[17,1825,30,31] Since CCBs in OD produce a hypoinsulinaemic state, glucose uptake into the cardiomyocytes cannot occur, impairing
cardiac contractility. Exogenous high-dose insulin and supplemental glucose therefore enable uptake of glucose and therefore improve myocardial contractility.
Targeted overexpression of the sarcoplasmic reticulum Ca2+-ATPase increases
cardiac contractility in transgenic mouse hearts.
We qualitatively assess
cardiac contractility and may find incidental pericardial effusions not detected by auscultation or physical examination.
Moreover, the reduction of proteotoxic stress by improving autophagic function has been proved to have positive impact on
cardiac contractility [31].
All these derangements further impair
cardiac contractility. In addition, inflammatory cytokines directly reduce contractility by interfering with SERCA2a [88].
[beta]-Arrestin signaling downstream of GLP1 receptor activation is another potential mechanism to increase
cardiac contractility. [beta]-arrestin, which is well-known for contributing to the termination of GPCR signaling [77], might regulate cardiac function and increase
cardiac contractility via [beta]-arrestin-mediated processes [78-80].
Interventions are required to decrease both preload and afterload as well as to improve
cardiac contractility and prevent precipitation of seizures preoperatively and postoperatively.
This finding suggested that patients with better
cardiac contractility before treatment could be better benefited from [sz]-receptor blockade, and patients in the early stage of septic shock who still had good
cardiac contractility could also be better benefited from [sz]-receptor blockade.
Hypothyroidism is recognised to cause many effects on the cardiovascular system, such as impaired
cardiac contractility, decreased cardiac output, increased systemic vascular resistance, and cardiac atrophy.18-20 This study on Saudi women with HF shows the prevalence of hypothyroidism in this cohort One-third patients had hypothyroidism of different severity.
In well-grown fetuses, the MCA PSV increase is related to the haemoglobin but not the partial pressure of oxygen (p[O.sub.2]), suggesting that this reflects decreased blood viscosity and increased venous return rather than an active fetal compensatory mechanism by p[O.sub.2]-related chemoreceptor stimulation (to increase
cardiac contractility and cause vasodilatation).
Excessive thyroid hormone production increased utilization of oxygen, increased blood flow, increased
cardiac contractility, and increased cardiac output and heart rate.