Force Of Myocardial Contraction Research Articles

Kinetic energy as a factor in assessing the work of the heart in patients with aortic stenosis

Goal. To analyze the evolution of the myocardial contraction force through the assessment of kinetic energy in patients with aortic stenosis based on intraventricular blood flowsMaterial and methods. According to the selection criteria, 21 healthy volunteers (age 34 ± 3) and 105 patients with aortic stenosis (age 62 ± 4) were examined before and after surgery for 7–10 days. Transthoracic echocardiography was performed on a Vivid E9 device in 2, 3 and 4 chamber positions with registration of intraventricular blood flows, calculation of the rate of change in volume and kinetic energy depending on the left ventricular EDV, pressure gradient (ΔP) on the aortic valve with an assessment of the displacement of the left ventricular endocardium contour, based on technologies for tracking speckles of ultrasonic images in the MultiVox program.Results. Our goal was to quantify kinetic energy (KE) during the entire cardiac cycle of the left ventricle (LV) using echocardiography. One of the main strengths identified in these studies is the high reproducibility of the assessment of LV blood flow and hemodynamics the average coefficient of variability 7 ± 2% for assessing LV function. Studies have shown increased diagnostic reliability without spending additional time. In systole, the KE before the LV operation was higher than normal values (0.62–0.78 J) after the operation, the KE approached the norm, averaging 0.55 J.Conclusion. Changes in intraventricular blood flow in patients with pressure overload of the heart demonstrate higher systolic energy compared to the control group. Different time values of energy in systole and diastole, observed in patients before surgery, represent an objective approach to assessing the work of the heart. The energy analysis reflects earlier signs of mechanical myocardial disorders, compared with the ejection fraction and, possibly, predict the development of cardiac remodeling. Adequate correction of the defect normalizes the work of the heart already in the early postoperative period.

Live cell screening identifies glycosides as enhancers of cardiomyocyte cell cycle activity.

Promoting cardiomyocyte proliferation is a promising strategy to regenerate the heart. Yet, so far, it is poorly understood how cardiomyocyte proliferation is regulated, and no factor identified to promote mammalian cardiomyocyte proliferation has been translated into medical practice. Therefore, finding a novel factor will be vital. Here, we established a live cell screening based on mouse embryonic stem cell-derived cardiomyocytes expressing a non-functional human geminin deletion mutant fused to Azami Green (CM7/1-hgem-derived cardiomyocytes). We screened for a subset of compounds of the small molecule library Spectrum Collection and identified 19 potential inducers of stem cell-derived cardiomyocyte proliferation. Furthermore, the pro-proliferative potential of identified candidate compounds was validated in neonatal and adult rat cardiomyocytes as well as human induced pluripotent stem cell-derived cardiomyocytes. 18 of these compounds promoted mitosis and cytokinesis in neonatal rat cardiomyocytes. Among the top four candidates were two cardiac glycosides, peruvoside and convallatoxin, the flavonoid osajin, and the selective α-adrenoceptor antagonist and imidazoline I1 receptor ligand efaroxan hydrochloride. Inhibition of PTEN and GSK-3β enhanced cell cycle re-entry and progression upon stimulation with cardiac glycosides and osajin, while inhibition of IP3 receptors inhibited the cell cycle-promoting effect of cardiac glycosides. Collectively, we established a screening system and identified potential compounds to promote cardiomyocyte proliferation. Our data suggest that modulation of calcium handling and metabolism promotes cardiomyocyte proliferation, and cardiac glycosides might, besides increasing myocardial contraction force, contribute to cardiac repair by inducing cardiomyocyte proliferation.

Blockade of α2-Adrenergic Receptors Inhibits Functional Parameters of Langendorff-Isolated Rat Heart.

