Effects of ischemia on sarcoplasmic reticulum and contractile myofilament activity in human myocardium

1993 ◽  
Vol 265 (4) ◽  
pp. H1334-H1341 ◽  
Author(s):  
G. B. Luciani ◽  
A. D'Agnolo ◽  
A. Mazzucco ◽  
V. Gallucci ◽  
G. Salviati
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Isometric Tension ◽  
Hill Coefficient ◽  
Calmodulin Antagonist ◽  
Contractile System ◽  
Cardiac Fiber ◽  
And Control

The effects of global ischemia on the contractile system and on sarcoplasmic reticulum (SR) function were studied by measuring the isometric tension and the SR Ca2+ release activity of chemically skinned cardiac fiber preparations from seven patients undergoing open-heart surgery. Ten minutes of ischemia caused 1) a decrease in the myofilament sensitivity to Ca2+ (expected Ca2+ concentration giving half-maximal tension; from 0.69 +/- 0.04 to 1.38 +/- 0.06 microM, n = 7) and in the cooperativity index (Hill coefficient; from 2.61 +/- 0.45 to 0.92 +/- 0.15, n = 7), 2) a decrease in myosin light chain phosphorylation, and 3) a 300% increase in the threshold caffeine concentration for SR Ca2+ efflux channel activation, with a 30% reduction in the rate of Ca2+ release by caffeine at threshold concentrations and a 23% reduction in the rate of release by 20 mM caffeine. After preincubation with 5 microM trifluoperazine, a calmodulin antagonist, the caffeine threshold of ischemic and control cardiac muscle became comparable. Most changes were reversed by reperfusion, while the caffeine threshold was still two times greater than control. These results indicate that ischemia caused alterations of the cardiac muscle contractile apparatus and the SR that were reversed only after reperfusion.

scholarly journals CardioVR-ReTone—Robotic Exoskeleton for Upper Limb Rehabilitation following Open Heart Surgery: Design, Modelling, and Control

Symmetry ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 81
Author(s):  
Bogdan Mocan ◽  
Claudiu Schonstein ◽  
Calin Neamtu ◽  
Mircea Murar ◽  
Mircea Fulea ◽  
...  
Keyword(s):  
Cardiac Rehabilitation ◽  
Dynamic Model ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Point Of View ◽  
Open Heart ◽  
Upper Limb Rehabilitation ◽  
Robotic Exoskeleton ◽  
Patients Experience ◽  
And Control

Following cardiac surgery, patients experience difficulties with the rehabilitation process, often finding it difficult, and therefore lack the motivation for rehabilitation activities. As the number of people aged 65 and over will rise by 207 percent globally by 2050, the need for cardiac rehabilitation will significantly increase, as this is the main population to experience heart problems. To address this challenge, this paper proposes a new robotic exoskeleton concept with 12 DoFs (6 DoFs on each arm), with a symmetrical structure for the upper limbs, to be used in the early rehabilitation of cardiac patients after open-heart surgery. The electromechanical design (geometric, kinematic, and dynamic model), the control architecture, and the VR-based operating module of the robotic exoskeleton are presented. To solve the problem of the high degree of complexity regarding the CardioVR-ReTone kinematic and dynamic model, the iterative algorithm, kinetic energy, and generalized forces were used. The results serve as a complete model of the exoskeleton, from a kinematic and dynamic point of view as well as to the selection of the electric motors, control system, and VR motivation model. The validation of the concept was achieved by evaluating the exoskeleton structure from an ergonomic point of view, emphasizing the movements that will be part of the cardiac rehabilitation.

Sarcoplasmic reticulum Ca2+ pump in pig coronary artery smooth muscle is regulated by a novel pathway

1996 ◽  
Vol 271 (1) ◽  
pp. C181-C187 ◽  
Author(s):  
A. K. Grover ◽  
A. Xu ◽  
S. E. Samson ◽  
N. Narayanan
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Phosphorylation Site ◽  
Cyclopiazonic Acid ◽  
Western Blots ◽  
Calmodulin Antagonist ◽  
Calmodulin Kinase ◽  
Kinase Phosphorylation

