Celiac Artery Vasculitis.

Isolated celiac artery vasculitis is an uncommon disease rarely reported in the Western literature. In this case report, we describe a 52-year-old Chinese male presenting with abdominal pain who was diagnosed with nonspecific celiac artery vasculitis and was successfully treated with a short course of oral corticosteroids.

Optimal management strategy for spontaneous isolated dissection of a visceral artery.

Objectives To describe our clinical experiences and recommend a management strategy for spontaneous isolated dissection of a visceral artery. Methods A retrospective study of patients from December 2005 to December 2015 was performed. Thirty-two patients had spontaneous isolated dissection of a visceral artery. Clinical features, computed tomography findings, the treatment method, and follow-up results were evaluated. Results There were 28 men and 4 women (mean age, 54 years). Dissection locations were the celiac artery in 10, superior mesenteric artery in 17, and celiac artery and superior mesenteric artery in 5 patients. Celiac artery stenosis existed with spontaneous isolated dissection of a visceral artery at a high rate. After diagnosis, the blood pressure of all patients was immediately controlled to a lower level. Three patients with arterial rupture and one patient with bowel infarction underwent operations for complications. Overall, the treatment of dissection involved drug therapy alone. The last follow-up computed tomography results of the true lumen residual ratio and the length of the dissected artery improved compared to the values on admission; the maximum diameter of the dissected artery did not enlarge. Eleven patients almost completely improved. No patients had any adverse event. Conclusions Most patients with spontaneous isolated dissection of a visceral artery can be first treated conservatively for dissection with strict blood pressure control and surveillance.

Medical therapy and intervention do not improve uncomplicated isolated mesenteric artery dissection outcomes over observation alone.

OBJECTIVE: Isolated dissection of the mesenteric vessels is rare but increasingly recognized. This study aimed to evaluate patient characteristics, primary treatment, and subsequent outcomes of mesenteric dissection using multi-institutional data. METHODS: All patients at participant hospitals between January 2003 and December 2015 with dissection of the celiac artery (or its branches) or dissection of the superior mesenteric artery (SMA) were included. Patients with an aortic dissection were excluded. Demographic, treatment, and follow-up data were collected. The primary outcomes included late vessel thrombosis (LVT) and aneurysmal degeneration (AD). RESULTS: Twelve institutions identified 227 patients (220 with complete treatment records) with a mean age of 55 ± 12.5 years. Median time to last follow up was 15 months (interquartile range, 3.8-32). Most patients were men (82% vs 18% women) and symptomatic at presentation (162 vs 65 asymptomatic). Isolated SMA dissection was more common than celiac artery dissection (n = 158 and 81, respectively). Concomitant dissection of both arteries was rare (n = 12). The mean dissection length was significantly longer in symptomatic patients than in asymptomatic patients in both the celiac artery (27 vs 18 mm; P = .01) and the SMA (64 vs 40 mm; P < .001). Primary treatment was medical in 146 patients with oral anticoagulation or antiplatelet therapy (n = 76 and 70, respectively), whereas 56 patients were observed. LVT occurred in six patients, and 16 patients developed AD (3% and 8%, respectively). For symptomatic patients without evidence of ischemia (n = 134), there was no difference in occurrence of LVT with medical therapy compared with observation alone (9% vs 0%; P = .35). No asymptomatic patient (n = 64) had an episode of LVT at 5 years. AD rates did not differ among symptomatic patients without ischemia treated with medical therapy or observed (9% vs 5%; P = .95). Surgical or endovascular intervention was performed in 18 patients (3 ischemia, 13 pain, 1 AD, 1 asymptomatic). Excluding the patients treated for ischemia, there was no difference in LVT with surgical intervention vs medical management (one vs five; P = .57). CONCLUSIONS: Asymptomatic patients with isolated mesenteric artery dissection may be observed and followed up with intermittent imaging. Symptomatic patients tend to have longer dissections than asymptomatic patients. Symptomatic isolated mesenteric artery dissection without evidence of ischemia does not require anticoagulation and may be treated with antiplatelet therapy or observation alone.