We studied the effect of α2-adrenoreceptor antagonist yohimbine in concentrations of 10-9-10-6 M on the inotropy, chronotropy, and coronary flow of the Langendorff-isolated rat heart. It was found that antagonist of α2-adrenoreceptors yohimbine changes all the studied parameters of the isolated heart. The force of left ventricular myocardial contraction, HR, and coronary flow decreased after application of all concentrations of α2-adrenoreceptor antagonist. The maximum inotropic, chronotropic, and vascular effects were observed when the antagonist was applied to the perfused solution in a concentration of 10-9 M. The minimum decrease in coronary flow and HR was observed when yohimbine was applied in a concentration of 10-8 M; minimum effect on myocardial contractility was revealed at α2-adrenoreceptor blocker concentration of 10-7 M.

Toxicities of opioid analgesics: respiratory depression, histamine release, hemodynamic changes, hypersensitivity, serotonin toxicity.

Opioid-induced respiratory depression is potentially life-threatening and often regarded as the main hazard of opioid use. Main cause of death is cardiorespiratory arrest with hypoxia and hypercapnia. Respiratory depression is mediated by opioid μ receptors expressed on respiratory neurons in the CNS. Studies on the major sites in the brainstem mediating respiratory rate suppression, the pre-Bӧtzinger complex and parabrachial complex (including the Kӧlliker Fuse nucleus), have yielded conflicting findings and interpretations but recent investigations involving deletion of μ receptors from neurons have led to greater consensus. Some opioid analgesic drugs are histamine releasers. The range of clinical effects of released histamine include increased cardiac output due to an increase in heart rate, increased force of myocardial contraction, and a dilatatory effect on small blood vessels leading to flushing, decreased vascular resistance and hypotension. Resultant hemodynamic changes do not necessarily relate directly to the concentration of histamine in plasma due to a range of variables including functional differences between mast cells and histamine-induced anaphylactoid reactions may occur less often than commonly believed. Opioid-induced histamine release rarely if ever provokes bronchospasm and histamine released by opioids in normal doses does not lead to anaphylactoid reactions or result in IgE-mediated reactions in normal patients. Hypersensitivities to opioids, mainly some skin reactions and occasional type I hypersensitivities, chiefly anaphylaxis and urticaria, are uncommon. Hypersensitivities to morphine, codeine, heroin, methadone, meperidine, fentanyl, remifentanil, buprenorphine, tramadol, and dextromethorphan are summarized. In 2016, the FDA issued a Drug Safety Communication concerning the association of opioids with serotonin syndrome, a toxicity associated with raised intra-synaptic concentrations of serotonin in the CNS, inhibition of serotonin reuptake, and activation of 5-HT receptors. Opioids may provoke serotonin toxicity especially if administered in conjunction with other serotonergic medications. The increasing use of opioid analgesics and widespread prescribing of antidepressants and psychiatric medicines, indicates the likelihood of an increased incidence of serotonin toxicity in opioid-treated patients.

Vasoactive Intestinal Peptide Changes the Frequency and Force of Myocardial Contraction in Rats.

We studied the effect of non-selective agonist of VIP receptors of vasoactive intestinal polypeptide in different concentrations on the frequency, force, and duration of isometric contraction of myocardial strips of the right atrium under conditions of spontaneous activity, as well as the force and duration of contractions of the right ventricle in rats. It was found that the agonist produced a positive inotropic and chronotropic effect that depended on its concentration. The maximum effect was observed at vasoactive intestinal peptide concentration of 10-11 M.