Coronary artery smooth muscle expresses an alternative splice (SERCA2b) of the sarcoplasmic reticulum (SR) Ca2+ pump gene SERCA2, which is also expressed in cardiac muscle (SERCA2a), but how the activity of this transporter is regulated in the coronary artery is not known. SERCA2a in the cardiac muscle can be regulated via phospholamban or, as recently reported, by a direct phosphorylation of this protein by calmodulin kinase (Xu, A., C. Hawkins, and N. Narayanan. J.Biol. Chem. 268:8394-8397, 1993). Because both SERCA2a and SERCA2b contain this calmodulin kinase phosphorylation site, we examined the effect of endogenous calmodulin kinase phosphorylation of the SR Ca2+ pump in the coronary artery. SR-enriched membranes were isolated from coronary artery smooth muscle and washed in ethylene glycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid to remove bound calmodulin. When these membranes were incubated with MgATP2- in the presence of Ca2+/calmodulin, a 115-kDa protein was phosphorylated. This phosphorylated 115-kDa protein was identified as SERCA2b in Western blots and by immunoprecipitation using a SERCA2-selective antibody. Preincubating the membranes in MgATP2- in the presence of Ca2+/calmodulin stimulated the subsequent Ca2+ uptake in the presence of oxalate plus MgATP2- and azide. The stimulation of Ca2+ uptake was inhibited by including the SR Ca2+ pump inhibitors thapsigargin and cyclopiazonic acid in the Ca2+ uptake medium or by including the calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide or the calmodulin kinase II peptide fragment 290-309 in the phosphorylation solution. Thus an endogenous calmodulin-dependent kinase phosphorylated SERCA2b and activated it. Phospholamban could not be detected in these membranes in Western blots. Therefore, the regulation of the SR Ca2+ pump activity in coronary artery smooth muscle may involve a direct phosphorylation of the pump protein by an endogenous calmodulin-dependent kinase.

Store-operated Ca2+ entry modulates sarcoplasmic reticulum Ca2+ loading in neonatal rabbit cardiac ventricular myocytes

2006 ◽  
Vol 290 (6) ◽  
pp. C1572-C1582 ◽  
Author(s):  
Jingbo Huang ◽  
Casey van Breemen ◽  
Kuo-Hsing Kuo ◽  
Leif Hove-Madsen ◽  
Glen F. Tibbits
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Heart Surgery ◽  
Ventricular Myocytes ◽  
Open Heart Surgery ◽  
Cell Types ◽  
Reverse Mode ◽  
Nonselective Cation Channels ◽  
Intracellular Ca ◽  
Neonatal Cardiomyocyte

Store-operated Ca2+ entry (SOCE), which is Ca2+ entry triggered by the depletion of intracellular Ca2+ stores, has been observed in many cell types, but only recently has it been suggested to occur in cardiomyocytes. In the present study, we have demonstrated SOCE-dependent sarcoplasmic reticulum (SR) Ca2+ loading (loadSR) that was not altered by inhibition of L-type Ca2+ channels, reverse mode Na+/Ca2+ exchange (NCX), or nonselective cation channels. In contrast, lowering the extracellular [Ca2+] to 0 mM or adding either 0.5 mM Zn2+ or the putative store-operated channel (SOC) inhibitor SKF-96365 (100 μM) inhibited loadSR at rest. Interestingly, inhibition of forward mode NCX with 30 μM KB-R7943 stimulated SOCE significantly and resulted in enhanced loadSR. In addition, manipulation of the extracellular and intracellular Na+ concentrations further demonstrated the modulatory role of NCX in SOCE-mediated SR Ca2+ loading. Although there is little knowledge of SOCE in cardiomyocytes, the present results suggest that this mechanism, together with NCX, may play an important role in SR Ca2+ homeostasis. The data reported herein also imply the presence of microdomains unique to the neonatal cardiomyocyte. These findings may be of particular importance during open heart surgery in neonates, in which uncontrolled SOCE could lead to SR Ca2+ overload and arrhythmogenesis.

scholarly journals Extracorporeal Hemadsorption versus Glucocorticoids during Cardiopulmonary Bypass: A Prospective, Randomized, Controlled Trial

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Gordana Taleska Stupica ◽  
Maja Sostaric ◽  
Marija Bozhinovska ◽  
Lea Rupert ◽  
Zoran Bosnic ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Clinical Outcome ◽  
Usual Care ◽  
Heart Surgery ◽  
Inflammatory Responses ◽  
Open Heart Surgery ◽  
Control Group ◽  
Outcome Parameters ◽  
Cd163 Expression ◽  
And Control

