Painful Blue Finger-Achenbach's Syndrome: Two Case Reports.

INTRODUCTION: Herein, two cases of a rare, self resolving condition are described. Vascular surgeons are often called to see patients with spontaneous discolouration of extremities and digits. Often after extensive investigations no diagnosis can be ascertained and the condition resolves spontaneously. REPORT: Two cases are described here, which presented with spontaneous onset of this condition and after extensive testing no cause was ascertained. The condition resolved spontaneously. DISCUSSION: Achenbach's syndrome is a benign, self-limiting condition of unknown aetiology and clinicians should be aware of it to avoid unnecessary time consuming and expensive investigations.

Emergency endovascular management of acute thoracic aortic pathology A safe and feasible option.

Endovascular repair has revolutionised the emergency treatment of thoracic aortic disease. We report our 10 year experience using this treatment in emergency cases. A prospectively maintained vascular database was analysed. Patients' medical records and CT images stored on the hospital PACS system were also reviewed. Statistical analysis was done using IBM SPSS V21. There were a total of 59 thoracic aortic stenting procedures of which 33 (60% males with a mean age of 58 yrs) were performed for emergency thoracic pathologies: traumatic transection (n = 10), ruptured aneurysm (n = 6), non-traumatic dissection (n = 8) and penetrating aortic ulcer (n = 9). All patients had self-expanding endografts implanted. Two patients required debranching procedures before the endovascular treatment. Thirty-day mortality was 12.1% (4/33). 70% of patients received a single device. There were 7 procedure related complications, 6 requiring re-intervention: thoracotomy and drainage in 2 patients, proximal graft extension in 2, open drainage of groin haematoma in 1 and open repair of a common femoral artery pseudo-aneurysm in one patient. In total 23 patients were transferred from 11 centres nationwide. There were no mortalities or other complications related to patient transfer from peripheral centres. Although acute thoracic aortic pathology is life threatening, appropriate blood pressure management and treatment of associated injuries can result in favourable outcomes. Endovascular repair is a safe and effective treatment option which enables patients to be treated with reduced morbidity and mortality. Transfer of patients with acute pathology to a tertiary centre can safely be performed.

Dopamine modulates peripheral purinergic neurotransmission through multiple presynaptic receptors: tissue-dependent effects.

This study investigated the identity of presynaptic receptors involved in dopaminergic modulation of purinergic transmission in peripheral tissues including isolated rat vas deferens and urinary bladder. Isometric muscle twitches were established in the two tissues by low frequency electric field-stimulation (0.05 Hz, 1-ms duration, and supramaximal voltage). Exposure to prazosin, 50 nmol l-1 (vas deferens), or atropine, 3 micromol l-1 (urinary bladder), had no effect on the developed twitches. In contrast, desensitisation of P2X-purinoceptors by alpha,beta-methylene ATP (alpha,beta-mATP, 30 micromol l-1) abolished the twitches in both tissues, confirming their purinergic origin. Dopamine (1.8x10(-7) to 4.2x10(-5) mol l-1) reduced the twitch response in a concentration-related manner. Yohimbine (alpha2-adrenoceptor antagonist, 0.3 micromol l-1) significantly (P<0.05) attenuated the inhibitory effects of dopamine and caused an upward shift in the concentration-response curves in the vas deferens and the urinary bladder. On the other hand, a blockade of DA2-dopaminoceptors by domperidone (1 micromol l-1) produced significant (P<0.05) reductions in dopamine responses only in rat vas deferens, with no effect in the urinary bladder. These data suggest that dopamine exerts inhibitory influences on purinergically-mediated muscle twitches in rat vas deferens and urinary bladder. More importantly, the nature of presynaptic receptors (alpha2-adrenergic and/or DA2-dopaminergic) involved in mediating dopamine effects is dependent on the tissue under investigation.

Prazosin-induced blockade of extraneuronal uptake facilitates dopaminergic modulation of muscle twitches in rat vas deferens.

Preliminary findings in our laboratory have shown that prazosin augmented the inhibitory effects of dopamine on the electrically-evoked muscle twitches in rat vas deferens. In this study, we opted to investigate the underlying mechanism and whether a prazosin-induced blockade of extraneuronal uptake process may be involved. Cumulative additions of dopamine (1.8 x 10(-7)-4.4 x 10(-5) M) elicited slight (< 30%) but dose-related inhibition of electrically-evoked (0.05 Hz, 1 ms duration and supramaximal voltage) muscle twitches of the vas deferens. Pretreatment with cocaine (10 microM), prazosin (50 nM) or oestradiol (10 microM) produced comparable potentiation of the inhibitory responses of dopamine; the pD2 values to dopamine amounted to 4.47 +/- 0.20, 4.72 +/- 0.21 and 4.56 +/- 0.19, respectively. A lower concentration of prazosin (5 nM) failed to alter dopaminergic responses. Further potentiation of dopamine responses was demonstrated in tissues preincubated with a combination of cocaine plus prazosin (50 nM), or cocaine plus oestradiol (pD2, 5.40 +/- 0.11 and 5.42 +/- 0.05, respectively). However, a mixture of all three drugs failed to elicit any further increase in dopamine responses, a finding that may suggest an extraneuronal uptake blocking activity for prazosin. Inhibition of muscle twitches evoked by bromocriptine, a dopaminoceptor agonist which is not a substrate for extraneuronal uptake, was not affected by prazosin (50 nM) pretreatment. The findings presented in this study emphasize the role of dopamine in modulating noradrenergic neurotransmission in rat vas deferens. More importantly, the results suggest that prazosin may act to block the extraneuronal uptake at noradrenergic sites, an effect that may account for its capability to facilitate dopaminergic modulation of noradrenergic neurotransmission.