EMOTIONAL STATES OF ELDERLY WOMEN WITH ISCHEMIC HEART DISEASE AS A COMPLEX PERSONALITY PHENOMENON

The article examines emotional states of elderly people with ischemic heart disease (IHD) as a complex personality phenomenon.  An individual’s emotional experience is manifested in different emotions, feelings and emotional states, which are evaluative and have negative/positive poles.  The main purpose of this work was to analyse theoretically the emotional states of elderly people with ischemic heart disease as a complex personality phenomenon that has mental, psychophysiological and behavioural levels. We have determined theoretically that negative feelings worsen a functional state of the heart, causing its electromagnetic destabilization.  The main mechanisms of the pathogenic influence of stresses on IHD are: the increased release of catecholamines, which leads to increased myocardial oxygen consumption as a result of an increased heart rate, higher blood pressure and stronger myocardial contraction force; a violated vascular tone of the epicardial arteries and worsened microcirculation; increased platelet aggregation, secretion of certain blood coagulation factors, decreased fibrinolytic activity of the blood. Considering the problem of negative emotional states, the scientific literature notes the following states that characterize an individual in difficult life situations: anxiety, depression, asthenia, hostility. Long-term emotional overstrain, acute and chronic traumas of the psyche, psychological-emotional disorders, the most significant of which are depressive and anxiety-phobic, influence significantly on older women’s ischemic heart disease.  In addition, at the case of depression, behavioural factors such as patients’ reluctance to take medications or to comply with the prescribed regimen have a significant effect. The article determines that elderly women’s emotional states are mainly negative, they are caused by chronic emotional stresses, emotional overstrain (distress) and psychological-emotional disorders and increases the risk of coronary heart disease. &nbsp

A New Approach to Evaluating the Pumping Function of the Heart by the Myocardial Work.

The function of left ventricular (LV) contractility consists of two aspects, the force of myocardial contraction, which provides a sufficient pressure gradient to open the heart valves, and deformation, which determines the actual cardiac output [1, 2]. The relationship between the characteristics of LV deformation and LV volume parameters remains poorly understood. The LV work may reflect the dependence between the volume and deformation characteristics of the left ventricle. Myocardial work indexes can more accurately describe the systolic LV function when the LV ejection fraction (EF) and global longitudinal strain (GLS) are not informative enough [3, 4]. A new approach was proposed for evaluating the LV pumping function, and a parameter was developed to characterize the efficiency of myocardial work for the cardiac cycle period from the aortic valve opening (AVO) to its closure (AVC), that is, the phase of blood ejection from the left ventricle.

The Ionotropic P2X4 Receptor has Unique Properties in the Heart by Mediating the Negative Chronotropic Effect of ATP While Increasing the Ventricular Inotropy.

Background: Mounting evidence indicate that reducing the sinoatrial node (SAN) activity may be a useful therapeutic strategy to control of heart failure. Purines, like ATP and its metabolite adenosine, consistently reduce the SAN spontaneous activity leading to negative cardiac chronotropy, with variable effects on the force of myocardial contraction (inotropy). Apart from adenosine A1 receptors, the human SAN expresses high levels of ATP-sensitive ionotropic P2X4 receptors (P2X4R), yet their cardiac role is unexplored. Methods: Here, we investigated the activity of P2 purinoceptors on isolated spontaneously beating atria (chronotropy) and on 2 Hz-paced right ventricular (RV, inotropy) strips from Wistar rats. Results: ATP (pEC 50 = 4.05) and its stable analogue ATPγS (pEC 50 = 4.69) concentration-dependently reduced atrial chronotropy. Inhibition of ATP breakdown into adenosine by NTPDases with POM-1 failed to modify ATP-induced negative chronotropy. The effect of ATP on atrial rate was attenuated by a broad-spectrum P2 antagonist, PPADS, as well as by 5-BDBD, which selectively blocks the P2X4R subtype; however, no effect was observed upon blocking the A1 receptor with DPCPX. The P2X4R positive allosteric modulator, ivermectin, increased the negative chronotropic response of ATP. Likewise, CTP, a P2X agonist that does not generate adenosine, replicated the P2X4R-mediated negative chronotropism of ATP. Inhibition of the Na+/Ca2+ exchanger (NCX) with KB-R7943 and ORM-10103, but not blockage of the HCN channel with ZD7288, mimicked the effect of the P2X4R blocker, 5-BDBD. In paced RV strips, ATP caused a mild negative inotropic effect, which magnitude was 2 to 3-fold increased by 5-BDBD and KB-R7943. Immunofluorescence confocal microscopy studies confirm that cardiomyocytes of the rat SAN and RV co-express P2X4R and NCX1 proteins. Conclusions: Data suggest that activation of ATP-sensitive P2X4R slows down heart rate by reducing the SAN activity while increasing the magnitude of ventricular contractions. The mechanism underlying the dual effect of ATP in the heart may involve inhibition of intracellular Ca2+-extrusion by bolstering NCX function in the reverse mode. Thus, targeting the P2X4R activation may create novel well-tolerated heart-rate lowering drugs with potential benefits in patients with deteriorated ventricular function.

