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PubMed1999

Effect of batroxobin on spontaneous echo contrast and hemorheology in left atrial appendage in atrial fibrillation assessed by transesophageal echocardiograpy.

Controversy exists regarding the effect of defibrination on spontaneous echo contrast and flow dynamics in left atrial appendage (LAA) in atrial fibrillation. We aimed to investigate the effect of batroxobin, which decreases plasma fibrinogen level, on the echo intensity of spontaneous echo contrast in LAA. In 36 patients with atrial fibrillation (duration 7 +/- 4 years), transesophageal echocardiography was performed at baseline and 24 hours after batroxobin administration (0.2 U/kg). At the orifice of the LAA, integrated backscatter of echo contrast and peak velocity of LAA emptying flow were measured. Plasma fibrinogen and whole blood viscosity were also measured. Fibrinogen and viscosity were significantly lower after batroxobin administration (96 +/-38 mg/dl and 4.35 +/- 0.56 cp) than those at baseline (320 +/- 61 mg/dl and 4.71 +/- 0.61 cp, both p <0.001). A significant positive correlation between changes in plasma fibrinogen and whole blood viscosity (r = 0.49, p = 0.002) was shown. The integrated backscatter significantly decreased from 14 +/- 3 to 12 +/- 3 decibels after batroxobin (p <0.001), and the changes in integrated backscatter and plasma fibrinogen was significantly correlated. Therefore, batroxobin administration improved blood rheology and decreased blood cell aggregation, which are effective in preventing left atrial thrombus formation.

Aged↗
PubMed1996

Batroxobin accelerates lipid accumulation of peroxidized low density lipoprotein in mouse peritoneal macrophages.

Mouse peritoneal macrophages were incubated in DMEM medium with batroxobin (DF-521) to determine the effect of batroxobin on the internalization of peroxidized low-density lipoprotein (pox-LDL) by transmission electron microscopy. Although the morphology of the mouse peritoneal macrophages after incubation with DMEM, normal LDL (n-LDL) and n-LDL plus batroxobin was similar to that of the cells before incubation, they exhibited numerous cytoplasmic lipid droplets after incubation with pox-LDL for 4 h. After addition of batroxobin to the medium containing pox-LDL, the production of lipid droplets in the mouse peritoneal macrophages was tremendously accelerated. Batroxobin accelerates the phagocytosis and degradation of pox-LDL by macrophages.

Animals↗
PubMed2001

Effect of batroxobin on neuronal apoptosis during focal cerebral ischemia and reperfusion in rats.

We have found that Batroxobin plays a protective role in ischemic brain injury, which attracted us to investigate the effect of Batroxobin on apoptosis of neurons during cerebral ischemia and reperfusion. The apoptotic cells in ischemic rat brains at different reperfusion intervals were tested with method of TdT-mediated dUTP-DIG nick end labeling (TUNEL) and the effect of Batroxobin on the apoptosis of neurons was studied in left middle cerebral artery (LMCA) occlusion and reperfusion in rat models (n = 18). The results showed that few scattered apoptosis cells were observed in right cerebral hemispheres after LMCA occlusion and reperfusion, and that a lot of apoptosis cells were found in left ischemic cortex and caudoputamen at 12 h reperfusion, and they reached peak at 24 h-48 h reperfusion. However, in the rats pretreated with Batroxobin, the number of apoptosis cells in left cerebral cortex and caudoputamen reduced significantly and the neuronal damage was much milder at 24 h reperfusion than that of saline-treated rats. The results indicate that administration of Batroxobin may reduce the apoptosis of neurons induced by cerebral ischemia and reperfusion and afford significant cerebroprotection in the model of focal cerebral ischemia and reperfusion.

Animals↗
PubMed2004

[Effectiveness of urokinase used in combination with batroxobin (DF-521) in rat model of focal cerebral ischemia-reperfusion].

