pubmed/22902240

«Where an individual cannot change much in his or her genetic constitution, circulating hormones and systemic inflammation, (s)he can still significantly slow the rate of muscle ageing by an adequate dietary intake and regular physical activity. Finally, it is suggested that age-related alterations in the capillary bed may negatively affect muscle mass.»