A missense mutation within the C6-domain of cMyBP-C results in cardiac enlargement and depressed ventricular function

Cardiac myosin-binding protein-C (cMyBP-C) plays a key role in determining the force and kinetics of myocardial contraction, primarily by binding to either myosin subfragment-2 or actin or both. By modulating the probability of myosin cross-bridge binding to actin, cMyBP-C normally acts to govern the kinetics of force development and relaxation. To determine the effects on cardiac morphology and function due to a novel cMyBP-C W792R missense mutation associated with clinical hypertrophic cardiomyopathy in humans. We generated cMyBP-C-W792R heterozygous and homozygous knock-in mice to investigate the structural and functional phenotypes associated with a missense mutation within the C6-domain of cMyBP-C. Compared to wild-type, homozygous W792R knock-in hearts exhibited significant ventricular and atrial dilation. While the W792R mutant protein was expressed at equivalent levels as in wild-type mice, the extent of phosphorylation of the mutant cMyBP-C protein was markedly reduced. Measurements of steady-state force and cross-bridge cycling kinetics showed that homozygous cMyBP-C W792R skinned myocardium exhibited a significant increase in the Ca2+-sensitivity of force and accelerated cross-bridge cycling kinetics (ktr) at maximal levels of Ca2+-activation, compared to WT myocardium. Cardiac function, as assessed by transthoracic echocardiography, revealed depressed indices of systolic and diastolic ventricular function in the homozygous W792R KI mice. These results demonstrate that a mutation within the mid-region of cMyBP-C can disrupt the dynamic regulation between myosin and actin that is normally governed by cMyBP-C, thereby leading to aberrant cardiac enlargement and commensurate diminution of in vivo ventricular function.

Identification of phosphorylation sites on β1-adrenergic receptor in the mouse heart

β1-adrenergic receptor (Adrb1) belongs to the superfamily of G-protein-coupled receptors (GPCRs) and plays a critical role in the regulation of heart rate and myocardial contraction force. GPCRs are phosphorylated at multiple sites to regulate distinct signal transduction pathways in different tissues. However, little is known about the location and function of distinct phosphorylation sites of Adrb1 in vivo. To clarify the mechanisms underlying functional regulation associated with Adrb1 phosphorylation in vivo, we aimed to identify Adrb1 phosphorylation sites in the mouse heart using phosphoproteomics techniques with nano-flow liquid chromatography/tandem mass spectrometry (LC-MS/MS). We revealed the phosphorylation residues of Adrb1 to be Ser274 and Ser280 in the third intracellular loop and Ser412, Ser417, Ser450, Ser451, and Ser462 at the C-terminus. We also found that phosphorylation at Ser274, Ser280, and Ser462 was enhanced in response to stimulation with an Adrb1 agonist. This is the first study to identify Adrb1 phosphorylation sites in vivo. These findings will provide novel insights into the regulatory mechanisms mediated by Adrb1 phosphorylation.