Cholecystokinin-33, but not cholecystokinin-8 shows gastrointestinal site specificity in regulating feeding behaviors in male rats.

Two separate experiments were performed to localize the gastrointestinal sites of action regulating meal size (MS), intermeal interval (IMI) length and satiety ratio (SR, IMI/MS) by cholecystokinin (CCK) 8 and 33. Experiment 1: CCK-8 (0, 0.05, 0.15, 0.25nmol/kg) was infused in the celiac artery (CA, supplies stomach and upper duodenum) or the cranial mesenteric artery (CMA, supplies small and part of the large intestine) prior to the onset of the dark cycle in free feeding, male Sprague Dawley rats and MS (normal rat chow), IMI and SR were recorded. Experiment 2: CCK-33 (0, 0.05, 0.15, 0.25nmol/kg) were infused in the CA or the CMA, under the same experimental conditions above, and MS, IMI and SR were recorded. Experiment 1 found that CCK-8 reduces MS, prolongs the IMI and increases the SR at sites supplied by both arteries. Experiment 2 found that CCK-33 reduces MS and increases the SR at sites supplied by the CMA. We conclude that in male rats the feeding behaviors evoked by CCK-33, but not CCK-8, are regulated at specific gastrointestinal sites of action.

The BB2 receptor antagonist BW2258U89 attenuates the feeding responses evoked by exogenous gastrin releasing peptide-29.

This confirmatory work is aimed to test that the hypothesis that the gastrin releasing peptide (GRP) receptor - the BB2 receptor - is necessary for reduction of meal size (MS) and prolongation of the intermeal interval (IMI) by the small and the large forms of GRP in the rat, GRP-10 and GRP-29, and to confirm the sites of action regulating such responses - the vascular bed of the celiac artery (CA, supplying stomach and upper duodenum). To pursue these aims we measured first MS and IMI length in response to GRP-10 and GRP-29 (0, 0.5nmol/kg) infused in the CA (n=8 rats) and the cranial mesenteric artery (CMA, supplying the small and part of the large intestine, n=8 rats) in near spontaneously free feeding rats pretreated with the BB2 receptor antagonist BW2258U89 (0.1mg/kg) in the same arteries prior to the onset of the dark cycle. We found that GRP-29, but not GRP-10, infused by the CA reduced MS and prolonged the IMI by decreasing meal latency and meal duration and the BB2 receptor antagonist BW2258U89 infused in the same artery attenuated these responses. These results suggest that the BB2 receptor is necessary for reduction of MS and prolongation of the IMI by exogenous GRP-29, and the vascular bed of the CA, stomach and upper duodenum, contains sites of action regulating these feeding responses.

Exogenous glucagon-like peptide-1 acts in sites supplied by the cranial mesenteric artery to reduce meal size and prolong the intermeal interval in rats.

Three experiments were done to better assess the gastrointestinal (GI) site(s) of action of GLP-1 on food intake in rats. First, near-spontaneous nocturnal chow meal size (MS), intermeal intervals (IMI) length and satiety ratios (SR = MS/IMI) were measured after infusion of saline, 0.025 or 0.5 nmol/kg GLP-1 into the celiac artery (CA, supplying the stomach and upper duodenum), cranial mesenteric artery (CMA, supplying small and all of the large intestine except the rectum), femoral artery (FA, control) or portal vein (PV, control). Second, infusion of 0.5 nmol/kg GLP-1 was tested after pretreatment with the GLP-1 receptor (GLP-1R) antagonist exendin-4(3-39) via the same routes. Third, the regional distribution of GLP-1R in the rat GI tract was determined using rtPCR. CA, CMA and FA GLP-1 reduced first MS relative to saline, with the CMA route more effective than the others. Only CMA GLP-1 prolonged the IMI. None of the infusions affected second MS or later eating. CA and CMA GLP-1 increased the SR, with the CMA route more effective than the CA route. CMA exendin-4 (3-39) infusion reduced the effect of CMA GLP-1. Finally GLP-1R expression was found throughout the GI tract. The results suggest that exogenous GLP-1 acts in multiple GI sites to reduce feeding under our conditions and that GLP-1R in the area supplied by the CMA, i.e., the small and part of the large intestine, plays the leading role.