OBJECTIVE: This study was designed to use urokinase (UK) in combination with batroxobin in thrombolytic therapy so as to see whether batroxobin(DF-521) would be effective for neuroprotection. METHODS: The model of right middle cerebral artery occlusion (MCAO) in male SD rats was established. 120 rats were randomized into 9 groups, namely control group, sham control group, and groups that were treated with batroxobin and urokinase together or separately. Each group comprised 15 rats. Intracranial bleeding, infarct volume ratio and neurological function were observed. RESULTS: Intracranial bleeding was found in 5 rats of the UK 5000 U/kg group, in 4 rats of the UK 5000 U/kg (2 h) + DF-521 5 BU/kg (2 h) group, and in only 1 rat of the UK 5000 U/kg (2 h) + DF-521 5 BU/kg (1 h) group. Cerebral infarct volume ratio was obviously reduced in 5 BU/kg batroxobin group. No difference was observed in neurological deficit scores. CONCLUSION: 5000 U/kg urokinase increased the risk of intracranial hemorrhage in rat MCAO model. Batroxobin either used separately or in combination with urokinase would not increase the risk of intracranial hemorrhage in rat MCAO model.

Animals↗
PubMed1996

[The effect of batroxobin on coronary segmental resistance and coronary blood flow in acute myocardial ischemic dogs].

To study the effects of batroxobin on coronary circulation and cardiac performance in acute myocardial ischemia, Batroxobin was given intravenously to dogs with experimental coronary stenosis. A dose-dependent increase of coronary blood flow (CBF) was observed. Forty minutes after batroxobin (2 BU.kg-1 at infusion rate 0.1 BU.kg-1.min-1) administration, CBF increased by 12% (P < 0.05), small coronary resistance(RS) decreased from 4.1 +/- 0.5 to 3.2 +/- 0.5 mmHg.min.ml-1 (P < 0.01), while large coronary resistance(RL) changed insignificantly from 3.9 +/- 0.8 to 3.8 +/- 0.7 mmHg.min.ml-1 (P > 0.05). Two hours following drug administration, the changes in CBF, RS and RL still remained and RT decreased by 13% (P < 0.05). The + LV(dp/dt)max and -LV(dp/dt)max increased by 14% and 16% (P < 0.05) respectively compared with those in control group. It is concluded that batroxobin improves the ischemic canine coronary circulation and cardiac performance by way of lowering the small coronary resistance and thus increasing CBF. The data also suggest the benificial effect of batroxobin in acute myocardial ischemia.

Animals↗
PubMed1988

Preventive effects of batroxobin on experimental canine coronary thrombosis.

The thrombolytic effects of urokinase (UK) and preventive effects of batroxobin, heparin, and aspirin on the recurrence of thrombosis in the coronary artery were studied in 118 anesthetized dogs with severe endothelial denudation and luminal stenosis of the coronary artery. Occlusive thrombi developed in 68 (58%) preparations (dogs), accompanied by a decrease of coronary blood flow and pressure, an electrocardiographic ST elevation, and epicardial cyanosis. An intravenous infusion of 20,000 IU/kg of UK reopened the occluded coronary artery in all 32 preparations with 1-h-old thrombi, in 6 (86%) of 7 preparations with 2-h-old thrombi, and in 5 (83%) of 6 preparations with 3-h-old thrombi. However, recanalization was not observed in preparations with thrombi more than 4-h-old. Occlusion recurred within 6 h after recanalization in 2 (18%) of 18 preparations pretreated with batroxobin (1-2 BU/kg) (p less than .005 vs. control UK group), in 1 (14%) of 7 preparations administered a continuous infusion of 30 U/kg per h of heparin (p less than .05 vs. control UK group), in 4 (57%) of 7 preparations pretreated with 2 mg/kg of aspirin, and in 7 (64%) of 11 preparations not pretreated (control UK group). Complete prevention was observed only in the group administered 2 BU/kg of batroxobin. Histologically, these thrombi closely simulated clinical arterial thrombi. Myocardial hemorrhage and contraction band necrosis were observed in the reperfused hearts. In conclusion, experimental canine coronary thrombi more than 4-h-old were resistant to thrombolytic therapy, and batroxobin and heparin were effective in the prevention of coronary reocclusion.

