https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12744 Thu 03 Sep 2020 09:11:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:2925 Sat 24 Mar 2018 08:32:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:2832 Sat 24 Mar 2018 08:29:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:2825 Sat 24 Mar 2018 08:28:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:1436 Sat 24 Mar 2018 08:28:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12710 A) was maintained sequentially at 22°C, 12°C, 22°C and 35°C, with an accuracy of ±1°C. Neither thalamic nor pontine rabbits could maintain core temperature in cold or heat. At T 35°C, thalamic and pontine animals did not pant, indicating that telencephalic responses were necessary for the integration of mechanisms promoting respiratory heat loss. Thalamic animals, however, could inhibit ear vascular sympathetic tone in the heat, but the response was absent in pontine animals, suggesting diencephalic responses were essential for the integration of mechanisms promoting ear skin heat loss. Thus, the neural adjustments to thermal stress depend on mechanisms of integration distributed longitudinally throughout the central nervous sytem, and different components of the reflex cardiorespiratory response depend on different sites in the central nervous system for their full expression.]]> Sat 24 Mar 2018 08:16:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12113 Sat 24 Mar 2018 08:12:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12191 Sat 24 Mar 2018 08:08:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12201 Sat 24 Mar 2018 08:08:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33273 2+ release, leading to sarcoplasmic reticulum Ca²⁺ depletion, reduced cardiac function, and providing cell protection against ischemia-reperfusion injury. Anesthetic activation of ryanodine receptor 2 is poorly defined, leaving aspects of the protective mechanism uncertain. Methods: Ryanodine receptor 2 from the sheep heart was incorporated into artificial lipid bilayers, and their gating properties were measured in response to five halogenated anesthetics. Results: Each anesthetic rapidly and reversibly activated ryanodine receptor 2, but only from the cytoplasmic side. Relative activation levels were as follows: halothane (approximately 4-fold; n = 8), desflurane and enflurane (approximately 3-fold,n = 9), and isoflurane and sevoflurane (approximately 1.5-fold, n = 7, 10). Half-activating concentrations (Kₐ) were in the range 1.3 to 2.1 mM (1.4 to 2.6 minimum alveolar concentration [MAC]) with the exception of isoflurane (5.3 mM, 6.6 minimum alveolar concentration). Dantrolene (10 µM with 100 nM calmodulin) inhibited ryanodine receptor 2 by 40% but did not alter the Kₐ for halothane activation. Halothane potentiated luminal and cytoplasmic Ca²⁺ activation of ryanodine receptor 2 but had no effect on Mg²⁺ inhibition. Halothane activated ryanodine receptor 2 in the absence and presence (2 mM) of adenosine triphosphate (ATP). Adenosine, a competitive antagonist to ATP activation of ryanodine receptor 2, did not antagonize halothane activation in the absence of ATP. Conclusions: At clinical concentrations (1 MAC), halothane desflurane and enflurane activated ryanodine receptor 2, whereas isoflurane and sevoflurane were ineffective. Dantrolene inhibition of ryanodine receptor 2 substantially negated the activating effects of anesthetics. Halothane acted independently of the adenine nucleotide-binding site on ryanodine receptor 2. The previously observed adenosine antagonism of halothane activation of sarcoplasmic reticulum Ca²⁺ release was due to competition between adenosine and ATP, rather than between halothane and ATP.]]> Mon 24 Sep 2018 13:26:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12206 10%. Distortion of pulsed Doppler signal peaks occurred in the conscious rabbit at peak aortic velocities, at which Reynold's number for turbulence was exceeded and the Doppler shift surpassed the Nyquist limit of 31.25 kHz for the velocimeter. Although the Doppler shift-volume flow relationship is linear at < 5 kHz, in some cases at higher Doppler shifts and blood flow velocities the relationship may become nonlinear, thus causing the volume flow rate to be underestimated by up to 38%. The cause of this phenomenon may be "aliasing" and/or the consequence of the range control capability of the velocimeter selectively sampling changing velocity profiles and flow disturbances in the central stream at higher velocities.]]> Fri 27 Sep 2019 16:32:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12664 τ) has been calculated in dogs from the rearranged Kubicek formula: p_τ = (SV · Z₀²)/(L² dZ/dt_max·T), where SV was measured by the electromagnetic flowmeter (EM). Hematocrit (Hct) in the dog was varied by hemorrhage and infusion. In contrast to the direct and exponential bench p-Hct relationship, p_τ varies inversely with Hct, but by no more than +6.3 Ω · cm (at Hct 26%) and -11.8 Ω · cm (at Hct 66%) about a mean p_τ of 135 ± 1.0 Ω · cm (at Hct 40%). Impedance SV calculated using p_τ over a wide range of SV bears a linear relationship to EM values with a 95% prediction limit for a single SV estimate of ±0.84 about a mean value of 26.9 ml. The findings suggest that p_τ is virtually constant during a variety of physiological disturbances.]]> Fri 27 Sep 2019 16:12:28 AEST ]]>