This study aimed to observe the effects of prilocaine chloridate (P) and the associations of P with felypressin (P+F), and epinephrine (P+E) on the heart rate and force of contraction on the isolated hearts of rats. The hearts were perfused according to Langendorff's method. The experiments were performed with the following substances: prilocaine (P), felypressin (F), and epinephrine (E). P was used in doses of 1.25, 2.5, and 5.0 mg. The same doses of F and P (1.0, 1.5 and 3.0 microg) were used in association with the P, respectively. Right after the application of the three doses of P, a reduction in the force of contraction was observed, with higher intensity at a higher dose, which led to cardiac arrest. A similar result was obtained with the administration of the three associations of P+F. Also the application of the three associations P+E resulted in a reduction of the force of contraction, that was, however, less intense with the associations of 1.25 mg P + 1.0 microg E and 2.5 mg P+1.5 microg E, as compared to the same doses of P alone and P+F. The two higher doses of P and P+F on the heart rate elicited a significant reduction in relation to the control, but with the associations of P+E no alterations were observed, with any one of the doses used. The results obtained in the present study suggest that an association of P and E must be used in local anesthesia, since epinephrine may well protect the heart from the depressive effects of the anesthetic salts.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/s1043-6618(03)00180-4 | DOI Listing |
J Mol Cell Cardiol
March 2025
Voiland School of Chemical and Bioengineering, Washington State University, Pullman, WA 99163-1062, USA; Department of Integrative Physiology and Neuroscience, Washington State University, Pullman, WA 99163-1062, USA. Electronic address:
Sarcomere length-dependent activation (LDA) is essential to engaging the Frank-Starling mechanism in the beat-to-beat regulation of cardiac output. Through LDA, the heart increases the Ca sensitivity of myocardial contraction at a longer sarcomere length, leading to an enhanced maximal force at the same level of Ca. Despite its importance in both normal and pathological states, the molecular mechanism underlying LDA, especially the origin of the sarcomere length (SL) induced increase in myofilament Casensitivity, remains elusive.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
March 2025
Randall Centre for Cell and Molecular Biophysics and British Heart Foundation Centre of Research Excellence, New Hunt's House, Guy's Campus, King's College London, London SE1 1UL, United Kingdom.
Muscle contraction is driven by myosin motors from the thick filaments pulling on the actin-containing thin filaments of the sarcomere, and it is regulated by structural changes in both filaments. Thin filaments are activated by an increase in intracellular calcium concentration [Ca] and by myosin binding to actin. Thick filaments are activated by direct sensing of the filament load.
View Article and Find Full Text PDFPLoS One
March 2025
Center for Rehabilitation Research, Texas Tech University Health Sciences Center, Lubbock, Texas, United States of America.
This study investigated the effects of mental fatigue on rate of force development (RFD) and peak force during an isometric mid-thigh pull (IMTP), as well as its impact on muscle activation measured by electromyography (EMG) median frequency. Sixteen healthy, resistance-trained males completed two sessions: a control condition and a mentally fatigued state induced by a 30-minute modified Stroop task. IMTP performance and muscle activation were assessed before and after the mental fatigue task.
View Article and Find Full Text PDFWearable Technol
February 2025
Neuromuscular Robotics Laboratory, Department of Biomechanical Engineering, University of Twente, Enschede, the Netherlands.
Research in lower limb wearable robotic control has largely focused on reducing the metabolic cost of walking or compensating for a portion of the biological joint torque, for example, by applying support proportional to estimated biological joint torques. However, due to different musculotendon unit (MTU) contractile speed properties, less attention has been given to the development of wearable robotic controllers that can steer MTU dynamics directly. Therefore, closed-loop control of MTU dynamics needs to be robust across fiber phenotypes, that is ranging from slow type I to fast type IIx in humans.
View Article and Find Full Text PDFJ Mol Cell Cardiol
March 2025
Voiland School of Chemical Engineering and Bioengineering, Washington State University, Pullman, WA 99163-1062, USA; Department of Integrative Physiology and Neuroscience, Washington State University, Pullman, WA 99163-1062, USA. Electronic address:
Sarcomere length-dependent activation (LDA) is the key cellular mechanism underlying the Frank-Starling law of the heart, in which sarcomere stretch leads to increased Ca sensitivity of myofilament and force of contraction. Despite its key role in both normal and pathological states, the precise mechanisms underlying LDA remain unclear but are thought to involve multiple interactions among sarcomere proteins, including troponin of the thin filament, myosin, titin and myosin binding protein C (MyBP-C). Our previous study with permeabilized rat cardiac fibers demonstrated that the mechanism underlying the increase in Ca sensitivity of thin filament induced by sarcomere stretch may involve sarcomere length (SL)-induced interactions between troponin and weakly bound, disordered relaxed state (DRX) myosin heads in diastole, rather than strong myosin-actin crossbridge interactions.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!