Inotropes and vasopressors

Inotropic agents are used to increase myo-cardial contraction while vasopressors are used to increase vascular tone. They are often used for treatment of patients whose tissue perfusion is insufficient to meet metabolic requirements. Therefore, these agents are usually administered in inten-sive care units where continuous and inva-sive monitoring of cardiac function can be applied.Inotropic agents can be divided into those that increase cAMP levels and those that do not. Adrenergic receptor agonists and phosphodiesterase inhibitors (PDEi) in-crease cAMP levels and are currently the mainstay of positive inotropic therapy. Le-vosimendan acts as calcium sensitizer and increases myocardial contraction force without increasing intracellular calcium levels. In addition to existing inotropic agents, new promising inotropes are be-ing developed. These include sarcoplasmic reticulum calcium pump (istaroxime), cardiac myosin activators (omecamtivme-carbil), gene therapy, nitroxyl donors and ryanodine receptor stabilizers.Current treatments of heart failure are aimed at prolonging survival and not just alleviating symptoms. This review pro-vides a short description of the physiology of myocardial contraction and adrenergic receptors. We also provide a short descrip-tion of commonly used inotropic agents and vasopressor drugs as well as a short re-view of agents that are expected are in use in the future.Inotropes are agents used to increase myo-cardial contractility, while vasopressors are administered to increase vascular tone (1). Their use ismostly confined to critically ill patients whose hemodynamic impairment is such that tissue perfusion is insufficient to meet metabolic requirements (2). Pa-tients in need of inotropic or vasopressor support are often presented with septic or cardiogenic shock and severe heart failure, and are victims of major trauma or un-dergoing major surgery.These drugs are therefore administered usually to patients treated in intensive care settings where continuous monitoring of cardiac rhythm, arterial oxygenation, urine output and other invasive hemodynamic monitoring can be applied.Inotropic and vasopressor drugs should be administered through a central venous catheter via infusion pumps that can deliver precise flow rates. These agents are mostly short acting with rapid onset and offset of action. Therefore, they can be used without an initial bolus and can be titrated frequently. Abrupt dis-continuation should be avoided because of possible hypotension.

Effective treatment of polydatin weakens the symptoms of collagen-induced arthritis in mice through its anti-oxidative and anti-inflammatory effects and the activation of MMP-9.

Polydatin is a natural extract used in traditional Chinese medicine, which leads to a marked improvement in the microcirculation perfusion and enhances the animal myocardial contraction force. The present study aimed to determine whether an effective treatment of polydatin ameliorates the symptoms of collagen‑induced arthritis (CIA), and also to explore the potential mechanism. Male DBA/1J mice were induced into CIA model mice. The administration of polydatin effectively suppressed CIA in mice. The serum levels of malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor‑α (TNF‑α) and interleukin1β (IL‑1β) were effectively increased following the induction of CIA in the model mice compared with the control group. The elevated serum levels of MDA, SOD, TNF‑α and IL‑1β were markedly suppressed by the effective treatment of polydatin in CIA mice, compared with the CIA model group. However, an increase in the level of matrix metalloproteinase‑9 (MMP‑9) was markedly induced in the CIA mice compared with the control group. As compared with the CIA group, the expression of MMP‑9 was substantially reduced by the effective treatment of polydatin. Taken together, the effective treatment of polydatin ameliorated the symptoms of CIA through an exertion of its antioxidative and anti‑inflammatory effects, and also via activation of the expression of matrix metalloproteinase-9 (MMP-9) in mice.

Vigorous Vascular Contraction Mimicking Myocardial Bridge Resulting from Digoxin Treatment in an Elderly Patient

Summary Myocardial bridge is defined as the intramyocardial course of a segment of a coronary artery. Digoxin increases the force of myocardial contraction, which augments the compression of the vessel. An 86-year-old woman was admitted to hospital because of chest tightness on exertion. Coronary angiography showed a myocardial bridge in the left anterior descending coronary artery that was absent 6 years previously. There was >80% reduction in the minimal luminal diameter during systole. Digoxin was discontinued. Repeat coronary angiography performed approximately 4 months later revealed that systolic compression of the myocardial bridge had decreased significantly, and the reduction was

How to administer inotropic drugs

Rationale and key pointsThis article aims to help nurses to administer inotropic drugs in a safe, effective and patient-centred manner. The mode of action of inotropic drugs makes them well suited to treat haemodynamic compromise experienced by critically ill patients. Effects such as increased force of myocardial contraction and vasoconstriction make them highly potent.▶Knowledge relating to cardiovascular physiology and the mode of action of inotropes enables the nurse to deliver inotropic drugs safely.▶Invasive blood pressure monitoring should be established before administering inotropic drugs, because of their rapid action.▶Inotropes should be administered via a central venous catheter.▶Drug administration procedures should be followed stringently.Reflective activityClinical skills articles can help update your practice and ensure it remains evidence based. Apply this article to your practice. Reflect on and write a short account of:1.The ways in which this article and the useful resources have enhanced your knowledge.2.How your practice, local policy and this article compare in the care of a patient receiving inotropic drugs. Could your practice be enhanced?Subscribers can upload their reflective accounts at: rcni.com/portfolio.

