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Nathan Goodyear

Direct effects of thyroid hormones on rat coronary... [Thyroid. 1998] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...9709915

T3 vasodilation rT3

shared by Nathan Goodyear on 01 Feb 11 - No Cached
  • Our results also suggest that thyroid hormones may play a role in preventing myocardial ischemia by inducing coronary artery vasodilation.
  • Nathan Goodyear on 01 Feb 11
     
    T3 increases vasodilation of arteries and improves cardiac blood flow in rat model; rT3 does not
Nathan Goodyear

Testosterone: a vascular hormone in health and disease - 0 views

joe.endocrinology-journals.org/...R47.full

testosterone hormone health disease hormones men male cardiovascular disease CVD

shared by Nathan Goodyear on 13 May 13 - No Cached
  • Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation
  • In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure.
  • testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells
  • ...54 more annotations...
  • Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis
  • there is no compelling evidence that testosterone replacement to levels within the normal healthy range contributes adversely to the pathogenesis of CVD (Carson & Rosano 2011) or prostate cancer (Morgentaler & Schulman 2009)
  • bidirectional effect between decreased testosterone concentrations and disease pathology exists as concomitant cardiovascular risk factors (including inflammation, obesity and insulin resistance) are known to reduce testosterone levels and that testosterone confers beneficial effects on these cardiovascular risk factors
  • Achieving a normal physiological testosterone concentration through the administration of testosterone replacement therapy (TRT) has been shown to improve risk factors for atherosclerosis including reducing central adiposity and insulin resistance and improving lipid profiles (in particular, lowering cholesterol), clotting and inflammatory profiles and vascular function
  • It is well known that impaired erectile function and CVD are closely related in that ED can be the first clinical manifestation of atherosclerosis often preceding a cardiovascular event by 3–5 years
  • no decrease in the response (i.e. no tachyphylaxis) of testosterone and that patient benefit persists in the long term.
  • free testosterone levels within the physiological range, has been shown to result in a marked increase in both flow- and nitroglycerin-mediated brachial artery vasodilation in men with CAD
  • Clinical studies, however, have revealed either small reductions of 2–3 mm in diastolic pressure or no significant effects when testosterone is replaced within normal physiological limits in humans
  • Endothelium-independent mechanisms of testosterone are considered to occur primarily via the inhibition of voltage-operated Ca2+ channels (VOCCs) and/or activation of K+ channels (KCs) on smooth muscle cells (SMCs)
  • Testosterone shares the same molecular binding site as nifedipine
  • Testosterone increases the expression of endothelial nitric oxide synthase (eNOS) and enhances nitric oxide (NO) production
  • Testosterone also inhibited the Ca2+ influx response to PGF2α
  • one of the major actions of testosterone is on NO and its signalling pathways
  • In addition to direct effects on NOS expression, testosterone may also affect phosphodiesterase type 5 (PDE5 (PDE5A)) gene expression, an enzyme controlling the degradation of cGMP, which acts as a vasodilatory second messenger
  • the significance of the action of testosterone on VSMC apoptosis and proliferation in atherosclerosis is difficult to delineate and may be dependent upon the stage of plaque development
  • Several human studies have shown that carotid IMT (CIMT) and aortic calcification negatively correlate with serum testosterone
  • t long-term testosterone treatment reduced CIMT in men with low testosterone levels and angina
  • neither intracellular nor membrane-associated ARs are required for the rapid vasodilator effect
  • acute responses appear to be AR independent, long-term AR-mediated effects on the vasculature have also been described, primarily in the context of vascular tone regulation via the modulation of gene transcription
  • Testosterone and DHT increased the expression of eNOS in HUVECs
  • oestrogens have been shown to activate eNOS and stimulate NO production in an ERα-dependent manner
  • Several studies, however, have demonstrated that the vasodilatory actions of testosterone are not reduced by aromatase inhibition
  • non-aromatisable DHT elicited similar vasodilation to testosterone treatment in arterial smooth muscle
  • increased endothelial NOS (eNOS) expression and phosphorylation were observed in testosterone- and DHT-treated human umbilical vein endothelial cells
  • Androgen deprivation leads to a reduction in neuronal NOS expression associated with a decrease of intracavernosal pressure in penile arteries during erection, an effect that is promptly reversed by androgen replacement therapy
