Variability in response to cryoprecipitate treatment for hemostatic defects in uremia

Cryoprecipitate is frequently administered as treatment for hemostatic defects in patients with uremia. The only published data supporting this approach however, involves seven patients described by Janson and colleagues in whom bleeding times were shortened and bleeding complications reduced after cryoprecipitate infusion. We retrospectively reviewed our institution's experience with cryoprecipitate in this setting. Five patients had sufficiently complete data for evaluation of the efficacy of therapy with cryoprecipitate, including pretreatment bleeding time greater than 15 minutes, normal coagulation studies, and platelet count greater than 100,000/microliters. Two patients had normalization of their bleeding time and a favorable clinical outcome after cryoprecipitate infusion. Three patients failed to shorten their bleeding time after cryoprecipitate infusion or, in one case, multiple infusions. One of these latter patients had correction of his abnormal bleeding time after subsequent administration of deamino-8-D-arginine vasopressin (DDAVP). We conclude that the hemostatic response to cryoprecipitate therapy is variable, and that cryoprecipitate therapy does not achieve restoration of normal hemostasis in some patients with uremic bleeding.     

Vasopressin and 1-deamino-8-d-arginine-vasopressin (DDAVP) reduce elevated plasma catecholamine levels in rats with hypothalamic deafferentation

1. Anterolateral cut (ALC) of the medial basal hypothalamus (MBH) in rats produces an elevation of plasma catecholamine levels, especially of norepinephrine (NE), in unstressed animals and a more pronounced rise of plasma NE levels in response to immobilization (IMO). Animals with ALC have a destroyed corresponding vasopressin (AVP) and other peptides containing innervation of the median eminence and the posterior pituitary, resulting in the prevention of increased AVP secretion during the early intervals of IMO. 2. The administration of AVP (Pitressin, 7 days, 1 IU per rat i.m.) or of 1-deamino-8-D-arginine-vasopressin (DDAVP), an AVP analogue without pressoric activity, taken in drinking water (about 100 micrograms per day) was almost equally potent in decreasing the elevated water consumption and plasma NE levels in unstressed rats with ALC. However, the stress-induced potentiation of plasma NE levels in rats with ALC was not influenced by AVP substitution and only partly reduced by DDAVP in the late IMO intervals. 3. The lack of circulating vasopressin is the main factor in the mechanism of increased activity of the sympathoadrenal system induced by ALC in unstressed rats. 4. The regulation of sympathoadrenal activity by vasopressin and DDAVP in rats with ALC seems to be mediated predominantly by V2-subtype receptors. 5. In stressed rats with ALC the potentiation of plasma NE levels was not reduced after AVP or DDAVP administration, suggesting that some addition regulatory mechanisms were involved.     

Effect of 1-desamino-8-D-arginine vasopressin (DDAVP) on vasopressin release and blood pressure during hemorrhage.

Whether or not 1-desamino-8-D-arginine-vasopressin (DDAVP) reduces blood pressure or affects the release of arginine vasopressin (AVP) and renin is controversial, although evidence suggests AVP and renin are important in maintaining blood pressure during hemorrhage. We therefore investigated the effect of DDAVP on endogenous release of AVP and renin and on blood pressure during hemorrhage in dogs. In the control group the hemorrhage was performed at a rate of 0.4 ml.kg-1.min-1 for 40 min from the femoral artery. The plasma AVP concentration and renin activity (PRA) increased progressively in response to the hemorrhage, from 7.5 +/- 0.5 to 40.3 +/- 7.3 pg.ml-1, and from 11.8 +/- 1.5 to 20.5 +/- 4.2 ng.ml-1.h-1, respectively, while blood pressure decreased slightly. In the DDAVP group, intravenous infusion of DDAVP (2.5 ng.kg-1.min-1 for 40 min) and hemorrhage were simultaneously performed. The plasma DDAVP concentration increased progressively to 218 +/- 21.0 pg.ml-1. There was no significant difference, however, between the control and DDAVP groups in the response of AVP, PRA and blood pressure. The results suggested that DDAVP may not affect the release of AVP and renin or blood pressure during hemorrhage.     

