https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16571 Wed 11 Apr 2018 13:35:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:8251 Sat 24 Mar 2018 08:40:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13287 Sat 24 Mar 2018 08:16:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16909 A antagonist bicuculline methiodide (BMI; 40 pmol/100 nl) into the DMH-evoked increases in heart rate (HR), left ventricular pressure (LVP), myocardial contractility (LVdP/dt), arterial pressure, and respiratory rate. DMH disinhibition also precipitated multiple ventricular and supraventricular ectopic beats. DMH-induced increases in HR, LVP, LVdP/dt, and in the number of ectopic beats dependent on the side of stimulation, with R-DMH provoking larger responses. In contrast, pressor and respiratory responses did not depend on the side of stimulation. Newly described DMH-induced inotropic responses were rate-, preload- and (largely) afterload-independent; they were mediated by sympathetic cardiac pathway, as revealed by their sensitivity to β-adrenergic blockade. We conclude that recruitment of DMH neurons causes sympathetically mediated positive chronotropic and inotropic effects, and that there is an asymmetry, at the level of the DMH, in the potency to elicit these effects, with R-DMH > L-DMH.]]> Sat 24 Mar 2018 07:59:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48450 Fri 17 Mar 2023 09:25:55 AEDT ]]>