Correlations of inhaled NO with the cTnI levels and the plasma clotting factor in rabbits with acute massive pulmonary embolism

Abstract Purpose: To investigate the correlation of inhaled nitric oxide (NO) on plasma levels of cardiac troponin I (cTnI) and von Willebrand factor (vWF), glycoprotein (GP) IIb/IIIa, granule membrane protein 140 (GMP-140) in rabbits with acute massive pulmonary embolism (PE). Methods: Thirty apanese white rabbits were divided into 3 groups, thrombus were injected in model group (n = 10), NO were inhalated for 24 h after massive PE in NO group (n = 10), saline were injected in control group (n = 10). The concentrations of vWF, GP IIb/IIIa, GMP-140 and cTnI were tested at 4, 8, 12, 16, 20, and 24 h, Correlation analyses were conducted between cTnI and vWF, GP IIb/IIIa, and GMP-140 by Pearson's correlation. Results: The concentration of cTnI and vWF, GP IIb/IIIa, and GMP-140 was increased in the model group, compared to control group. In the inhaled group, the concentrations of cTnI, vWF, GP IIb/IIIa, and GMP-140 were reduced compared to model group. There was a positive correlation between cTnI and vWF, GP IIb/IIIa, and GMP-140. Conclusion: Inhaled nitric oxide can lead to a decrease in levels of cardiac troponin I, von Willebrand factor, glycoprotein, and granule membrane protein 140, after an established myocardial damage, provoked by acute massive pulmonary embolism.

Enoxaparin versus unfractionated heparin in acute ischemic stroke [in-evolution type]. Differential effects of enoxaparin on von willebrand factor release and a possible relation to improved clinical outcomes

The significance of low-molecular-weight heparins [LMWHs] in the management of acute stroke remains controversial. Investigating the effect of early administration of Enoxaparin [ENOX] on risk reduction of early recurrent ischemic strokes compared with Unfractionated Heparin [UFH]. Besides, exploring whether these benefits of ENOX might lead to reduction in death and disability. One hundred patients with acute ischemic stroke in evolution were enrolled [with symptoms of stroke within eight hours randomization]. Patients were randomized to receive UFH or ENOX for ten days. National Institutes of Health Stroke Scale [NIHSS] and Computed Tomography [ct] scan were performed at the time of admission, and after 48 hours of randomization. The mean baseline of [NIHSS] were 9.14 +/- 0.62 and 7.86 +/- 0.54 among patients randomized to UFH and ENOX respectively [P-value 0.2]. At discharge, the mean NIHSS showed a statistically significant difference in favor of the ENOX group [7.9 +/- 0.82 vs 4.96 +/- 0.54 for ENOX and UFH respectively [P-value = 0.002]] The mean NIHSS after therapy in patients who demonstrated neurological improvement was 5.6 +/- 0.46 in the UFH arm compared to 3.65 +/- 0.39 in the ENOX arm [P-valne=0.001]. A deterioration in the clinical neurological condition [progressive stroke symptoms] inspite of treatment with anticoagulant therapy was seen in 20% [n=10] of the patients in the UFH treatment arm compared to none [n=0] in the ENOX treatment arm [P-value=0.005]. ENOX + aspirin was superior to UFH + aspirin in reducing adverse neurological disability after acute ischemic stroke in evolution

Enoxaparin versus unfractionated heparin in acute ischemic stroke [in-evolution type] differential effects of enoxaparin on von Willebrand factor release and a possible relation to improved clinical outcomes

The significance of low-molecular-weight heparins [LMWHs] in the management of acute stroke remains controversial. One hundred patients with acute ischemic stroke in evolution were enrolled [with symptoms of stroke within eight hours of randomization]. Patients were randomized to receive Unfractionated Heparin [UFH] at a dose 5000 IU by IV bolus, followed by a continuous IV infusion; or to Enoxaparin [ENOX] at a dose of 0.5 mg per kilogram body weight. Therapy was continued for 10 days. National Institutes of Health Stroke Scale [NIHSS] and Computed Tomography [CT] scan were performed in all patients at the time of admission, and after 48 hours of randomization. It was found that, the mean baseline National Institutes of Health Stroke Score [NIHSS] was 9.14 +/- 0.62 among patients randomized to UFH, vs. 7.86 +/- 0.54 among patients randomized to ENOX [p = 0.2]. At discharge, the mean NIHSS showed a statistically significant difference in favor of the ENOX group [7.9 +/- 0.82 for the UFH arm versus 4.96 +/- 0.54 for the ENOX arm; p = 0.002]. The mean NIHSS after therapy in patients who demonstrated neurological improvement was 5.6 +/- 0.46 in the UFH arm, as opposed to 3.65 +/- 0.39 in the ENOX arm [p = 0.001]. A deterioration in the clinical neurological condition [progressive stroke symptoms] inspite of treatment with anticoagulant therapy was seen in 20% [n = 10] of the patients in the UFH treatment arm and no patients in the ENOX treatment arm showed this condition [p = 0.005]. No statistically significant differences were observed for pulmonary embolism, deep venous thrombosis, recurrent strokes, or death. It was concluded that, Enoxaparin [+ aspirin] was superior to UFH [+ aspirin] in reducing adverse neurological disability after acute ischemic stroke in evolution. This superiority was not associated with reductions in mortality, and could be explained by blunting of von Willebrand factor release by Enoxaparin