Collecting duct-specific knockout of adenylyl cyclase type VI causes a urinary concentration defect in mice

Collecting duct (CD) adenylyl cyclase VI (AC6) has been implicated in arginine vasopressin (AVP)-stimulated renal water reabsorption. To evaluate the role of CD-derived AC6 in regulating water homeostasis, mice were generated with CD-specific knockout (KO) of AC6 using the Cre/loxP system. CD AC6 KO and controls were studied under normal water intake, chronically water loaded, or water deprived; all of these conditions were repeated in the presence of continuous administration of 1-desamino-8-d-arginine vasopressin (DDAVP). During normal water intake or after water deprivation, urine osmolality (U(osm)) was reduced in CD AC6 KO animals vs. controls. Similarly, U(osm) was decreased in CD AC6 KO mice vs. controls after water deprivation+DDAVP administration. Pair-fed (with controls) CD AC6 KO mice also had lower urine osmolality vs. controls. There were no detectable differences between KO and control animals in fluid intake or urine volume under any conditions. CD AC6 KO mice did not have altered plasma AVP levels vs. controls. AVP-stimulated cAMP accumulation was reduced in acutely isolated inner medullary CD (IMCD) from CD A6 KO vs. controls. Medullary aquaporin-2 (AQP2) protein expression was lower in CD AC6 KO mice vs. controls. There were no differences in urinary urea excretion or IMCD UT-A1 expression; however, IMCD UT-A3 expression was reduced in CD AC6 KO mice vs. controls. In summary, AC6 in the CD regulates renal water excretion, most likely through control of AVP-stimulated cAMP accumulation and AQP2.     

Involvement of the V2 receptor in vasopressin-stimulated translocation of placental leucine aminopeptidase/oxytocinase in renal cells.

The placental leucine aminopeptidase (P-LAP)/oxytocinase is a membrane-bound enzyme thought to play an important role during pregnancy. In this study, we identified the presence of P-LAP protein in the renal distal tubules and collecting ducts. In rat NRK52E cells derived from renal tubules, P-LAP was localized mainly in the intracellular compartment. Upon the treatment of cells with 8-arginine-vasopressin (AVP), a significant increase in the surface level of P-LAP was observed. [deamino-Cys1, d-Arg8]-vasopressin (DDAVP), a specific V2 receptor agonist, increased the surface level of P-LAP, while [adamantaneacetyl1, O-Et-d-Tyr2, Val4, aminobutyryl6, Arg8,9]-vasopressin (AEAVP), a potent V2 receptor antagonist, blocked the AVP-stimulated enhancement. Moreover, reagents known to enhance the intracellular level of cAMP have also been shown to increase the surface level of P-LAP. When we examined the colocalization of P-LAP with the cell surface water channel aquaporin-2 (AQP-2) that is regulated by AVP, the P-LAP-containing vesicles had a relatively higher density than the AQP-2-containing vesicles, suggesting that P-LAP and AQP-2 are differently distributed in NRK52E cells. These results suggest that AVP induces the translocation of P-LAP via V2 receptor and P-LAP plays a role in the regulation of excessive AVP level in the renal collecting duct, acting as a negative feedback mechanism for the AVP action of regulating water reabsorption.     