Animals↗
PubMed1983

The effects of defibrinogenation with batroxobin on endotoxin-induced disseminated intravascular coagulation in rats.

Experimental disseminated intravascular coagulation (DIC) can be induced by a 4-hr sustained infusion of endotoxin at a dose of 100 mg/kg in rats. This experimental model of DIC in rats was used to study the effects of defibrinogenation with batroxobin against DIC. One hour before the infusion of endotoxin, 200 batroxobin unit (BU)/kg of batroxobin was injected intraperitoneally. Immediately after the injection, fibrinogen level markedly decreased and fibrinogen and fibrin degradation products increased. Prothrombin time and partial thromboplastin time were also prolonged. Blood counts, platelet counts and hematocrit level only showed a slight decrease after the injection. The preventive effect against DIC was noted by the partial inhibition of the fall in the platelet counts and lessened number of renal glomeruli with fibrin thrombi, in the rats treated with 200 BU/kg of batroxobin 1 hr before the infusion of endotoxin (100 mg/kg/4 hr). From these results, it was shown that fibrinogen metabolism plays an important role in the DIC state.

Animals↗
PubMed1993

Comparison of the sequence of fibrinopeptide A cleavage from fibrinogen fragment E by thrombin, atroxin, or batroxobin.

In order to investigate the sequence of fibrinopeptide release from the amino terminal end of a dimeric fibrinogen-derived substrate by thrombin or batroxobins, we studied their effects on plasmic fragment E1, a core fragment from the central domain of fibrinogen containing both A alpha chain fibrinopeptide A (FPA) sequences. Isoelectric focussing (IEF) was employed as a means of resolving des A-fragment E1, from which one FPA had been cleaved, from des AA-fragment E1 resulting from the loss of both FPA's. Using densitometric gel scanning for quantification of the levels of intact fragment E1, des A-fragment E1, and des AA-fragment E1, in mixtures incubated with enzyme for various periods of time, we found similar catalytic rate constants (k1, k2) for release of the first fibrinopeptide A, (FPA1) or the second, (FPA2) from fragment E1, with either thrombin or batroxobin (k2:k1 ratios of 1.10 +/- 0.42, 1.34 +/- 0.26 respectively). Atroxin released FPA2 more slowly than FPA1 with a k2:k1 ratio of 0.34 +/- 0.1. Th finding that the cleavage of FPA2 by Atroxin is three-fold slower than thrombin and almost four-fold slower than batroxobin, suggest that batroxobin and thrombin cleavage of FPA2 may be cooperative in nature. However, the cooperativity in the cleavage sequence is insufficient to markedly suppress the evolution of intermediate des A fragment E species during early and intermediate phases of FPA cleavage from fragment E.

Amino Acid Sequence↗
PubMed1982

The effect of hypofibrinogenemia with batroxobin on rat Masugi nephritis.

The effect of hypofibrinogenemia with batroxobin on proliferative glomerular lesions of Masugi nephritis was examined in the rat. Batroxobin-treated rats had a relatively low level of plasma fibrinogen and a reduction in glomerular fibrin deposition. Mean nuclear counts in the outer cortical glomeruli were less in the batroxobin-treated group than in the untreated group on the 7th day. However, the difference in the overall severity of the glomerular histologic lesions between the two groups was not significant. Continual injections of the same dosage of batroxobin failed to maintain hypofibrinogenemia, possibly due to the antibody formation. These results suggest that relatively low plasma levels of fibrinogen are obviously not effective enough to prevent the development of the proliferative lesions in rat Masugi nephritis.