  • Observational evidence suggests that several pro-inflammatory cytokines (including interleukin 1β (IL1β), IL6, tumour necrosis factor α (TNFα), and highly sensitive CRP) and serum testosterone levels are inversely associated in patients with CAD, T2DM and/or hypogonadism
  • patients with the highest IL1β concentrations had lower endogenous testosterone levels
  • TRT has been reported to significantly reduce TNFα and elevate the circulating anti-inflammatory IL10 in hypogonadal men with CVD
  • testosterone treatment to normalise levels in hypogonadal men with the MetS resulted in a significant reduction in the circulating CRP, IL1β and TNFα, with a trend towards lower IL6 compared with placebo
  • parenteral testosterone undecanoate, CRP decreased significantly in hypogonadal elderly men
  • Higher levels of serum adiponectin have been shown to lower cardiovascular risk
  • Research suggests that the expression of VCAM-1, as induced by pro-inflammatory cytokines such as TNFα or interferon γ (IFNγ (IFNG)) in endothelial cells, can be attenuated by treatment with testosterone
  • Testosterone also inhibits the production of pro-inflammatory cytokines such as IL6, IL1β and TNFα in a range of cell types including human endothelial cells
  • decreased inflammatory response to TNFα and lipopolysaccharide (LPS) in human endothelial cells when treated with DHT
  • The key to unravelling the link between testosterone and its role in atherosclerosis may lay in the understanding of testosterone signalling and the cross-talk between receptors and intracellular events that result in pro- and/or anti-inflammatory actions in athero-sensitive cells.
  • testosterone functions through the AR to modulate adhesion molecule expression
  • pre-treatment with DHT reduced the cytokine-stimulated inflammatory response
  • DHT inhibited NFκB activation
  • DHT could inhibit an LPS-induced upregulation of MCP1
  • Both NFκB and AR act at the transcriptional level and have been experimentally found to be antagonistic to each other
  • As the AR and NFκB are mutual antagonists, their interaction and influence on functions can be bidirectional, with inflammatory agents that activate NFκB interfering with normal androgen signalling as well as the AR interrupting NFκB inflammatory transcription
  • prolonged exposure of vascular cells to the inflammatory activation of NFκB associated with atherosclerosis may reduce or alter any potentially protective effects of testosterone
  • DHT and IFNγ also modulate each other's signalling through interaction at the transcriptional level, suggesting that androgens down-regulate IFN-induced genes
  • (Simoncini et al. 2000a,b). Norata et al. (2010) suggest that part of the testosterone-mediated atheroprotective effects could depend on ER activation mediated by the testosterone/DHT 3β-derivative, 3β-Adiol
  • TNFα-induced induction of ICAM-1, VCAM-1 and E-selectin as well as MCP1 and IL6 was significantly reduced by a pre-incubation with 3β-Adiol in HUVECs
  • 3β-Adiol also reduced LPS-induced gene expression of IL6, TNFα, cyclooxygenase 2 (COX2 (PTGS2)), CD40, CX3CR1, plasminogen activator inhibitor-1, MMP9, resistin, pentraxin-3 and MCP1 in the monocytic cell line U937 (Norata et al. 2010)
  • This study suggests that testosterone metabolites, other than those generated through aromatisation, could exert anti-inflammatory effects that are mediated by ER activation.
  • The authors suggest that DHT differentially effects COX2 levels under physiological and pathophysiological conditions in human coronary artery smooth muscle cells and via AR-dependent and -independent mechanisms influenced by the physiological state of the cell
  • There are, however, a number of systematic meta-analyses of clinical trials of TRT that have not demonstrated an increased risk of adverse cardiovascular events or mortality
  • The TOM trial, which was designed to investigate the effect of TRT on frailty in elderly men, was terminated prematurely as a result of an increased incidence of cardiovascular-related events after 6 months in the treatment arm
  • trials of TRT in men with either chronic stable angina or chronic cardiac failure have also found no increase in either cardiovascular events or mortality in studies up to 12 months
  • Evidence may therefore suggest that low testosterone levels and testosterone levels above the normal range have an adverse effect on CVD, whereas testosterone levels titrated to within the mid- to upper-normal range have at least a neutral effect or, taking into account the knowledge of the beneficial effects of testosterone on a series of cardiovascular risk factors, there may possibly be a cardioprotective action
  • The effect of testosterone on human vascular function is a complex issue and may be dependent upon the underlying androgen and/or disease status.
  • the majority of studies suggest that testosterone may display both acute and chronic vasodilatory effects upon various vascular beds at both physiological and supraphysiological concentrations and via endothelium-dependent and -independent mechanisms
  • Nathan Goodyear on 13 May 13
     