Diabetes Diminishes the Portal-Systemic Collateral Vascular Response to Vasopressin via Vasopressin Receptor and Gα Proteins Regulations in Cirrhotic Rats

Liver cirrhosis may lead to portal-systemic collateral formation and bleeding. The hemostatic effect is influenced by the response of collateral vessels to vasoconstrictors. Diabetes and glucose also influence vasoresponsiveness, but their net effect on collaterals remains unexplored. This study investigated the impact of diabetes or glucose application on portal-systemic collateral vasoresponsiveness to arginine vasopressin (AVP) in cirrhosis. Spraque-Dawley rats with bile duct ligation (BDL)-induced cirrhosis received vehicle (citrate buffer) or streptozotocin (diabetic, BDL/STZ). The in situ collateral perfusion was done after hemodynamic measurements: Both were perfused with Krebs solution, D-glucose, or D-glucose and NaF, with additional OPC-31260 for the BDL/STZ group. Splenorenal shunt vasopressin receptors and G_α proteins mRNA expressions were evaluated. The survival rate of cirrhotic rats was decreased by STZ injection. The collateral perfusion pressure changes to AVP were lower in STZ-injected groups, which were reversed by OPC-31260 (a V₂R antagonist) and overcome by NaF (a G protein activator). The splenorenal shunt V₂R mRNA expression was increased while G_α proteins mRNA expressions were decreased in BDL/STZ rats compared to BDL rats. The G_αq and G_α11 mRNA expressions also correlated with the maximal perfusion pressure changes to AVP. Diabetes diminished the portal-systemic collateral vascular response to AVP in rats with BDL-induced cirrhosis, probably via V₂ receptor up-regulation and G_α proteins down-regulation.     

AT1a receptor signaling is required for basal and water deprivation-induced urine concentration in AT1a receptor-deficient mice

It is well recognized that ANG II interacts with arginine vasopressin (AVP) to regulate water reabsorption and urine concentration in the kidney. The present study used ANG II type 1a (AT(1a)) receptor-deficient (Agtr1a(-/-)) mice to test the hypothesis that AT(1a) receptor signaling is required for basal and water deprivation-induced urine concentration in the renal medulla. Eight groups of wild-type (WT) and Agtr1a(-/-) mice were treated with or without 24-h water deprivation and 1-desamino-8-d-AVP (DDAVP; 100 ng/h ip) for 2 wk or with losartan (10 mg/kg ip) during water deprivation. Under basal conditions, Agtr1a(-/-) mice had lower systolic blood pressure (P < 0.01), greater than threefold higher 24-h urine excretion (WT mice: 1.3 ± 0.1 ml vs. Agtr1a(-/-) mice: 5.9 ± 0.7 ml, P < 0.01), and markedly decreased urine osmolality (WT mice: 1,834 ± 86 mosM/kg vs. Agtr1a(-/-) mice: 843 ± 170 mosM/kg, P < 0.01), without significant changes in 24-h urinary Na(+) excretion. These responses in Agtr1a(-/-) mice were associated with lower basal plasma AVP (WT mice: 105 ± 8 pg/ml vs. Agtr1a(-/-) mice: 67 ± 6 pg/ml, P < 0.01) and decreases in total lysate and membrane aquaporin-2 (AQP2; 48.6 ± 7% of WT mice, P < 0.001) and adenylyl cyclase isoform III (55.6 ± 8% of WT mice, P < 0.01) proteins. Although 24-h water deprivation increased plasma AVP to the same levels in both strains, 24-h urine excretion was still higher, whereas urine osmolality remained lower, in Agtr1a(-/-) mice (P < 0.01). Water deprivation increased total lysate AQP2 proteins in the inner medulla but had no effect on adenylyl cyclase III, phosphorylated MAPK ERK1/2, and membrane AQP2 proteins in Agtr1a(-/-) mice. Furthermore, infusion of DDAVP for 2 wk was unable to correct the urine-concentrating defects in Agtr1a(-/-) mice. These results demonstrate that AT(1a) receptor-mediated ANG II signaling is required to maintain tonic AVP release and regulate V(2) receptor-mediated responses to water deprivation in the inner medulla.     

Urinary excretion of aquaporin-2 and inappropriate secretion of vasopressin in hyponatremic patients after cerebral infarction.