Afibrinogenemia↗
PubMed2000

Effect of batroxobin on expression of c-Jun in left temporal ischemic rats with spatial learning and memory disorder.

The effect of Batroxobin on expression of c-Jun in left temporal ischemic rats with spatial memory disorder was investigated by means of Morri's water maze and immunohistochemistry methods. The results showed that the mean reaction time and distance of temporal ischemic rats for searching a goal were significantly longer than those of sham-operated rats, and at the same time c-Jun expression of left temporal ischemic region was significantly increased. However, the mean reaction time and distance of Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of c-Jun immune reactive cells of Batroxobin-treated rats was also less than that of ischemic group. In conclusion, Batroxobin can improve spatial memory disorder in temporal ischemic rats, and the down-regulation of the expression of c-Jun is probably related to the neuroprotective mechanism.

Animals↗
PubMed2000

Effects of batroxobin on spatial learning and memory disorder of rats with temporal ischemia and the expression of HSP32 and HSP70.

The effect of Batroxobin on spatial memory disorder of left temporal ischemic rats and the expression of HSP32 and HSP70 were investigated with Morri's water maze and immunohistochemistry methods. The results showed that the mean reaction time and distance of temporal ischemic rats in searching a goal were significantly longer than those of the sham-operated rats and at the same time HSP32 and HSP70 expression of left temporal ischemic region in rats was significantly increased as compared with the sham-operated rats. However, the mean reaction time and distance of the Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of HSP32 and HSP70 immune reactive cells of Batroxobin-treated rats was also less than that of the ischemic group. In conclusion, Batroxobin can improve spatial memory disorder of temporal ischemic rats; and the down-regulation of the expression of HSP32 and HSP70 is probably related to the attenuation of ischemic injury.

Animals↗
PubMed2001

Metabolic changes in rats with photochemically induced cerebral infarction and the effects of batroxobin: a study by magnetic resonance imaging, 1H- and 31P-magnetic resonance spectroscopy.

Metabolic changes in rats with photochemically induced cerebral infarction and the effects of batroxobin were investigated 1, 3, 5 and 7 days after infarction by means of magnetic resonance imaging (MRI), 1H- and 31P-magnetic resonance spectroscopy (MRS). A region of T2 hyperintensity was observed in left temporal neocortex in infarction group and batroxobin group 1, 3, 5 and 7 days after infarction. The volume of the region gradually decreased from 1 day to 7 days after infarction. The ratio of NAA/Cho + Cr in the region of T2 hyperintensity in the infarction group was significantly lower than that in the corresponding region in the sham-operated group 3, 5 and 7 days after infarction respectively (P < 0.05). Lac appeared in the region of T2 hyperintensity in the infarction group 1, 3, 5 and 7 days after infarction, but it was not observed in the corresponding region in sham-operated group at all time points. Compared with the sham-operated group, the ratios of beta ATP/PME + PDE and PCr/PME + PDE of the whole brain in the infarction group were significantly lower 1, 3 and 5 days after infarction respectively (P < 0.05), and the ratio of beta ATP/PCr also was significantly lower 1 day after infarction (P < 0.05). Batroxobin significantly decreased the volume of the region of T2 hyperintensity 1 and 3 days after infarction (P < 0.05), significantly increased the ratio of NAA/Cho + Cr in the region 5 and 7 days after infarction (P < 0.05), significantly decreased the ratios of Lac/Cho + Cr and Lac/NAA in the region 5 and 7 days after infarction (P < 0.05), and significantly increased the ratios of beta ATP/PME + PDE and beta ATP/PCr in the whole brain 1 day after infarction (P < 0.05). The results indicated that the infracted region had severe edema, increased Lac and apparent neuronal dysfunction and death, and energy metabolism of the whole brain decreased after focal infarction, and that batroxobin effectively ameliorated the above-mentioned abnormal changes.

Animals↗
PubMed2000

[The effects of batroxobin on the healing of and microcirculatory blood flow volume in deep partial thickness burn wounds in rats].