The Effect of Milrinone on Splanchnic and Cerebral Perfusion in Infants With Congenital Heart Disease Prior to Surgery: An Observational Study.

Despite the advancement in the postoperative care of neonates with congenital heart disease (CHD), there is little information on preoperative management of systemic and regional hemodynamics, which may be related to outcomes. We aimed to determine the preoperative effect of milrinone, a phosphodiesterase III inhibitor, on cardiac output and splanchnic and cerebral perfusion in neonates with CHD. Neonates with CHD requiring cardiac surgery were enrolled in a prospective, single-blinded study once a clinical decision of starting milrinone (0.75 µg/kg per minute intravenously) using institutional criteria was made. Demographic and clinical variables and outcomes were recorded. Combined cardiac output and measures of splanchnic (superior mesenteric and celiac arteries) and cerebral (anterior and middle cerebral arteries) perfusion were determined by Doppler studies at 0, 6, 24, and 48 h after milrinone infusion. Investigators were unaware of intervention time points and patients in analyzing blood flow measurements. Seventeen term (39.2 ± 1.3 weeks) neonates were included with hypoplastic left-sided heart syndrome (78.5%) as the most common diagnosis. Combined cardiac output increased by 28% within 48 h (613 ± 154 vs. 479 ± 147 mL/kg per minute at baseline, P < 0.05). Superior mesenteric artery mean velocity increased at 6 h and throughout 48 h of milrinone infusion (P < 0.05). Peak and mean velocities at cerebral arteries increased with milrinone infusion (P < 0.05~0.08), and the corresponding changes at celiac artery were modest. There were no significant changes in splanchnic and cerebral resistive and pulsatility indices during milrinone infusion. Milrinone increases cardiac output with concurrent effects on splanchnic and cerebral blood flows during the short-term preoperative use in neonates with CHD.

The circulatory and renal sympathoinhibitory effects of gastric leptin are altered by a high fat diet and obesity.

Gastric leptin elicits its cardiovascular and splanchnic sympathoinhibitory responses via a vagal afferent mechanism, however the latter are blunted/abolished in animals fed a medium high fat diet (MHFD). In a diet-induced obesity model we sought to determine whether the renal sympathetic nerve discharge (RSND) and regional vasodilator responses to gastric leptin are also affected by diet and/or obesity. The diet induced obesity model was used in 2 separate studies. After 13 weeks on a MHFD the animals were classified as either obesity prone (OP) or obesity resistant (OR) depending on their weight gain. Control animals were fed a low fat diet for an equivalent period. Arterial pressure (AP) and heart rate (HR) were monitored in isoflurane-anaesthetised, artificially ventilated animals and RSND or regional vascular responses to leptin (15 µg/kg) administered close to the coeliac artery were evaluated. OP rats had higher baseline AP compared to control/OR rats (P<0.05). Close arterial leptin inhibited RSND in control animals but this response was abolished in OR and OP animals (P<0.01 for both). Leptin administration increased renal vascular conductance in control animals but this response was significantly attenuated only in OP animals (P<0.05). The vasodilator response in the superior mesenteric artery was not significantly different in any of the groups (P>0.05). Together these results suggest that, while the renal sympathoinhibitory responses to gastric leptin are affected by diet, the vasodilator responses to leptin in the renal vascular bed are only affected in OP animals. These changes may impact on cardiovascular homeostatic mechanisms in obesity.

Intravenous vasopressin for the prevention of nontarget gastrointestinal embolization during liver-directed cancer treatment: experimental study in a porcine model.