    Good deep look into the testosterone and CVD link.
Nathan Goodyear

Testosterone relaxes coronary arteries by opening the large-conductance, calcium-activa... - 0 views

ajpheart.physiology.org/...H1720.full

testosterone vasodilation DHT androgens calcium channels potassium channels

shared by Nathan Goodyear on 14 May 13 - No Cached
  • Nathan Goodyear on 14 May 13
     
    The androgens testosterone and DHT elicit vasodilation via calcium and potassium channel activation.  The vasodilatory effect of the androgens is through, in part, due to K activated Ca channels.  Also of note, DHT had the same effect and DHT cannot be aromatized to estrogen.
Nathan Goodyear

Selective Inhibition of L-Type Ca2+ Channels in A7r5 Cells by Physiological Levels of T... - 0 views

endo.endojournals.org/...2675

testosterone vasodilation calcium channel blocker cardiovascular CVD calcium channel blocker

shared by Nathan Goodyear on 14 May 13 - No Cached
  • Nathan Goodyear on 14 May 13
     
    Physiologic levels of testosterone shown to induce Calcium channel blockade.  This induces the beneficial cardiovascular vasodilation.  It is known that testosterone binds to the same receptor as the common calcium channel blocker nifedipine.
Nathan Goodyear

Testosterone-induced vasorelaxation in the rat mesenteric arterial bed is mediated pred... - 0 views

onlinelibrary.wiley.com/...661A9547BF5ECEB8423866F.d02t01

testosterone men male aromatase aromatase inhibition vasodilation

shared by Nathan Goodyear on 14 May 13 - No Cached
  • Nathan Goodyear on 14 May 13
     
    Testosterone induces vasodilation and even with aromatase inhibition, the vasodilatory effect of testosterone is maintained.
Nathan Goodyear

Testosterone Relaxes Rabbit Coronary Arteries and Aorta - 0 views

circ.ahajournals.org/...1154.abstract

testosterone aromatase aromatase inhibition men male vasodilation

shared by Nathan Goodyear on 14 May 13 - No Cached
  • Nathan Goodyear on 14 May 13
     
    In this animal study, testosterone induces vasodilation via a non-classical genomic pathway.  Likely independent of androgen receptor.  Also, aromatase inhibition does not diminish the vasodilatory effect of testosterone.
Nathan Goodyear

Vitamin C Improves Endothelium-Dependent Vasodilation by Restoring Nitric Oxide Activit... - 0 views

circ.ahajournals.org/...2222

eNOS NO nitric oxide vitamin C hypertension

shared by Nathan Goodyear on 16 Jan 17 - No Cached
  • Nathan Goodyear on 16 Jan 17
     
    vitamin C, in small study in patient with/without hypertension, found to increase endothelial vasodilation via increasing eNOS activity.
Nathan Goodyear

Comparisons of normal saline and lactated Ringer's resuscitation on hemodynamics, metab... - 0 views

