ABSTRACT
The traditional medical experiment based on animal studies fails to reflect competency-oriented goal, and is not closely combined with clinical and scientific research, which does not meet the need for early clinical and scientific training. In order to cultivate the first-class medical talents, medical experimental teaching should conform to the trend of modern medical education, innovate teaching ideas and models, and update the hardware and software in time. Therefore, our teaching center adopts the triad medical experimental system which consists of "animal experiments, human functional experiments, and electronic standardized patient (ESP)-based virtual simulation experiments", and uses one system to integrate basic and clinical medicine, practice and virtual learning, teaching and scientific training. The system retains the core content of traditional animal experiments, and includes the most mature and widely used human physiological experiments to increase students' learning experience. With medical simulation experiment, it explains the specific physiological and pathophysiological processes of human body to improve students' cognitive and thinking ability. Here, we provide a systematic description on our triad medical experimental system, and discuss the experience to establish this novel system.
Subject(s)
Animals , Humans , Learning , StudentsABSTRACT
Chemical stimulation of the kidney increases sympathetic activity and blood pressure in rats. The hypothalamic paraventricular nucleus (PVN) is important in mediating the excitatory renal reflex (ERR). In this study, we examined the role of molecular signaling in the PVN in mediating the capsaicin-induced ERR and sympathetic activation. Bilateral PVN microinjections were performed in rats under anesthesia. The ERR was elicited by infusion of capsaicin into the cortico-medullary border of the right kidney. The reflex was evaluated as the capsaicin-induced changes in left renal sympathetic nerve activity and mean arterial pressure. Blockade of angiotensin type 1 receptors with losartan or inhibition of angiotensin-converting enzyme with captopril in the PVN abolished the capsaicin-induced ERR. Renal infusion of capsaicin significantly increased NAD(P)H oxidase activity and superoxide anion production in the PVN, which were prevented by ipsilateral renal denervation or microinjection of losartan into the PVN. Furthermore, either scavenging of superoxide anions or inhibition of NAD(P)H oxidase in the PVN abolished the capsaicin-induced ERR. We conclude that the ERR induced by renal infusion of capsaicin is mediated by angiotensin type 1 receptor-related NAD(P)H oxidase activation and superoxide anion production within the PVN.
ABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of dopamine receptor (DR2) activation on hypoxia/reperfusion injury (HRI) in the neonatal rat cardiomyocytes, and to explore its mechanism.</p><p><b>METHODS</b>The hypoxia/reperfusion (H/R) injury model was established in primarily cultured neonatal rat cardiomyocytes, and randomly assigned: control, H/R, bromocriptine (Bro) and haloperidol (Hal) groups. The cell apoptosis was detected using inverted microscope, transmission electron microscope and flow cytometry (FCM). The lactate dehydrogenase(LDH) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in cell medium were analyzed. The expression of mRNA and protein of caspase-3, caspase-8, caspase-9, Fas, Fas-L, Cyt C and Bcl-2 were detected by RT-PCR and Western blot, respectively.</p><p><b>RESULTS</b>Compared with the control group, apoptosis rate, LDH activity, MDA content and the expression of pro-apoptotic factors and anti-apoptotic factors were increased, but SOD activity was decreased in H/R group. Compared with the H/R group, all index above-mentioned were down-regulated or reversed in Bro-group, and had no obvious differences in Hal-group.</p><p><b>CONCLUSION</b>The neonatal rat cardiomyocytes injury and apoptosis caused by hypoxia/reperfusion can be inhibited with DR2 activation, which mechanism is related to scavenging oxygen radical.</p>