Aquaporin-2, a water-channel protein, is known to increase water permeability due to vasopressin binding to V2 receptors at the renal collecting duct and is excreted into the urine. It is still unclear whether a hyponatremic state is caused by vasopressin-dependent aquaporin-2 in patients clinically diagnosed with the syndrome of inappropriate secretion of antidiuretic hormone. To determine this, we measured urinary aquaporin-2 and vasopressin by radioimmunoassay in normonatremic or hyponatremic patients after cerebral infarction and in healthy controls. In the normonatremia group, urinary aquaporin-2 and plasma AVP levels were higher than in controls. In the hyponatremia group, plasma AVP was relatively high despite low plasma osmolality in each patient. However, urinary aquaporin-2 in hyponatremia was significantly increased when compared with the other two groups. In conclusion, AQP-2 increment does not directly reflect non-osmotic AVP secretion in a hyponatremic state. This result indicates that the urinary excretion of AQP-2 is not only AVP-dependent in hyponatremic states.     

Shortening of bleeding time after intranasal administration of 1-deamino-8-D-arginine vasopressin to patients with chronic uremia

1-deamino-8-D-arginine vasopressin (DDAVP) was administered intranasally in a dose of 2 micrograms/kg BW to 17 uremic patients (16 maintained on chronic hemodialysis and 1 treated conservatively). The bleeding time was significantly shortened 120 minutes after DDAVP administration (from 18.1 +/- 7.5 minutes to 12.3 +/- 6.4 minutes p less than 0.001). Factor VIII related antigen (VIII: Ag) did not change. Factor VIII ristocetin cofactor activity (VIII: RCof) significantly increased (from 251.2 +/- 162.0 to 336.5 +/- 167.2 p less than 0.025). Platelet count decreased significantly after DDAVP (from 174.9 +/- 43.8 X 10(9)/l to 155.6 +/- 45.9 X 10(9)/l 30 minutes p less than 0.01 and 129.8 +/- 45.2 X 10(9)/l p less than 0.005 120 minutes after DDAVP). Antithrombin III concentration, and hematocrit did not change. Our data indicate that further clinical studies of intranasal DDAVP in uremic patients during episodes of bleeding are warranted.     

Upregulation of collecting duct aquaporin-2 by metabolic acidosis: role of vasopressin

Metabolic acidosis is associated with alteration in fluid and electrolyte reabsorption in a number of nephron segments. However, the effects of metabolic acidosis on urine osmolality and aquaporin-2 (AQP-2) remain poorly understood. In these studies, we examined the effects of chronic metabolic acidosis on water handling by the kidney. Rats were placed in metabolic cages and subjected to water (control) or 280 mM NH₄Cl loading for 120 h to induce metabolic acidosis. The results indicated a significant increase in urine osmolality with no change in urine volume or urinary Na⁺ excretion in acid-loaded animals. This effect was independent of alteration in fluid intake or salt/Cl^- loading. Immunoblotting and Northern hybridization studies indicated that AQP-2 protein abundance and mRNA expression levels increased significantly along the collecting duct system of NH₄Cl-but not NaCl-loaded animals. RIA results indicated that metabolic acidosis was associated with a fourfold increase in circulating levels of vasopressin (AVP) and a significant increase in brain AVP mRNA expression levels. In conclusion, metabolic acidosis upregulates the expression levels of AQP-2 and increases urine osmolality, suggesting an adaptive increase in water reabsorption in the collecting duct. A concomitant increase in AVP synthesis and secretion likely plays an essential role in the adaptation of AQP-2 in metabolic acidosis. kidney; acid-base; urine osmolality; sodium excretion rate     