www.ncbi.nlm.nih.gov/...PMC4029282

IV fluids lactated ringers normal saline LR NS

shared by Nathan Goodyear on 03 Jul 18 - No Cached
  • NS contains 154 mM Na+ and Cl-, with an average pH of 5.0 and osmolarity of 308 mOsm/L.
  • LR solution has an average pH of 6.5, is hypo-osmolar (272 mOsm/L), and has similar electrolytes (130 mM Na+, 109 mM Cl-, 28 mM lactate, etc.) to plasma
  • hyperchloremic acidosis
  • ...26 more annotations...
  • LR’s acid base balance is superior to that of NS’s
  • There were no significant differences between LR and NS groups in fibrinogen concentrations or platelet count
  • Total protein dropped
  • no significant differences in Hct (Table  1) or total protein between LR and NS groups
  • Bicarbonate HCO3- levels were decreased by hemorrhage but returned to pre-hemorrhage values by 3 h after LR resuscitation, whereas no return was observed with NS resuscitation
  • Na+ was increased after NS resuscitation
  • No changes in Na+ or K+ were observed
  • K+ did not change initially after NS resuscitation but was elevated at 6 h afterwards
  • Ca++ was similarly decreased
  • Cl- was elevated for 6 h after NS resuscitation, with no changes shown after LR resuscitation
  • PT was similarly prolonged by resuscitation with LR (from 11.2 ± 0.2 sec at baseline to 12.1 ± 0.2 sec at 6 h) and NS
  • Plasma aPTT was also similarly prolonged by resuscitation with LR (from 17.1 ± 0.5 sec baseline to 20.1 ± 1.2 sec at 6 h) or NS
  • NS resuscitation resulted in better oxygen delivery and oxygen delivery-to-oxygen demand ratio as an index of oxygen debt
  • NS had better tissue perfusion and oxygen metabolism than LR
  • LR resuscitation returned BE and bicarbonate to pre-hemorrhage levels within 3 h, but no return of BE or bicarbonate was observed for 6 hr with NS resuscitation
  • current blood bank guidelines state that LR should not be mixed with blood to prevent the risk of clot formation from calcium included in LR
  • LR resuscitation should not be given with blood through the same iv-line and crystalloids should be avoided in patients with blood transfusion
  • PT and aPTT were prolonged for 6 h after hemorrhage and resuscitation, suggesting a hypocoagulable states
  • potential thrombotic risk from LR resuscitation is unlikely.
  • we suspected that the blood pressure after NS resuscitation would be lower than that of LR due to its vasodilator effects
  • NS required a larger resuscitation volume and was associated with poor acid base status and elevated serum potassium in this model
  • NS required 50% more volume and was associated with a higher cardiac output and lower peripheral resistance, as compared to LR resuscitation
  • These differences are possibly due to the vasodilator effects from NS
  • an elevation of K+ was observed at 6 h post NS resuscitation, while no change of K+ was observed after LR resuscitation
  • The mechanism for the increase of K+ from NS is not fully known
  • NS is associated with vasodilator effects and the risks of metabolic acidosis and hyperkalemia
  • Nathan Goodyear on 03 Jul 18
     
    LR vs NS crystalloid.
Nathan Goodyear

Vitamin C Improves Endothelium-Dependent Vasodilation by Restoring Nitric Oxide Activit... - 0 views

circ.ahajournals.org/...2222.long

vitamin C hypertension eNOS IV vitamin C NO nitric oxide

shared by Nathan Goodyear on 18 Dec 17 - No Cached
  • Nathan Goodyear on 18 Dec 17
     
    IV Vitamin C improves endothelial vasodilation in essential hypertension.  The Vitamin C reduces the oxygen free radicals which allowed eNOS to increase NO production.  Two take homes: oxygen free radicals may be responsible for the endothelial dysfunction that leads to essential hypertension and vitamin C, particularly IV, can be used to counter this process.  Other studies have shown IV vitamin C to be anti-hypertensive in its action.
Nathan Goodyear

Testosterone: a vascular hormone in health and disease - 0 views

joe.endocrinology-journals.org/...JOE-12-0582.full.pdf+html

low T low Testosterone testosterone low cardiovascular cardiovascular disease CVD health hormone hormones men male

shared by Nathan Goodyear on 23 Apr 13 - No Cached
  • Nathan Goodyear on 23 Apr 13
     
    testosterone therapy has tremendous cardiovascular benefit in men with low T.  The key here is physiologic replacement of Testosterone.  Testosterone is a vasodilator and anti-inflammatory agent in men with low T.  Testosterone therapy improves cardiac function in those with DHF and angina.  Testosterone is found to be a Ca++ channel blocker--anyone say hypertension treatment?
Nathan Goodyear