OBJECTIVE: To investigate the effects of batroxobin on the healing of and microcirculatory blood flow in deep partial thickness burn wound in rats. METHODS: Wistar rat inflicted by 4 cmx 4 cm deep partial thickness scalding on the back was taken as the model. Twenty male rats were randomly divided into scalding burn group and batroxobin treatment group. Cutaneous blood flow volume was measured before and at 0.5, 2, 4, 6, 12, 24 and 72 postburn hours (PBH). Scalding and residual burn wound areas were measured immediately and on the 14th and 18th postburn day (PBD). The rats were sacrificed on 30th PBD and the cutaneous samples were harvested for hair follicle counting and histological examination with LM. RESULTS: The cutaneous blood flow volume of rats in single burn group decreased progressively during 2-72 PBHs. But in batroxobin treating group, cutaneous blood flow volume improved evidently and the wound healing accelerated obviously with increased cutaneous appendages formation. CONCLUSION: Batroxobin might restore the blood circulation of stasis band of burn wound, so as to accelerate wound healing and to improve the quality of healed skin.

Animals↗
PubMed2001

Effect of batroxobin on expression of neural cell adhesion molecule in temporal infarction rats and spatial learning and memory disorder.

The effect of Batroxobin expression of neural cell adhesion molecule (NCAM) in left temporal ischemic rats with spatial memory disorder was investigated by means of Morri's water maze and immunohistochemical methods. The results showed that the mean reaction time and distance of temporal ischemic rats for searching a goal were significantly longer than those of sham-operated rats and at the same time NCAM expression of left temporal ischemic region was significantly increased. However, the mean reaction time and distance of Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of NCAM immune reactive cells of Batroxobin-treated rats was more than that of ischemic group. In conclusion, Batroxobin can improve spatial memory disorder of temporal ischemic rats and the regulation of the expression of NCAM is probably related to the neuroprotective mechanism.

Animals↗
PubMed2002

[The establishment of a guinea pig model of inflammatory pleural effusion and the effect of batroxobin in the prevention of pleural encapsulation].

OBJECTIVE: To establish an animal model of inflammatory pleural effusion and to investigate the role of batroxobin in preventing encapsulation of pleural effusion. METHODS: (1) Forty guinea pigs were divided into two groups: the animal model group received injection of 1% carrageenan (0.8 approximately 1.0 ml) in the right chest cavity; the control animals received injection of normal saline (1 ml). (2) Sixty guinea pigs were injected with 1% carrageenan (0.8 approximately 1.0 ml) in the right chest cavity, and then divided into a treatment group and a control group. Batroxobin (3 BU) was injected into the right chest cavity of the animals in the treatment group, while normal saline was used in the control group. The animals were killed at different time points. RESULTS: In the animal model group, pleural effusion appeared in 24 hours and reached maximum amount within 2 approximately 3 days. Neutrophils accumulated in the effusion and pleural inflammation intensified at the same time. Fibrosis and pleural adhesion appeared by the seventh day, became prominent by the tenth day, and encapsulated pleurisy was evident by the fourteenth day. With batroxobin treatment, pleural effusion and inflammation attenuated. The fibrinogen (Fbg) level decreased, and the levels of tissue plasminogen activator (t-PA) and D-dimer increased in the effusion. No pleural encapsulation was observed. CONCLUSIONS: Carrageenan was successfully used to establish an animal model of inflammatory pleural effusion in guinea pigs. Batroxobin was effective in reducing inflammation and pleural effusion and in preventing pleural fibrosis and encapsulation.

Animals↗
PubMed2003

Lipopolysaccharide attenuates thrombolysis in batroxobin-induced lung vasculature fibrin deposition but not in ferrous chloride-induced carotid artery thrombus in rats: role of endogenous PAI-1.

