Comparison of Therapeutic Efficacy of Anticoagulation and Its Combination with Catheter-directed Thrombolysis for Deep Venous Thrombosis of Lower Extremities / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To investigate the therapeutic efficacy of anticoagulation(AC) and its combination with catheter-directed thrombolysis(CDT) for deep venous thrombosis of lower extremities.</p><p><b>METHODS</b>One hundred and thirty-nine patients with deep venous thrombosis of early lower extremities treated in our hospital from May 2011 to September 2013 were selected and randomly divided into the AC group(n= 66) and CDT+AC group(n= 73). The thrombolytic effects, adverse reactions, post-thrombotic syndrome (PTS) and quality of life were evaluated.</p><p><b>RESULTS</b>There were no serious adverse events during treatment and after treatment in the 2 groups. Hematomas in 2 cases and gross hematuria in 3 cases were observed in the CDT+AC group. The gums bleed or gross hematuria in 3 cases were observed in the AC group. Compared with the AC group, the number of grade I thrombolysis in CDT+AC group decreased significantly (60.61% vs 9.59%)(P< 0.05), and the number of grade III thrombolysis increased significantly(7.57% vs 49.31%)(P< 0.05). During follow-up, the incidence of PTS in both groups showed increase year by year, and none of the patients had severe PTS. The incidence PTS in CDT+AC group at 12 months and 18 months were lower than those of AC group(17.81% vs 33.33%, 24.66% vs 43.94%)(P< 0.05). Compared with the AC group, the scores of physiological role and vitality in CDT+AC group at 6 months, 12 months and 18 months were higher (P< 0.05).</p><p><b>CONCLUSION</b>Catheter-directed thrombolysis combined with AC therapy can promote the mitigation of clinical symptoms in patients with DVT of lower extremities and is beneficial to promoting the life quality of patients.</p>

Effect of hypothalamic supraoptic nucleus on acupuncture analgesia in the rat.

Hypothalamic supraoptic nucleus (SON) has been demonstrated to involve in pain modulation. Acupuncture analgesia is a very useful clinical skill for pain relief, which has over 2500-year history in China. The present study investigated the effect of SON on acupuncture analgesia in the rat. Electrical stimulation of the SON or microinjection of a small dose L-glutamate sodium into the SON enhanced acupuncture analgesia in a dose-dependent manner, while cauterization of the SON weakened acupuncture analgesia. Pituitary removal did not influence the effect of L-glutamate sodium that enhanced acupuncture analgesia in the SON. The data suggested that the neurons and not the nerve fibers in the SON played an important role in acupuncture analgesia, which effect might be through the central nervous system rather than the hypothalamo-neurohypophyseal system.

Investigating the role of the hypothalamic supraoptic nucleus in nociception in the rat.

We investigated the role of the hypothalamic supraoptic nucleus (SON) in nociception in the rat. Electrical stimulation of the SON or microinjection of a small dose of L-glutamate sodium into the SON elevated the nociceptive threshold in a dose-dependent manner, while cauterization of the SON decreased the nociceptive threshold. Pituitary removal did not influence the antinociceptive effect of L-glutamate sodium in the SON. The data suggested that the neurons and not the nervous fibers in the SON played an important role in antinociception.

Central oxytocin enhances antinociception in the rat.

The study aimed to investigate the effect of oxytocin on antinociception in the rat. The pain threshold was elevated by oxytocin following intraventricular (icv) or intrathecal injection (ith), and reduced by anti-oxytocin serum (icv or ith). But the pain threshold was not altered by intravenous injection (iv) of oxytocin or anti-oxytocin serum. Pain stimulation induced oxytocin concentration decrease in the hypothalamic supraoptic nucleus, and increase in the locus coeruleus, raphe magnus nucleus, caudate nucleus and spinal cord, but no change in the hypothalamic paraventricular nucleus and plasma. The results indicated that central, not peripheral oxytocin could enhance antinociception.

Arginine vasopressin enhances periaqueductal gray synthesis and secretion of enkephalin and endorphin in the rat.

Previous study has proven that arginine vasopressin (AVP) enhances periaqueductal gray (PAG) secreting enkephalin and endorphin in vivo in the rat. Present work investigated that AVP effect on PAG secretion and synthesis of enkephalin and endorphin in vitro. Radioimmunoassy results showed that AVP increased leucine-enkephalin (L-Ek), methionine-enkephalin (M-Ek), beta-endorphin (beta-Ep) rather than dynorphin A(1-13) (DynA(1-13)) concentrations in PAG slice culture liquid, and V(2) receptor antagonist: d(CH(2))(5)[D-Ile(2), Ile(4), Ala(9)-NH(2)]AVP decreased L-Ek, M-Ek and beta-Ep, not DynA(1-13) concentrations in PAG slice culture liquid in a dose-dependent manner, but V(1) receptor antagonist: d(CH(2))(5)Tyr(Me)AVP did not change these peptide concentrations in PAG slice culture liquid. RT-PCR data displayed that AVP enhanced proenkephalin and proopiomelanocortin (Pro-beta-Ep) rather than prodynorphin mRNA expressions in culture PAG tissues, and V(2) receptor antagonist weakened proenkephalin and proopiomelanocortin (Pro-beta-Ep), not prodynorphin mRNA expressions in culture PAG tissues, but V(1) receptor antagonist did not influence these mRNA expressions in culture PAG tissues. The data suggest that AVP enhances PAG synthesizing and secreting enkephalin and endorphin rather than dynorphin through V(2) receptors.

Through the central V2, not V1 receptors influencing the endogenous opiate peptide system, arginine vasopressin, not oxytocin in the hypothalamic paraventricular nucleus involves in the antinociception in the rat.

Our previous study has proven that hypothalamic paraventricular nucleus (PVN) played a role in the antinociception. The central bioactive substances involving in the PVN regulating antinociception were investigated in the rat. The results showed that electrical stimulation of the PVN increased the pain threshold, and L-glutamate sodium injection into the PVN elevated the pain threshold, but the PVN cauterization decreased the pain threshold; pain stimulation raised the arginine vasopressin (AVP), not oxytocin (OXT), leucine-enkephalin (L-Ek), beta-endorphin (beta-Ep) and DynorphinA1-13 (DynA1-13) concentrations in the PVN tissue using micropunch method, heightened AVP, L-Ek, beta-Ep and DynA1-13, not OXT concentrations in the PVN perfuse liquid, and reduced the number of AVP-, not OXT, L-Ek, beta-Ep and DynA1-13-immunoreactive neurons in the PVN especially in the posterior magnocellular part of the PVN using immunocytochemistry. There was a negative relationship between the PVN AVP concentration and the pain threshold; pain stimulation enhanced the AVP, not OXT mRNA expression in the PVN using in situ hybridization and RT-PCR; intraventricular injection of anti-AVP serum completely reversed L-glutamate sodium injection into the PVN-induced antinociception, and administration of naloxone - the opiate peptide antagonist, partly blocked this L-glutamate sodium effect, but anti-OXT serum pretreatment did not influence this L-glutamate sodium effect; L-glutamate sodium injection into the PVN-induced analgesia was inhibited by V2 receptor antagonist - d(CH2)5[D-Ile2, Ile4, Ala-NH2(9)]AVP, not V1 receptor antagonist - d(CH2)5Tyr(Me)AVP. The data suggested that the PVN was limited to the central AVP, not OXT, which was through V2, not V1 receptors influencing the endogenous opiate peptide system, to regulate antinociception.