Effects of Testosterone on Coronary Vasomotor Regulation in Men With Coronary Heart Dis... - 0 views

circ.ahajournals.org/...1690.long

Testosterone CVD CAD heart heart disease cardiovascular heart disease cardiovascular disease men male hormone hormones

shared by Nathan Goodyear on 17 Jul 12 - No Cached
  • Nathan Goodyear on 17 Jul 12
     
    Testosterone therapy, injected intracoronary, resulted in vasodilation and improved blood flow in men with CAD.
Nathan Goodyear

Testosterone and the Cardiovascular System: A Comprehensive Review of the Clinical Lite... - 0 views

jaha.ahajournals.org/...e000272

low T Testosterone cardiovascular disease CAD CHF insulin resistance type II diabetes diabetes obesity men male hormone hormones therapy

shared by Nathan Goodyear on 13 May 14 - No Cached
  • Nathan Goodyear on 13 May 14
     
    Some startling statistics in this 2013 review on Testosterone in men.  Studies reflect an inverse relationship between Testosterone and CAD severity.  That is, the lower the Testosterone levels, the increase in severity of CAD. This same association was also found with CHF.  Low Testosterone is common in those with CAD, CHF, type II diabetes, increased IMT in carotids and aorta, and obesity when compared to "healthy" individuals.  Testosterone therapy in those with CAD found benefits: prolongation of ST segment depression, coronary vasodilation, improved exercise capacity in those with CHF, shift to type I muscle fibers, shorten the QTc interval.  Testosterone therapy has been shown to improve insulin resistance, improve HgbA1c and decrease waist circumference and fat loss in obese individuals.  Otherwise, a good review of the association between a declining Testosterone and cardiovascular disease.
Nathan Goodyear

Ascorbic Acid-Induced Modulation of Venous Tone in Humans | Hypertension - 0 views

hyper.ahajournals.org/...949

vitamin C IV vitamin C hypertension blood pressure cardiovascular disease CVD

shared by Nathan Goodyear on 20 Dec 17 - No Cached
  • Nathan Goodyear on 20 Dec 17
     
    Acute vasodilation with IV vitamin C found to be independent of NO.
Nathan Goodyear

The acute effect of high-dose intravenous vitamin C and other nutrients on blood pressu... - 0 views

www.ncbi.nlm.nih.gov/...PMC4864764

vitamin C IV vitamin C hypertension vitamin B12 blood pressure cardiovascular disease CVD

shared by Nathan Goodyear on 14 Aug 17 - No Cached
  • the reduction in BP within the first 10–20 min may be primarily attributed to a direct vasodilatory physiological effect, described as venodilation
  • BP reduction observed after 70–90 min is likely attributable to pharmacokinetically plausible vitamin C absorption and vasodilation because of nitric oxide release
  • Pharmacokinetic studies of IVC administration observed peak plasma levels within the first 90 min, with plasma levels reaching 13350 μmol/l for 50 g of IVC
  • ...6 more annotations...
  • Essential hypertension, associated with endothelial dysfunction because of an impaired nitric oxide/l-arginine pathway and impaired vasodilation can be restored by vitamin C
  • marked increase in BP response when IVB12 is administered
  • The mean BP increased significantly up to 12–16 mmHg systolic and diastolic independent of the dosage of vitamin B12
  • The production of norepinephrine, which can stimulate angiotensin-II production, which in turn influences BP, has been suggested as a possible mechanism for the increase in BP with IVB12
  • excess norephinephrine levels stimulate the sympathetic nervous system, leading to increased cortisol production, which has also been linked to increases in BP
  • Animal studies have found higher serum levels of norepinephrine (noradrenaline) in the adrenal medulla of rats receiving methylcobalamin (methyl-vitamin B12)
  • Nathan Goodyear on 14 Aug 17
     
    IV vitamin C in mostly normotensive patients (> 30 grams) reduced blood pressure.  Some of the patients were pre-hypertensive. Vitamin B12 increase the blood pressure.
Nathan Goodyear

Testosterone Induces Dilation of Canine Coronary Conductance and Resistance Arteries In... - 0 views

circ.ahajournals.org/...2614.abstract

testosterone vasodilation androgen receptor AR androgen receptor antagonist blockade antagonist male men

shared by Nathan Goodyear on 14 May 13 - No Cached
  • Nathan Goodyear on 14 May 13
     
    another animal study, but blockade of androgen receptor, in this study, was not found to diminish the vasodilatory effect of testosterone.  This indicates that some of the vasoactive responses to testosterone are independent of AR and this has been shown in other studies ie. AR knockout mice.
Nathan Goodyear