ASSA14-03-36 Guanxinkeli protects myocardial cells from ischemia-reperfusion injury in rats via JNK signal pathway

Background To study the protective effect and potential mechanism of Guanxinkeli (GXKL) which may plays an important role in resisting the reperfusion injury of the ischaemic myocardium on myocardial ischemia and reperfusion injuries. Methods Thirty-six rats were randomly divided into three groups: control group, ischemia reperfusion injury group and GXKL group, there were 12 rats in each group. The rat hearts were subjected to 15 min ischemia, followed by 30 min reperfusion. HR, LVDP, LVEDP and ± dp /dtmax were recorded before ischemia and at 30 min of reperfusion. The coronary effulents were collected before ischemia and at 30 min of reperfusion to measure the CK and LDH activity and the arrhythmia scores were determined. JNK protein Level was derermined by western blotting assay. Results GXKL enhanced LVEDP, LVDP and ± dp /dtmax. The arrhythmia score, CK and LDH activities in GXKL group were lower than those in ischemia and reperfusion group. The phosphorylated JNK protein was also lower in GXKL group. Conclusions GXKL may obviously improve the anti-ischaemic myocardial ischemia/reperfusion ability, increase myocardial contraction force, alleviate arrhythmia, the protective effect may be correlated with JNK signalling pathway.

Role of neuropeptide Y in myocardial contractility of rats during early postnatal ontogeny.

We studied the effect of neuropeptide Y in concentrations of 10(-10)-10(-6) M on myocardial contractility of rats at the age of 7, 21, and 100 days. Studying the isometric contraction of myocardial strips showed that neuropeptide Y decreases the force of myocardial contraction in 7-day-old rat pups. Exogenous neuropeptide Y produced a biphasic effect in 21-day-old rats, which was manifested in the increase and subsequent decrease in myocardial contractility. Neuropeptide Y had little effect on myocardial contractility of 100-day-old animals.

Cardiovascular activity of total protein extract of Morinda morindoïdes (baker) Miln-Redhon on rabbit blood pressure and isolated rat heart

Total protein extract of the leaves of Morinda morindoides were investigated for rabbit blood pressure and mechanical activity of isolated rat heart. Total proteins of M. morindoides (PT-Mm) were extracted according the saturation related to Dawson method. The blood pressure was analysed using the mercury manometer of Ludwig. The mechanical activity of the heart was realized with the Langendorff method. PT-Mm produced a reversible hypotension at doses ranging from 5.55 to 27.77 mg/kgBw, and irreversible hypotension to 55.55 mg/kg resulting in the death of the animal. PT-Mm showed a significant decrease (31.77 ± 2.72%) in average of the arterial blood pressure in a dose-related manner. Also, PT-Mm (10-8 to 10-1mg/ml) decreased both the force and rate of myocardial contraction, respectively (28.58 ± 2.47 and 33.35% ± 2.35) in a concentration dependent manner. The hypotensive effect of PT-Mm was inhibited by atropine sulfate. The hypertensive effect of adrenaline was strongly reduced by PT-MN extract (77.44 ± 2.23%). In conclusion, total proteins extract of M. morindoides has blood pressure lowering effect which would result from the combined actions of myocardial depression and activation of muscarinic cholinergic receptors mediated by vascular smooth muscle relaxation. Key words: Cardiovascular activity, Morinda morindoides, Total proteins, Blood pressure, Heart rate.

A Family of microRNAs Encoded by Myosin Genes Governs Myosin Expression and Muscle Performance

Myosin is the primary regulator of muscle strength and contractility. Here we show that three myosin genes, Myh6, Myh7, and Myh7b, encode related intronic microRNAs (miRNAs), which, in turn, control muscle myosin content, myofiber identity, and muscle performance. Within the adult heart, the Myh6 gene, encoding a fast myosin, coexpresses miR-208a, which regulates the expression of two slow myosins and their intronic miRNAs, Myh7/miR-208b and Myh7b/miR-499, respectively. miR-208b and miR-499 play redundant roles in the specification of muscle fiber identity by activating slow and repressing fast myofiber gene programs. The actions of these miRNAs are mediated in part by a collection of transcriptional repressors of slow myofiber genes. These findings reveal that myosin genes not only encode the major contractile proteins of muscle, but act more broadly to influence muscle function by encoding a network of intronic miRNAs that control muscle gene expression and performance.