"U"字缝合止血法对前置胎盘剖宫产患者术中出血量的影响

目的:探讨"U"字缝合止血法对前置胎盘剖宫产患者术中出血量的影响。方法:将2015年9月至2017年9月在西北妇女院儿童医院行前置胎盘剖宫产术的产妇96例作为研究对象,将其随机分组为两组,每组各48例患者。两组均给予常规止血处理,对照组采用"8"字缝合止血法,观察组为"U"字缝合止血法,比较两组手术指标及止血效果。结果:观察组手术时间、止血时间、术中出血量均显著少(短)于对照组(P0.05),凝血酶时间(TT)、血浆凝血酶还原时间(PT)、D-二聚体(D-D)、血小板(PLT)以及活化部分凝血活化酶时间(APTT)水平均明显低于对照组(P0.05),血红蛋白(HGB)、纤维蛋白原(FIB)水平均显著高于对照组(P0.05);止血有效率[97.92%(47/48)]显著高于对照组[85.42%(41/48)](P0.05),患者下床活动时间、住院治疗时间均显著短于对照组(P0.05)。结论:在前置胎盘剖宫产术中,实施"U"字缝合止血法可快速止血,且操作简单,确保降低出血量,降低对患者的损害,保证产妇健康和安全。     

Effect of vasopressin and its analogs on blood coagulation in rats

A change in the response of the blood coagulation system to the intravenous injection of vasopressin (AVP), DDAVP and DGAVP has been studied in the experiments on white rats. Intensification of the procoagulant activity on AVP is of the dose-dependent character. Maximal effect is observed 5-15 min after i.v. injection of AVP in a dose of 4 mg/kg. The administration of this peptide increases the fibrinolytic activity, that is connected with an increase in the level of plasminogen activator. DDAVP and DGAVP have a weaker effect on fibrinolysis. AVP and DDAVP increase the level of FVIII by 5-6% during the first minutes, but DGAVP increases the level of FVIII only after 15-30 minutes. While using AVP, DDAVP and DGAVP in clinical practice it is necessary to allow for their hormonal action, the initial state of haemostasis and the age of patients.     

Intracellular pathways of V(1) and V(2) receptors activated by arginine vasopressin in rat hippocampal neurons.

To explore the intracellular pathways activated by vasopressin receptors, the effects of arginine vasopressin (AVP) and its analogues mediating glycine (Gly)-induced Cl(-) currents (I(Gly)) were examined in acutely dissociated rat hippocampal CA1 neurons using the whole-cell patch recording technique. AVP and its analogues inhibited I(Gly) in a concentration-dependent manner. The inhibitory actions of AVP(4-9) (AVP metabolite) and NC-1900 (AVP(4-9) analogue) were reversed by a V(1) receptor antagonist, or pretreatment with 1,2-bis(2-amino-5-fluorophenoxy)ethane-N,N,N', N'-tetraacetic acid. In contrast, these blocking procedures had no effect on the 1-desamino-8-D-AVP (DDAVP; V(2) agonist) action. A V(2) receptor antagonist did not block the inhibitory action of AVP(4-9) or NC-1900, but blocked that of DDAVP. The inhibitory action of AVP was completely blocked by the co-application of the V(1) and V(2) antagonists. The inhibitory action of NC-1900 was not affected by perfusion with a Ca(2+)-free external solution, but was strongly blocked by thapsigargin. The intracellular application of heparin or anti-inositol 1,4,5-triphosphate (IP(3)) also blocked the NC-1900 action. Furthermore, Ca(2+)/calmodulin (CaM) inhibitors blocked the NC-1900 action, while a CaM-dependent kinase II inhibitor and PKC modulators had no effect. 2',5'-Dideoxyadenosine (an adenylate cyclase inhibitor), H-89, and Rp-cAMPS blocked the inhibitory actions of NC-1900 and DDAVP. These results suggest that the activation of the V(1) receptor in the hippocampal neurons induces the production of IP(3), which releases Ca(2+) from the IP(3)-sensitive Ca(2+) storage sites. The Ca(2+) binds to CaM, resulting in the activation of Ca(2+/)CaM-sensitive adenylate cyclases. The activation of protein kinase A through the adenylate cyclase inhibits I(Gly).     