Androgens and penile erection: evidence for a direct relationship between free testoste... - 0 views

onlinelibrary.wiley.com/...abstract

ED testosterone men male

shared by Nathan Goodyear on 01 Jun 13 - No Cached
  • Nathan Goodyear on 01 Jun 13
     
    testosterone replacement in men found to improve penile blood flow and thus improve erectile function.
Nathan Goodyear

L-arginine-induced vasodilation in healthy humans: pharmacokinetic-pharmacodynamic rela... - 0 views

www.ncbi.nlm.nih.gov/...PMC1873701

L-Arginine NO

shared by Nathan Goodyear on 30 Apr 13 - No Cached
  • Nathan Goodyear on 30 Apr 13
     
    l-Arginine
Nathan Goodyear

Testosterone deficiency syndrome and cardiovascular health: An assessment of beliefs, k... - 0 views

www.ncbi.nlm.nih.gov/...PMC3929476

low T Testosterone cardiovascular disease physicians men male hormone hormones

shared by Nathan Goodyear on 03 Mar 14 - No Cached
  • The vast majority (88%) did not screen cardiac patients for TDS.
  • Testosterone deficiency has a prevalence of 7% in the general population, rising to 20% in elderly males
  • Males with CAD have lower testosterone levels than those with normal coronary angiograms of the same age,5 suggesting that the prevalence of testosterone deficiency is much higher in the CAD population
  • ...14 more annotations...
  • Men with hypertension, another established risk factor for CAD, have lower testosterone compared to normotensive men
  • Recent meta-analyses showed that testosterone levels are generally lower among patients with metabolic syndrome, regardless of the various definitions of metabolic syndrome that are used
  • Testosterone (total and bioavailable) and sex-hormone binding globulin (SHBG) are inversely associated with the prevalence of metabolic syndrome in men between the ages of 40 and 80, and this association persists across racial and ethnic backgrounds
  • ower levels of testosterone and SHBG predict a higher incidence of metabolic syndrome.
  • Low testosterone levels have been related to increased insulin resistance and cardiovascular mortality,12 even in the absence of overt type 2 diabetes mellitus.
  • testosterone levels (total and bioavailable) in middle-aged men are inversely correlated with insulin resistance
  • The Massachusetts Male Aging Study (MMAS) demonstrated that low levels of testosterone and SHBG are independent risk factors for the development of type 2 diabetes,
  • Andropausal men (age 58 ± 7 years) have a higher maximal carotid artery intima-media thickness
  • There is an inverse linear correlation between body mass index (BMI) and wait-to-hip ratio with testosterone and insulin-like growth factor-1 levels.
  • Testosterone supplementation for 1 year in hypogonadal men has been shown to cause a significant improvement in body weight, BMI, waist size, lipid profile, and C-reactive protein levels
  • TRT for 3 months in hypogonadal men with type 2 diabetes significantly improved fasting insulin sensitivity, fasting blood glucose and glycated hemoglobin.
  • Testosterone replacement can improve angina symptoms and delay the onset of cardiac ischemia, likely through a coronary vasodilator mechanism
  • ADT is associated with an increased risk of cardiovascular events, including myocardial infarction and cardiovascular mortality.
  • ADT significantly increases fat mass, decreases lean body mass,29,30 increases fasting plasma insulin and decreases insulin sensitivity31 and increases serum cholesterol and triglyceride levels
  • Nathan Goodyear on 03 Mar 14
     
    Startling study on the knowledge of Testosterone and cardiovascular disease in general practitioners and cardiologists in Canada.  Eight-eight percent did not screen patients with cardiovascular disease for low Testosterone.  A whopping 67% of physicians did not know that low T was a risk factor for cardiovascular disease, yet 62% believed Testosterone would increase exercise tolerance. The lack of knowledge displayed by physicians today is staggering and is an indictment of the governing bodies.  This was a survey conducted in Canada so there are obvious limitations to the strength/conclusion of this study.
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