In this study, we investigated if elevation of endogenous plasminogen activator inhibitor type 1 (PAI-1) by lipopolysaccharide (LPS) can retard thrombolysis in both a rat model of lung vasculature fibrin deposition and a platelet-rich thrombus model induced by endothelial injury. By 3 h following an intravenous bolus injection of 0.5 mg/kg LPS, the plasma PAI-1 level had increased to approximately 8 ng/ml. 125I-labeled fibrinogen was injected intravenously followed by an injection of batroxobin. Batroxobin converts fibrinogen into insoluble fibrin, which was then deposited in the lungs within 5 min, followed by spontaneous fibrinolysis that completely cleared fibrin deposition in the lungs by 30 min. In rats pre-treated with LPS, spontaneous fibrinolysis was significantly retarded. In the endothelial injury model, topical application of FeCl2 on the carotid artery induced an occlusive platelet-rich thrombus, which was not sensitive to endogenous thrombolysis. Exogenous tissue-type plasminogen activator (tPA) was required to recanalize the occlusive thrombus in a dose-dependent manner. Pre-treatment with LPS did not alter the dose-response curve of exogenous tPA-induced thrombolysis. These data indicate that batroxobin-induced lung vasculature fibrin deposition in rats, unlike the FeCl2 model, is sensitive to the impact of endogenous PAI-1 on fibrinolysis.

Animals↗
PubMed1999

Changes in mRNA levels of fibrinogen subunit polypeptides in rats defibrinogenated with batroxobin.

Batroxobin is a snake venom that is a thrombinlike enzyme used for clinical treatment. We analyzed hepatic mRNA levels for fibrinogen subunit polypeptides and prothrombin by reverse transcription-polymerase chain reaction as well as coagulation and fibrinolysis factors in plasma 1, 3, 5 and 24 hours after Batroxobin treatment (3 BU/100 g) in rats. The mRNA levels of alpha- and beta-chains of fibrinogen were significantly increased with decreases in plasma fibrinogen, alpha2-plasmin inhibitor, and plasminogen levels, while the mRNA levels for prothrombin remained unchanged. These results suggest that fibrinogen mRNA synthesis is regulated by plasma fibrinogen levels in Batroxobin-induced defibrinogenated rats.

Animals↗
PubMed2003

Batroxobin-induced clots exhibit delayed and reduced platelet contractile force in some patients with clotting factor deficiencies.

Thrombin causes platelet activation via multiple pathways, and deficient thrombin generation reduces platelet contractile force (PCF) during clot retraction. We hypothesized that PCF in blood samples from clotting factor-deficient patients would be diminished due to delayed or deficient thrombin generation. Blood samples from patients with fibrinogen, and factor V, VII, VIII, IX, X, XI and XIII deficiencies were compared to samples from normal controls. PCF in patient blood clotted with thrombin (1 NIH UmL(-1)) was compared to PCF in clots formed with batroxobin (0.25 micro g mL(-1)). PCF in the former should be normal, but PCF in the latter is dependent on thrombin generation within the sample and might be deficient. In factor VII-(n = 2, P < 0.05), factor VIII-(n = 6, P < 0.005) and factor XI-(n = 2, P < 0.05) deficient platelet-rich plasmas, PCF in batroxobin-induced clots was significantly lower than in thrombin-induced clots. In factor IX deficiency (n = 2), one patient had a dramatic reduction in PCF while a second patient had increased PCF. PCF was insignificantly (P = 0.346) reduced in two patients with factor X deficiency, and was normal in one patient with factor V deficiency. The factor X result is consistent with work in model systems, which indicates that as little as 1-3% factor X activity is sufficient to restore thrombin generation to normal. The factor V result probably indicates that the deficiency is incomplete. PCF in thrombin-induced clots was normal in all of these patients. Low fibrinogen and factor XIII deficiency reduced PCF in both thrombin- and batroxobin-induced clots. These results indicate that PCF is reduced, probably due to delayed thrombin generation, in some factor-deficient platelet-rich plasma samples.

Batroxobin↗