Extracorporeal hemadsorption may reduce inflammatory reaction in cardiopulmonary bypass (CPB) surgery. Glucocorticoids have been used during open-heart surgery for alleviation of systemic inflammation after CPB. We compared intraoperative hemadsorption and methylprednisolone, with usual care, during complex cardiac surgery on CPB, for inflammatory responses, hemodynamics, and perioperative course. Seventy-six patients with prolonged CPB were recruited and randomized, with 60 included in final analysis. Allocation was into three groups: Methylprednisolone (n = 20), Cytosorb (n = 20), and Control group (usual care, n = 20). Proinflammatory (TNF-α, IL-1β, IL-6, and IL-8) and anti-inflammatory (IL-10) cytokines which complement C5a, CD64, and CD163 expression by immune cells were analyzed within the first five postoperative days, in addition to hemodynamic and clinical outcome parameters. Methylprednisolone group, compared to Cytosorb and Control had significantly lower levels of TNF-α (until the end of surgery, p<0.001), IL-6 (until 48 h after surgery, p<0.001), and IL-8 (until 24 h after surgery, p<0.016). CD64 expression on monocytes was the highest in the Cytosorb group and lasted until the 5th postoperative day (p<0.016). IL-10 concentration (until the end of surgery) and CD163 expression on monocytes (until 48 h after surgery) were the highest in the Methylprednisolone group (p<0.016, for all measurements between three groups). No differences between groups in the cardiac index or clinical outcome parameters were found. Methylprednisolone more effectively ameliorates inflammatory responses after CPB surgery compared to hemadsorption and usual care. Hemadsorption compared with usual care causes higher prolonged expression of CD64 on monocytes but short lasting expression of CD163 on granulocytes. Hemadsorption with CytoSorb® was safe and well tolerated. This trial is registered with clinicaltrials.gov (NCT02666703).

scholarly journals Caffeine and micromolar Ca2+ concentrations can release Ca2+ from ryanodine-sensitive stores in crab and lobster striated muscle fibres

1996 ◽  
Vol 199 (11) ◽  
pp. 2419-2428 ◽  
Author(s):  
T Lea
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Striated Muscle ◽  
Abdominal Muscle ◽  
Isometric Tension ◽  
Muscle Fibres ◽  
Phasic Contraction ◽  
Crustacean Muscle ◽  
Time Integral ◽  
Variable Nature

Ca2+ release mechanisms were studied in striated muscle from the walking legs of crabs using isometric tension recordings from isolated myofibrillar bundles. Caffeine-induced phasic contractions had properties consistent with Ca2+ release from a sarcoplasmic store, which could be optimally loaded in the presence of ATP at pCa 6.4&shy;6.1. Ryanodine (10 &micro;mol l-1) abolished the caffeine-induced contractions and in solutions with low Ca2+ buffering (0.1 mmol l-1 EGTA) itself caused phasic contractions, indicative of Ca2+ release. Ca2+-induced Ca2+ release (CICR) was observed in a pCa 5.8 solution (buffered by 1 mmol l-1 EGTA) as a phasic contraction of variable nature, inhibited by ryanodine (10 &micro;mol l-1), procaine (10 mmol l-1) or benzocaine (5 mmol l-1). Ca2+ release was measured as a function of releasing pCa by using the force&shy;time integral of the caffeine-induced contraction as an estimate of the Ca2+ remaining in the store. After the Ca2+ store had been loaded for 2 min at pCa 6.6, CICR was measured in the presence of 1 mmol l-1 Mg2+, 1 mmol l-1 EGTA and 5 mmol l-1 ATP. The threshold pCa for CICR was 6.0&shy;6.4 under these conditions and more than 90 % of stored Ca2+ was released in 1 min by pCa values in the range 3.5&shy;5.3. Benzocaine totally inhibited the release and promoted extra Ca2+ loading. Preliminary experiments showed a similar caffeine-releasable store in lobster abdominal muscle, which was slightly less sensitive to free [Ca2+]. It is concluded that in crustacean muscle caffeine and micromolar [Ca2+] can release Ca2+ from a ryanodine-sensitive store, which in many respects is similar to the sarcoplasmic reticulum of vertebrate skeletal and cardiac muscle.

