Intra-arterial thrombolysis of acute hand ischaemia with or without microcatheter: preliminary experience and comparison with the literature

Purpose

This paper evaluates the indications, techniques, results, and complications of intra-arterial thrombolysis with or without a multihole microcatheter in three cases of acute hand ischaemia in comparison with the literature.

Materials and methods

Three men (mean age 39 years) with symptoms and signs of acute hand ischaemia (i.e. pain, pallor, cyanosis, decreased motor or sensory function) were studied with Doppler ultrasound and selective arteriography, which demonstrated acute clotting of wrist and/or hand arteries. They therefore underwent intra-arterial thrombolysis with the administration of urokinase and vasodilators and heparin if necessary, with (n=2) or without (n=1) multihole microcatheters.

Results

In all three cases, partial or complete recanalisation of the occluded arteries was achieved, with almost complete remission of clinical symptoms and good recovery of hand function.

Conclusions

Percutaneous intra-arterial thrombolysis is an effective therapeutic approach in cases of acute hand ischaemia and is a valid alternative to surgical thrombectomy. Multihole microcatheters allow the thrombolytic agent to be distributed more evenly into the clot and may help to reduce reactive arterial spasm.     

Characterization of motor,depressive-like and neurochemical alterations induced by a short-term rotenone administration

BackgroundRotenone exposure in rodents provides an interesting model for studying mechanisms of toxin-induced dopaminergic neuronal injury. However, several aspects remain unclear regarding the effects and the accuracy of rotenone as an animal model of Parkinson’s disease (PD). In this study, we investigated the motor and depressive-like behaviors associated to neurochemical alterations induced by a novel protocol of rotenone administration.MethodsIn the first experiment, we adopted the paw test to characterize an effective dose of rotenone able to promote nigrostriatal toxicity. In the second experiment, control and rotenone 2.5 mg/kg groups were injected (ip) for 10 consecutive days.ResultsThis test indicated that intraperitonial (ip) rotenone at 2.5 and 5.0 mg/kg promoted a significant neurotoxicity to striatum and nucleus accumbens. However, only 2.5 mg/kg of rotenone was associated to a negligible mortality rate. Open-field tests were conducted on 1, 7, 14 and 21 day after the last day of treatment and showed an important locomotor impairment, confined to 1 and 7 day. Besides, rotenone affected dopamine levels and increased its turnover in the striatum. Modified forced swim test (performed on 22 day) and sucrose preference test (performed on 14 and 21 day) demonstrated that rotenone produced impairments in the swimming and immobility. In parallel, increments in the serotonin and noradrenaline turnovers were observed in the striatum and hippocampus of the rotenone group.ConclusionsThese data suggest important participations of serotonin and noradrenaline in depressive-like behaviors induced by rotenone. Thus, it is proposed that the current rotenone protocol provides an improvement regarding the existing rotenone models of PD.     

Behavioral, Neurochemical and Histological Alterations Promoted by Bilateral Intranigral Rotenone Administration: A New Approach for an Old Neurotoxin

Rotenone exposure in rodents provides an interesting model for studying mechanisms of toxin-induced dopaminergic neuronal injury. However, several aspects remain unclear regarding the effects and the accuracy of rotenone as an animal model of Parkinson's disease (PD). In order to counteract these limitations, this study characterized a precise neurotoxin-delivery strategy employing the bilateral intranigral administration protocol of rotenone as a reliable model of PD. We performed bilateral intranigral injections of rotenone (12 μg) and subsequent general activity (1, 10, 20, and 30?days after rotenone) and cognitive (7, 8, 15, and 30?days after rotenone) evaluations followed by neurochemical and immunohistochemical tests. We have observed that rotenone was able to produce a remarkable reduction on the percentage of tyrosine hydroxylase immunoreactive neurons (about 60%) within the substantia nigra pars compacta. Dopamine (DA) was severely depleted at 30?days after rotenone administration, similarly to its metabolites. In addition, an increase in DA turnover was detected at the same time-point. In parallel, striatal serotonin and its metabolite were found to be increased 30?days after the neurotoxic insult, without apparent modification in the serotonin turnover. Besides, motor behavior was impaired, mainly 1?day after rotenone. Furthermore, learning and memory processes were severely disrupted in different time-points, particularly at the training and test session (30?days). We now provide further evidence of a time-dependent neurodegeneration associated to cognitive impairment after the single bilateral intranigral administration of rotenone. Thus, it is proposed that the current rotenone protocol provides an improvement regarding the existing rotenone models of PD.