Outpatient treatment of non-complicated deep venous thrombosis:is it still questionable?

At our medical community, we persist on treating all cases of acute deep venous throm boris in the hospital for fear of pulmonary embolism [PE] antobe-able to give unfractionated hearin [UFH] infusion, misguided by the apparent high cost of the low molecular weight heparin [LMWH]. The purpose of this study was to prove that out patient treatment [OPT] is not only safe and effective, but also more reasonable and economic in treating non complicated DVT. Out patient treatment [OPT] was given for patients with proven non-complicated DVT in the period between January 2004 and January 2005. Data regarding complications, vein clearance and recurrence were collected at: one week, 4 weeks, 3 and 6 months. The cost of this regimen was compared to the cost of receiving UFH infusion at a general and private hospitals. Patient compliance was also assessed. Fifty-three patients received OPT for DVT between January 2004 and 2005. Only one patient [1.8%] had minor PE. Two patients [3.7%] had remnant of the clot at the end of follow up period. Three patients [5.6%] had deep venous reflux and no one had recurrence during the follow up period. This type of treatment costs the same price when compared to the in-patient treatment using the UFH at a general hospital and less than half the price for treatment at a private one. All patients were compliant to the injections and 37 of them [70%] were compliant to the elastic stockings [ES] This study confirmed that OPT of non-ocomplioance is high and the treatment is presumably satisfying. Admitting patients with non-complicated DVT is no more justified or accepted

Effect of angiotensin-II Receptor blockade on experimental portal hypertension in rabbits

In this study, the effect of angiotensin- II receptor antagonist [Candesartan] was evaluated on the portal venous pressure and angiotensin II plasma level in normal and experimentally induced portal venous hypertension in rabbits [PHT] [by partial ligation of portal vein for 3 weeks]. It was found that candesartan administration reduces the portal venous pressure insignificantly from 7.23 +/- 0.47 mmHg in control group to 6.96 +/- 0.32 [P > 0.05] and caused an insignificant increase of angiotensin-II plasma level from 6.98 +/- 0.63 pg/ml in control group to 7.75 +/- 0.39 pg/ml [p> 0.05]. However, after partial ligation of portal veins, the portal venous pressure rises to 13.53 +/- 0.51 mmHg, and decreased significantly by Candesartan to 8.7 +/- 0.86 mmHg [p < 0.001]. Moreover, angiotensin-Il level increased in PHT rabbits to 11. 77 +/- 0.65 pg/ml [P < 0.001] and insignificantly increased by candesartan to 12.66 +/- 0.67 pg/ml. [P > 0.05]. In conclusion, angiotensin-II receptor antagonists may be of great value in treatment of patients with portal hypertension and esophageal varices

Chronic zinc administration improves endothelial cell function and vascular reactivity in experimentally induced diabetes mellitus in rats

An exaggerated oxidative stress has been postulated as the link between diabetes mellitus [D.M] and endothelial dysfunction. This study aimed to investigate the possible therapeutic effect of chronic zinc administration [0.5% in drinking water] on renal artery vascular reactivity and oxidative stress indices viz serum oxidized to reduced glutathione ratio [GSH/GSSG], trolox equivalent antioxidant capacity [TEAC] and lipohydroperoxides [LPO] in experimentally-induced D.M by streptozotocin [STZ] [60 mg/kg i.p single dose] in rats. Using Doppler technique in this study indicated that chronic zinc administration significantly [p<0.05] improved renal artery vascular reactivity to acetylcholine [Ach]. Such an effect which seemed to be mediated by two mechanisms: [1] Zinc restored plasma antioxidant defenses as it significantly [p<0.05] increased the GSH/GSSG ratio, the [TEAC] and significantly [Sp<0,05] decreased LPO. This resulted in lowering the quenching effect of free radicals on nitric oxide [NO] [2] Chronic zinc administrarion significantly [p<0.05] increased intracelular Mg 2+ concentration and significantly [p<0.05] decreased intracellular Ca 2+ content, thus protecting against oxidative cell damage and improving smooth vascular cell relaxation respectively

Zinc-metallothionein provides a protective role against experimentally induced myocardial infarction and arrhythmia in rabbits

Zinc-metallothionein [MT] is a low molecular weight [MW] zinc binding protein [600-700 Dalton]. MT has been proposed to participate in the transport, accumulation, and compartmentation of zinc in the biological system In addition to its role as a storehouse for zinc, MT acts as a free radical scavenger and protect against cadmium toxicity. The present work aimed to investigate the possible role of MT in providing a myocardial protection against isoprenaline-induced myocardial infarction [MI] and arrhythmias in rabbits. To induce myocardial MT, zinc sulfate was injected intraperitoneally 50mg/kg for three consecutive days. It was found that MT protected against MI as indicated by the lower levels of creatine kinase-MB, aspertate aminotransferase and lactate dehydrogenase enzymes. It has also potentiated verapamil effect to protect against tachyarrhythmias

role of blood flow rate and nitric oxide in gonadotropin-induced ovulation in rats

This study has attempted to investigate the role of changes in bood.flow and nitric oxide [NO] in human chorionic gonadotropin [HCG] induced ovulation in rats. A total number of 54 adult female albino rats weighting 300-350 grams were used for this study.The animals were divided into two main groups. The first group was examined for the effect of blood.flow changes. It was injected with HCG in a dose of 15 I.U subcutaneously then divided into six subgroup [uterine artery ligation group, uterine and ovarian artery ligation group and sham operation group] zero-hour [0-h] and 10-hour after HCG injection.The second group was divided into three equal subgroups. A control subgroup was injected with saline, a subgroup was injected with N-Omega-nitro-L-arginine methyl ester [L-NAME] 0.15 mmol kg intravenously and suhgroup was intravenously injected with sodium nitroprusside [0.5 mg kg], a nitric oxide generator, concomitantly with I-NAME.The above three subgroups were injected one-hour later with HCG in a dose of 15 I.U. subcutaneously.In the first group we found that uterine and ovarian artery ligation at zero-hour after HCG injection significantly inhibit ovulation and significantly decreased serum level of both estradiol ond progesterone.While uterine and ovarian artery ligation at 10 hour after HCG injection significantly reduced ovulation rate. However, uterine artery ligation at zero or ten-hour HCG injection lead to nonsignificant effect either on ovulation or serum concentrations of both estradiol and progesterone. In the second group we observed that L-NAME injection one-hour before HCG injection significamly reduced ovulation rate, serum progesterone level and significantly increased serum estradiol level. However, simultaneous injection of both sodium nitroprusside and L-NAME was resulted in significant increase of ovulation and serum progesterone level while, serum estradiol level significantly decreased In conclusion, the present study demonstrates that ovulation process is sensitive to disturbances in ovarian bood flow that is very essential for HCG induced ovulation. NO is an important mediator of vascular changes and tissue remodeling during the ovulatory process and luteinization, consequently L-NAME [NO synthase inhibitor] may be used as an inhibitor of ovulation when hormonal methods are contraindicated