PURPOSE: The aim of this study was to evaluate the potential for intravenous vasopressin to reduce the risk of nontarget gastrointestinal embolization during transcatheter liver-directed cancer therapies in a porcine model. MATERIALS AND METHODS: An angiographic catheter was used to select the celiac or common hepatic artery under fluoroscopic guidance in six anesthetized pigs. After angiography of the hepatic and splanchnic territories was performed, technetium-99m macroaggregated albumin ((99m)Tc-MAA) was injected through the catheter. Serial arteriograms were obtained before, every 5 minutes during, and after peripheral intravenous vasopressin infusion at 0.4 U/min for a minimum of 20 minutes. After 10 minutes of infusion, indium-111 ((111)In)-MAA was injected through the arterial catheter. Quantitative comparisons of liver and gastrointestinal activity using dual-isotope single-photon emission computed tomography (SPECT)/CT imaging were performed. RESULTS: Catheter angiography demonstrated reduced blood flow to the splanchnic vasculature while maintaining blood flow through the hepatic arteries during vasopressin infusion. Angiographic findings correlated with the relative distribution of (99m)Tc-MAA (before the vasopressin infusion) and (111)In-MAA (after the vasopressin infusion) on SPECT/CT. The increased ratio of liver to gastrointestinal tract activity during the vasopressin infusion was statistically significant (6.2:11.4, respectively; P = .018). CONCLUSIONS: Intravenous vasopressin reduces arterial blood flow to the splanchnic vasculature while preserving hepatic arterial blood flow in a healthy porcine model. Intraprocedural vasopressin administration has the potential to benefit liver-directed cancer therapies by enhancing tumor targeting as well as preventing the unintended delivery of bland embolic, chemoembolic, or radioembolic agents into the gastrointestinal vascular territories.

Proteus Takayasu's arteritis with unusual intracranial granulomatosis as initial manifestation.

Takayasu's arteritis (TA) is an inflammatory vasculitis of aorta and its branches, its low incidence limited our recognition to this entity. We sometimes can confuse this disease with polyarteritis nodosa and other vasculitis when no conventional "big artery" involved in TA cases. Here we report a 26-year-old man with Takayasu's arteritis who presented with a provisional intracranial granulomatosis first and then saccular aneurysms between celiac trunk and arteria hepatica communis and many other proteus manifestations, which is seldom described before.

Effects of fenoldopam mesylate infusion on splanchnic perfusion after myocardial revascularization on cardiopulmonary bypass: an ultrasound Doppler study.

OBJECTIVES: To measure the effects of fenoldopam mesylate infusion on splanchnic blood flow in patients undergoing myocardial revascularization with cardiopulmonary bypass. DESIGN: An experimental observational study. SETTING: A single-institution community hospital. PARTICIPANTS: Eighteen patients undergoing on-pump coronary artery bypass graft surgery. INTERVENTIONS: Fenoldopam mesylate infusion (0.1 µg/kg/min). MEASUREMENTS AND MAIN RESULTS: Blood flow through the celiac artery, superior mesenteric artery, portal vein and hepatic artery were assessed by means of Doppler measurements. The main hemodynamic variables were measured using echocardiography. The infusion of fenoldopam significantly increased the blood flow through both celiac and superior mesenteric arteries by decreasing vascular resistance. The percentage of cardiac output directed to these 2 vessels increased significantly; the increase through the superior mesenteric artery was greater compared with the celiac artery. Portal vein and hepatic artery blood flow also consistently increased. No significant variations were observed with respect to hemodynamic variables. CONCLUSIONS: The infusion of fenoldopam increased the flow through the celiac artery and superior mesenteric artery; the effect was higher for the latter. These changes did not affect the hemodynamic variables.

Cod CGRP and tachykinins in coeliac artery innervation of the Atlantic cod, Gadus morhua: presence and vasoactivity.