Anchorfibers and the Topography of Junctional SR

1977 ◽  
Vol 35 ◽  
pp. 582-583
Author(s):  
James Junker ◽  
Joachim R. Sommer
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Single Filament ◽  
Relaxation Cycle ◽  
10 Nm Filaments ◽  
Junctional Sarcoplasmic Reticulum

Junctional sarcoplasmic reticulum (JSR) in all its forms (extended JSR, JSR of couplings, corbular SR) in both skeletal and cardiac muscle is always located at the Z - I regions of the sarcomeres. The Z tubule is a tubule of the free SR (non-specialized SR) which is consistently located at the Z lines in cardiac muscle (1). Short connections between JSR and Z lines have been described (2), and bundles of filaments at Z lines have been seen in skeletal (3) and cardiac (4) muscle. In opossum cardiac muscle, we have seen bundles of 10 nm filaments stretching across interfibrillary spaces and adjacent myofibrils with extensions to the plasma- lemma in longitudinal (Fig. 1) and transverse (Fig. 2) sections. Only an occasional single filament is seen elsewhere along a sarcomere. We propose that these filaments represent anchor fibers that maintain the observed invariant topography of the free SR and JSR throughout the contraction-relaxation cycle.

Enhanced Effective Fibrinolysis following the Neutralization of Heparin in Open Heart Surgery Increases the Risk of Post-Surgical Bleeding

1990 ◽  
Vol 63 (02) ◽  
pp. 241-245 ◽  
Author(s):  
Jørgen Gram ◽  
Thomas Janetzko ◽  
Jørgen Jespersen ◽  
Hans Dietrich Bruhn
Keyword(s):  
Blood Loss ◽  
Plasminogen Activator ◽  
Heart Surgery ◽  
Degradation Products ◽  
Open Heart Surgery ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Chest Tube Drain ◽  
Median Blood Loss

SummaryThe tissue-type plasminogen activator related fibrinolytic system was studied in 24 patients undergoing cardiopulmonary bypass surgery. The degradation of fibrinogen and fibrin was followed during and after surgery by means of new sensitive and specific assays and the changes were related to the blood loss measured in the chest tube drain during the first 24 postoperative hours. Although tissue-type plasminogen activator was significantly released into the circulation during the period of extracor-poreal circulation (p <0.01), constantly low levels of fibrinogen degradation products indicated that a systemic generation of plasmin could be controlled by the naturally occurring inhibitors. Following extracorporeal circulation heparin was neutralized by protamine chloride, and in relation to the subsequent generation of fibrin, there was a short period with increased concentrations of fibrinogen degradation products (p <0.01) and a prolonged period of degradation of cross-linked fibrin, as detected by increased concentrations of D-Dimer until 24 h after surgery (p <0.01). Patients with a higher than the median blood loss (520 ml) in the chest tube drain had a significantly higher increase of D-Dimer than patients with a lower than the median blood loss (p <0.05).We conclude that the incorporation of tissue-type plasminogen activator into fibrin and the in situ activation of plasminogen enhance local fibrinolysis, thereby increasing the risk of bleeding in patients undergoing open heart surgery

The Hemostatic Mechanism after Open-Heart Surgery

1978 ◽  
Vol 39 (02) ◽  
pp. 474-487 ◽  
Author(s):  
E R Cole ◽  
F Bachmann ◽  
C A Curry ◽  
D Roby
Keyword(s):  
Extracorporeal Circulation ◽  
Heart Surgery ◽  
Polyacrylamide Gel Electrophoresis ◽  
Open Heart Surgery ◽  
Coagulation System ◽  
Open Heart ◽  
Time Activity ◽  
Post Surgery ◽  
Plasma Fractions ◽  
The Mean

SummaryA prospective study in 13 patients undergoing open-heart surgery with extracorporeal circulation revealed a marked decrease of the mean one-stage prothrombin time activity from 88% to 54% (p <0.005) but lesser decreases of factors I, II, V, VII and X. This apparent discrepancy was due to the appearance of an inhibitor of the extrinsic coagulation system, termed PEC (Protein after Extracorporeal Circulation). The mean plasma PEC level rose from 0.05 U/ml pre-surgery to 0.65 U/ml post-surgery (p <0.0005), and was accompanied by the appearance of additional proteins as evidenced by disc polyacrylamide gel electrophoresis of plasma fractions (p <0.0005). The observed increases of PEC, appearance of abnormal protein bands and concomitant increases of LDH and SGOT suggest that the release of an inhibitor of the coagulation system (similar or identical to PIVKA) may be due to hypoxic liver damage during extracorporeal circulation.

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