Upregulation and protein trafficking of aquaporin-2 attenuate cold-induced osmotic damage during cryopreservation

Aquaporins (AQPs) are a recently discovered family of proteins that function as transmembrane water channels. These proteins regulate the delicate osmotic balance across the cell plasma membrane. Given that osmotic damage is the major contributing factor to cell death during freezing, we hypothesized that regulation of AQPs may have an unrealized role in protecting cells from osmotic damage during cryopreservation. Rat kidney inner medullar collecting duct (IMCD) cells were treated with arginine vasopressin (AVP) to increase the amount of AQP2 in the external plasma membrane before freezing in University of Wisconsin solution at -4 degrees C for 24 h. This resulted in a significant increase in cell viability on warming. Conversely, treatment of IMCD cells with AVP and W7 (which inhibits AQP2 protein trafficking to the plasma membrane) before freezing resulted in a 55% decrease in cell viability. These preliminary data indicate that regulation of AQP2 can attenuate cold-induced osmotic damage in rat kidney IMCD cells.     

Study on mechanisms of a haemostatic effect of 1 deamino-8-D-arginine vasopressin (desmopressin) in uraemic patients.

The effect of 1 deamino-8-D-arginine vasopressin (DDAVP) on blood platelet serotonin and some parameters of haemostasis was investigated. DDAVP was administered intravenously in a dose of 0.4 micrograms/kg BW to 16 uraemic patients maintained on chronic haemodialysis in a double-blind crossover study compared with placebo. The bleeding time was significantly shortened after DDAVP administration from 21.3 +/- 8 minutes to 11.5 +/- 6 minutes (p less than 0.001). VIII: Ag increased from 239.1 +/- 94% to 473 +/- 293% (p less than 0.01). Euglobulin lysis time was shortened from 238 +/- 101 to 148 +/- 84 minutes (p less than 0.005). The platelet serotonin level was significantly reduced from 532 +/- 141 to 366 +/- 88 ng/10(9) platelets (p less than 0.02). There were no changes in haematocrit, platelet count, VIII: C levels and blood serotonin concentrations after DDAVP administration. In placebo group there were no changes in all investigated parameters. Our data indicate that DDAVP shortens prolonged bleeding time in uraemic probably by means of the serotonergic mechanism. Further studies are needed to confirm this suggestion.     

Hydroosmotic activities of arginine-vasopressins modified either in positions 1, 2 and 4 or at N-terminal extensions.

Vasopressin and its synthetic analogs were studied for their effect on transepithelial water flux in frog urinary bladder. As compared with AVP, 1-deamino-8-D-arginine vasopressin (dDAVP) was about 40 times less effective in stimulating osmotic water flow. The vasopressin analogs obtained by modification in positions 1 and 2 were: [1-(1-mercapto-4-tert-butylcyclohexaneacetic acid)] AVP (I); [1-(1-mercapto-4-methylcyclohexaneacetic acid)]AVP (II); [1-(1-mercapto-4-methylcyclohexaneacetic acid)-2-O-methyltyrosine]AVP (III); and those modified in position 4 were: [1-(1-mercaptocyclohexaneacetic acid)-4-arginine] AVP (IV); [1-(2-mercaptopropionic acid)-4-arginine]AVP (V). Any of the above analogs did not influence basal, but antagonized vasopressin-stimulated water flux. N-terminally extended analogs of AVP: Ala-AVP (VI); Ser-Ala-AVP (VII) and Thr-Ser-Ala-AVP (VIII) stimulated osmotic water flux to the same extent in concentration 200 times higher as that of AVP. We conclude from these studies that vasopressin analogs (I-V) competitively antagonize vasopressin-stimulated hydroosmotic activity in frog urinary bladder probably at the epithelial vasotocin V1 and/or V2 receptor site. N-terminal extension of the vasopressin molecule did not influence the capacity of AVP to induce V2 receptor-mediated action, even when used at higher concentrations.     

