Samsum ant venom modulates the immune response and redox status at the acute toxic dose in vivo

Background:Ant venoms express surface molecules that participate in antigen presentation involving pro- and anti-inflammatory cytokines. This work aims to investigate the expression of MHC-II, CD80 and CD86 on the polymorphonuclear cells (PMNs) in rats injected with samsum ant venom (SAV).Methods:Rats were divided into three groups - control, SAV-treated (intraperitoneal route, 600 μg/kg), and SAV-treated (subcutaneous route, 600 μg/kg). After five doses, animals were euthanized and samples collected for analysis.Results:The subcutaneous SAV-trated rats presented decreased levels of glutathione with increased cholesterol and triglyceride levels. Intraperitoneal SAV-treated animals displayed significantly reduced concentrations of both IFN-γ and IL-17 in comparison with the control group. However, intraperitoneal and subcutaneous SAV-treated rats were able to upregulate the expressions of MHC-II, CD80 and CD86 on PMNs in comparison with the control respectively. The histological examination showed severe lymphocyte depletion in the splenic white pulp of the intraperitoneal SAV-injected rats.Conclusion:Stimulation of PMNs by SAV leads to upregulation of MHC-II, CD 80, and CD 86, which plays critical roles in antigen presentation and consequently proliferation of T-cells. Subcutaneous route was more efficient than intraperitoneal by elevating MHC-II, CD80 and CD86 expression, disturbing oxidative stability and increasing lipogram concentration.

Evaluating the effect of midodrine on renal resistance index in patients with liver cirrhosis and ascites

Background: Portal hypertension, which occurs as a consequence of liver cirrhosis, leads to splenic vasodilatation and alterations in the systemic circulation. Arterial vasodilatation in the splanchnic circulation appears to play a central role in hemodynamic changes and in the decline in renalfunction in cirrhosis. Peripheral vasodilatation, which occurs as a part of alterations in the systemic circulation, may decrease the renal blood flow and subsequently raise plasma renin activity. Midodrine is a agonist and acts as a peripheral vasoconstrictor; therefore, it may reduce plasma renin activity and improve renal function

Aim of the work: The aim of the study was to evaluate the relationship between renal resistive indices [RIs]in cirrhotic patients before and after oral administration of 7.5 mg midodrine three times dailyfor 3 days

Patients and methods:The study was conducted on 40 patients with liver cirrhosis and ascites and on 40 healthy controls from October 2014 to March 2015 at Al Azhar University Hospital, Assiut, where allpatients were subjected to history and clinical examination as well as to routine investigations such as total bilirubin, albumin, international normalized ratio, and serum creatinine. Patients underwent an abdominal ultrasound with duplex Doppler examination of the kidneys, and RIwas calculated before and 3 days after oral intake of midodrine

Results: Patients with liver cirrhosis and ascites had significantly higher RI in the right kidney[0.69 +/- 0.101 vs. 0.57 +/- 0.055, P < 0.001] and in the left kidney [0.69 +/- 0.097 vs. 0.59 +/- 0.047,P < 0.001] compared with healthy controls. After oral administration of midodrine for 3 days,RI showed significant improvement [RI = 0.928, P < 0.001] in the right kidney and in theleft kidney [R = 0.993, P < 0.001]. RI had significant positive correlation with Child-Pughscore [R = 0.75, P < 0.001, in the right kidney and R = 0.75, P < 0.001, in the left kidney] and significant positive correlation with Model for End Stage Liver Disease score [R = 0.536,P < 0.008, in the right kidney and R = 0.487, P < 0.005, in the left kidney]

Conclusion: Oral midodrine improved renal hemodynamics as assessed by RI in cirrhotic patients. RI is correlated with severity of liver disease as assessed by Child-Pugh and Model for End StageLiver Disease scores