The term myocardial contractility is thought to have originated more than 125 years ago and has remained and enigma ever since. Although the term is frequently used in textbooks, editorials and contemporary manuscripts its definition remains illusive often being conflated with cardiac performance or inotropy. The absence of a universally accepted definition has led to confusion, disagreement and misconceptions among physiologists, cardiologists and safety pharmacologists regarding its definition particularly in light of new discoveries regarding the load dependent kinetics of cardiac contraction and their translation to cardiac force-velocity and ventricular pressure-volume measurements. Importantly, the Starling interpretation of force development is length-dependent while contractility is length independent. Most historical definitions employ an operational approach and define cardiac contractility in terms of the hearts mechanical properties independent of loading conditions. Literally defined the term contract infers that something has become smaller, shrunk or shortened. The addition of the suffix “ility” implies the quality of this process. The discovery and clinical investigation of small molecules that bind to sarcomeric proteins independently altering force or velocity requires that a modern definition of the term myocardial contractility be developed if the term is to persist. This review reconsiders the historical and contemporary interpretations of the terms cardiac performance and inotropy and recommends a modern definition of myocardial contractility as the preload, afterload and length-independent intrinsic kinetically controlled, chemo-mechanical processes responsible for the development of force and velocity.

Intravenous fluid therapy can alter plasma acid-base balance. The Stewart approach to acid-base balance is uniquely suited to identify and quantify the effects of the cationic and anionic constituents of crystalloid solutions on plasma pH. The plasma strong ion difference (SID) and weak acid concentrations are similar to those of the administered fluid, more so at higher administration rates and with larger volumes. A crystalloid's in vivo effects on plasma pH are described by 3 general rules: SID > [ {\text{HCO}}_3^{?} ] increases plasma pH (alkalosis); SID < [ {\text{HCO}}_3^{?} ] decreases plasma pH (alkalosis); and SID = [ {\text{HCO}}_3^{?} ] yields no change in plasma pH. The in vitro pH of commercially prepared crystalloid solutions has little to no effect on plasma pH because of their low titratable acidity. Appreciation of IV fluid composition and an understanding of basic physicochemical principles provide therapeutically valuable insights about how and why fluid therapy can produce and correct alterations of plasma acid-base equilibrium. The ideal balanced crystalloid should (1) contain species-specific concentrations of key electrolytes (Na⁺, Cl⁻, K⁺, Ca⁺⁺, Mg⁺⁺), particularly Na⁺ and Cl⁻; (2) maintain or normalize acid-base balance (provide an appropriate SID); and (3) be isosmotic and isotonic (not induce inappropriate fluid shifts) with normal plasma.

Objective To evaluate the quality of the veterinary literature investigating IV fluid therapy in dogs, cats, horses and cattle. Design Systematic review Procedures The preferred reporting of items for systematic review and Meta-Analysis protocols (PRISMA-P) was employed for systematic review of all relevant IV fluid therapy manuscripts published from January1969 through December 2016 in the commonwealth agricultural bureau international (CABI) database. Independent grading systems used to evaluate manuscripts included the updated CONsolidated Standards of Reporting Trials (CONSORT) 2012 checklist, risk of bias (RoB) for animal intervention studies, criteria for levels of evidence, and methodological quality (Jadad scale). The quality of articles published before and after 2010 was compared. Results One hundred and thirty nine articles (63 dog, 7 cat, 39 horse, 30 cattle) from 7258 met the inclusion criteria. More than 50% of the manuscripts did not comply with minimal requirements for reporting randomized controlled trials. The most noncompliant items included identification of specific predefined objectives or a hypothesis, identification of trial design, how sample size was determined, randomization and blinding procedures. Most studies were underpowered and at risk for selection, performance, and detection bias. The overall quality of the articles improved for articles published after 2010. Conclusion and Clinical Relevance Most of the veterinary literature investigating the administration of IV fluid therapy in dogs, cats, horses and cattle is descriptive, does not comply with standards for evidence or provide adequate translation to clinical practice. Authors should employ and journal editors should enforce international consensus recommendations and guidelines for publication of data from animal experiments investigating IV fluid therapy.

Potentially damaging “heart stress” is reversed using reactive nerve stimulation controlled by artificial intelligence.

Summary: Effects of low-flow ischemia and reperfusion of the large colon on mucosal architecture were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline values. Systemic hemodynamic and metabolic variables were maintained constant and in a normal physiologic range. Full-thickness biopsy specimens were obtained from the left ventral colon for histomorphologic and morphometric examination at baseline and at 30-minute intervals for 6 hours; additional biopsy specimens were collected at 185, 190, and 195 minutes (corresponding to 5-, 10-, and 15-minute periods of reperfusion in group-3 horses). There were no differences among groups at baseline or across time in group-1 horses for any of the histopathologic variables. There were significant (P < 0.05) increases in percentage of surface mucosal disruption, estimated and measured percentage depth of mucosal loss, mucosal hemorrhage, mucosal edema, and cellular debris index during 0 hour to 3 hours, compared with baseline, and from 3 hours to 6 hours, compared with 3 hours in horses of groups 2 and 3. Estimated percentage depth of mucosal loss and cellular debris index were significantly (P < 0.05) greater in group-3 horses, compared with group-2 horses during the interval from 3 to 6 hours. There were trends toward greater percentage of surface mucosal disruption and mucosal edema during the early phase of reperfusion (3 to 4 hours) and greater mucosal hemorrhage, measured percentage depth of mucosal loss, and mucosal interstitial-to-crypt ratio during the late phase (4 to 6 hours) of reperfusion in group-3 horses vs group-2 horses. Reestablishment of colonic arterial blood flow after low-flow ischemia caused greater mucosal injury than did a comparable period of continued ischemia. Thus, reperfusion injury was detected in the large colon of horses after low-flow arterial ischemia. The serial mucosal alterations that developed in the colon were comparable in horses of groups 2 and 3; however, reperfusion exacerbated colonic mucosal injury.