Rat renal cell monolayer culture: a sensitive method for investigating ADH and PTH actions on the kidney by determining adenosine 3' :5'-cyclic monophosphate

The response of cAMP to antidiuretic hormone (ADH) was studied using rat renal medullary cells in a monolayer culture. In addition, cAMP response to parathyroid hormone (PTH) was studied in renal cortical cells. As the culture aged, an increase in basal cAMP content and a gradual decrease in the cAMP responsiveness to arginine vasopressin (AVP) were observed. After 2 days of culture, AVP and hPTH-(1-34) produced a rapid increase in intracellular cAMP with single peaks, after 10 min and 5 min, respectively. Extracellular cAMP was increased linearly by both AVP and hPTH-(1-34). The response of cAMP to AVP was markedly greater in the medulla than in the cortex, while the response to hPTH-(1-34) was remarkable only in the cortex. Outstanding sensitivity of cAMP responsiveness was observed in this system, i.e., 10(-12) M AVP (1 pg/ml) and 2.43 X 10(-10) M hPTH-(1-34) (1 ng/ml) provoked significant increases in cAMP from the basal level of 0.31 +/- 0.04 and 0.59 +/- 0.05 pmol/dish to 0.79 +/- 0.03 and 1.07 +/- 0.13 pmol/dish, respectively (P less than 0.001). In the medulla, potencies of lysine vasopressin (LVP), DDAVP and oxytocin at a concentration of 10(-9) M were 76.1%, 154.2% and 8.1% of that of AVP, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Vasopressin analgesia: specificity of action and non-opioid effects

Recent neuroanatomical and behavioral evidence has indicated that vasopressin (VP) increases pain thresholds. In the present study intracerebroventricular (ICV) administration of both arginine VP (AVP: 75-500 ng) and 1-deamino-8-D-arginine vasopressin (DDAVP: 150-500 ng) elevated tail flick latencies. Oxytocin (OXY, ICV), also elevated tail-flick latencies (150-1000 ng); however this increase was accompanied by "barrel-roll" seizure activity. VP analgesia was eliminated by pretreatment with 1-deamino-penicillamine-2(O-methyl)tyrosine-AVP (dPTyr(me)AVP: 500 ng, ICV), a VP antagonist, but not naloxone (1 or 10 micrograms, ICV), suggesting that VP modulates nonciceptive thresholds through its own binding sites. Conversely, pretreatment with naloxone (1 micrograms, ICV) but not dPTyr(me)AVP (1 microgram, ICV) attenuated the analgesic efficacy of systemic morphine (10 mg/kg), further dissociating VP and central opiate analgesic processes. Finally, systemic pretreatment with dexamethasone potentiated VP analgesia. These data support the notion that VP is a specific non-opioid pain inhibitor.     

内镜止血在急性非静脉曲张性上消化道出血治疗中的临床应用

目的:探讨内镜下金属钛夹止血在急性非静脉曲张性上消化道出血治疗中的应用价值。方法:按照随机数字表法将2014年1月-2014年12月我院收治的40例急性非静脉曲张性上消化道出血患者分为观察组(n=20)及对照组(n=20),观察组行内镜下金属钛夹止血治疗,对照组予以内镜下药物注射,比较两组治疗后的止血效果、临床疗效及并发症情况。结果:观察组患者治疗后的有效止血率、即时止血率为95.00%、100.00%,分别高于对照组的65.00%、75.00%,差异有统计学意义(P0.05)。治疗后观察组临床疗效优于对照组,差异有统计学意义(P0.05)。治疗后两组患者均未出现严重并发症。结论:内镜下金属钛夹止血用于急性非静脉曲张性上消化道出血具有止血效果好、并发症少等特点,临床有重要的参考价值。