The velocity of the arterial pulse wave: a viscous-fluid shock wave in an elastic tube

BackgroundThe arterial pulse is a viscous-fluid shock wave that is initiated by blood ejected from the heart. This wave travels away from the heart at a speed termed the pulse wave velocity (PWV). The PWV increases during the course of a number of diseases, and this increase is often attributed to arterial stiffness. As the pulse wave approaches a point in an artery, the pressure rises as does the pressure gradient. This pressure gradient increases the rate of blood flow ahead of the wave. The rate of blood flow ahead of the wave decreases with distance because the pressure gradient also decreases with distance ahead of the wave. Consequently, the amount of blood per unit length in a segment of an artery increases ahead of the wave, and this increase stretches the wall of the artery. As a result, the tension in the wall increases, and this results in an increase in the pressure of blood in the artery.MethodsAn expression for the PWV is derived from an equation describing the flow-pressure coupling (FPC) for a pulse wave in an incompressible, viscous fluid in an elastic tube. The initial increase in force of the fluid in the tube is described by an increasing exponential function of time. The relationship between force gradient and fluid flow is approximated by an expression known to hold for a rigid tube.ResultsFor large arteries, the PWV derived by this method agrees with the Korteweg-Moens equation for the PWV in a non-viscous fluid. For small arteries, the PWV is approximately proportional to the Korteweg-Moens velocity divided by the radius of the artery. The PWV in small arteries is also predicted to increase when the specific rate of increase in pressure as a function of time decreases. This rate decreases with increasing myocardial ischemia, suggesting an explanation for the observation that an increase in the PWV is a predictor of future myocardial infarction. The derivation of the equation for the PWV that has been used for more than fifty years is analyzed and shown to yield predictions that do not appear to be correct.ConclusionContrary to the theory used for more than fifty years to predict the PWV, it speeds up as arteries become smaller and smaller. Furthermore, an increase in the PWV in some cases may be due to decreasing force of myocardial contraction rather than arterial stiffness.

Reactive Oxygen Species Mediate Sevoflurane- and Desflurane-Induced Preconditioning in Isolated Human Right Atria In Vitro

We examined the role of reactive oxygen species (ROS) in sevoflurane- and desflurane-induced preconditioning on isolated human right atrial myocardium. We recorded isometric contraction of human right atrial trabeculae suspended in an oxygenated Tyrode's solution (34 degrees C, stimulation frequency 1 Hz). In all groups, a 30-min hypoxic period was followed by 60 min of reoxygenation. Ten minutes before hypoxia reoxygenation, muscles were exposed to 5 min of sevoflurane 2% or desflurane 6%. In separate groups, the sevoflurane 2% (Sevo + N-(2-mercaptopropionyl)-glycine [MPG]) or desflurane 6% (Des + MPG) was administered in the presence of 0.1 mM MPG, a ROS scavenger. The effect of 0.1 mM MPG alone was tested. Recovery of force after a 60-min reoxygenation period was compared between groups (mean +/- sd). Preconditioning with sevoflurane 2% (85% +/- 4% of baseline) or desflurane 6% (86% +/- 7% of baseline) enhanced the recovery of the force of myocardial contraction after 60 min reoxygenation compared with the control group (53% +/- 11% of baseline, P < 0.001). This effect was abolished in the presence of MPG (56% +/- 12% of baseline for Sevo + MPG, 48% +/- 13% of baseline for Des + MPG). The effect of MPG alone on the recovery of force was not different from the control group (57% +/- 7% of baseline versus 53% +/- 11%; P = NS). In vitro, sevoflurane and desflurane preconditioned human myocardium against hypoxia through a ROS-dependent mechanism.