Medical Education Journal Club: Two years' experience at King Saud University

Objective: Medical Education Journal Club is an evidence-based approach to teach and learn critical appraisal techniques on available literature. This study evaluates the implementation and experience of two academic years of Journal club at Medical Education Department, King Saud University

Methods: We started JC in 2015 at medical education department, KSU. An invitation with a published paper and event poster were sent 2 weeks prior of the session to participants. A traditional one-group posttest design with open item survey were conducted at the end of every session

Results: A total of 12 sessions were conducted in total. The average attendance of 26 [Male: 42/79, 53.1%] and [Female: 31/79, 39.2%] with mix of professors, associate and assistant professors. The MEJC had a positive effect on participant's session expectations [45/79, 92.4%], and had increased their knowledge of the field [73/79, 92.4%]. It was observed that the attendance of event depends on the speaker for the event. The sessions have also arisen the need of trainings and other scientific activities

Conclusions: MEJC is an educational activity that can play important aspect in providing high quality healthcare teachings. We conclude that the success and consistency of MEJC depends on speaker. It commensurate the audience interest to attend and learn. While proper advertisement of event, and regular attendance also plays a vital role in this regard

Preservation of myocardial contractile function by aminoguanidine, a nitric oxide synthase inhibitors, in a rat model of hemorrhagic shock

Myocardial contractile dysfunction plays a major role in the outcome of trauma patients. Nitric oxide [NO] has been shown to increase following haemorrhagic shock. Peroxynitrite which is produced by the reaction of NO with reactive oxygen species leads to nitrosative stress mediated organ injury and myocardial contractile dysfunction. Aminoguanidine is a selective inhibitor of inducible nitric oxide synthase [iNOS]. The aim of this study was to determine the protective effects of inhibiting the production of NO using aminoguanidine [AG] on myocardial contractility, following hemorrhagic shock and resuscitation in rats. Male Sprague-Dawley rats were assigned to 3 experimental groups [n = 6 per group]:1] Normotensive rats [N], 2] Hemorrhagic shock rats [HS], and 3] Hemorrhagic shock rats treated with AG 60 mg/kg AG intra-arterially [HS-AG]. Rats were hemorrhaged over 60 minutes to reach a mean arterial blood pressure of 40 mmHg. Rats were treated with 1 ml of 60 mg/Kg AG intra-arterially after 60 minutes haemorrhagic shock,. Resuscitation was performed in vivo by the reinfusion of the shed blood for 30 minutes to restore normo-tension. Hearts were harvested and ex vivo perfused in the Langendorff System and myocardial function was determined by measuring the left ventricular end diastolic pressure [LVEDP] and left ventricular systolic pressure [LVSP]. Left ventricular generated pressure [LVGP] and + dP/dt max was calculated. Hemorrhagic shock rats treated with AG exhibited a significant increase in left ventricular generated pressure LVGP [137.1 +/- 9.4 mmHg] and + dP/dtmax [589.6 +/- 110.7 mmHg/sec] compared with the untreated group [44.43 +/- 20.18 mmHg, 289.8 +/- 25.0 mmHg/sec]. Treatment with AG protects the myocardium from post-resuscitation myocardial dysfunction