The presence and vasoactive effects of native calcitonin gene-related peptide (CGRP), substance P (SP), and neurokinin A (NKA) were studied on isolated small branches of the coeliac artery from Atlantic cod, Gadus morhua, using immunohistochemistry and myograph recordings, respectively. Immunohistochemistry revealed nerve fibers containing CGRP- and SP/NKA-like material running along the wall of the arteries. CGRP induced vasorelaxation of precontracted arteries with a pD(2) value of 8.54 +/- 0.17. Relaxation to CGRP (10(-8) M) was unaffected by L-NAME (3 x 10(-4) M) and indomethacin (10(-6) M) suggesting no involvement of nitric oxide or prostaglandins in the CGRP-induced relaxation. SP and NKA (from 10(-10) to 3 x 10(-7) M) contracted the unstimulated arteries at concentrations from 10(-8) M and above in 42% and 33%, respectively, of the vessels. It is concluded that the innervation of the cod celiac artery includes nerves expressing CGRP-like and tachykinin-like material, and that a vasodilatory response to CGRP is highly conserved amongst vertebrates while the response to tachykinins is more variable.

Effects of a divided high loading dose of caffeine on circulatory variables in preterm infants.

BACKGROUND: A single high loading dose of 25 mg/kg caffeine has been shown to be effective for the prevention of apnoea, but may result in considerable reductions in blood flow velocity (BFV) in cerebral and intestinal arteries. OBJECTIVE: To assess the effects of two loading doses of 12.5 mg/kg caffeine given four hours apart on BFV in cerebral and intestinal arteries, left ventricular output (LVO), and plasma caffeine concentrations in preterm infants. DESIGN: Sixteen preterm neonates of <34 weeks gestation were investigated one hour after the first oral dose and one, two, and 20 hours after the second dose by Doppler sonography. RESULTS: The mean (SD) plasma caffeine concentrations were 31 (7) and 29 (7) mg/l at two and 20 hours respectively after the second dose. One hour after the first dose, none of the circulatory variables had changed significantly. One hour after the second caffeine dose, mean BFV in the internal carotid artery and anterior cerebral artery showed significant reductions of 17% and 19% (p = 0.01 and p = 0.003 respectively). BFV in the coeliac artery and superior mesenteric artery, LVO, PCO2, and respiratory rate had not changed significantly. Total vascular resistance, calculated as the ratio of mean blood pressure to LVO, had increased significantly one and two hours after the second dose (p = 0.049 and p = 0.023 respectively). CONCLUSION: A divided high loading dose of 25 mg/kg caffeine given four hours apart had decreased BFV in cerebral arteries after the second dose, whereas BFV in intestinal arteries and LVO were not affected.

Expression and functional role of the RhoA/Rho-kinase pathway in rat coeliac artery.

1. Rho-kinase (ROK) stimulation represents a key step in the maintenance of agonist-induced contraction, an effect counteracted by nitric oxide (NO) released from the endothelium. The aim of the present study was to characterize the involvement of ROK in smooth muscle contraction of the rat coeliac artery using functional and expression studies. 2. Rings of rat coeliac artery were mounted in 5 mL myographs containing warmed and oxygenated Krebs' solution. Rings were connected to isometric transducers and data were recorded in a PowerLab system (ADInstruments, Colorado Springs, CO, USA). After a 60 min equilibration period, preparations were precontracted with phenylephrine (1 micromol/L). Endothelial integrity was assessed by treating the vessels with acetylcholine (1 micromol/L). Expression of ROKalpha, ROKbeta and RhoA was analysed using western blot, whereas Rho guanine nucleotide exchange factors (RhoGEF) were measured at the mRNA level. 3. The addition of Y-27632 (0.01-30 micromol/L) caused sustained relaxation of rings contracted with phenylephrine (PE; 1 micromol/L), with intact or denuded endothelium (pEC50 = 6.38 +/- 0.03 and 5.65 +/- 0.02, respectively). NG-Nitro-L-arginine methyl ester (100 micromol/L) or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10 micromol/L), but not indomethacin (10 micromol/L), caused marked rightward shifts of the concentration-response curves to Y-27632. The contractile response to KCl (80 mmol/L) was significantly reduced by Y-27632, with a maximal inhibition of 57 +/- 6%. Nifedipine (0.1-100 nmol/L) fully blocked KCl-evoked contractions, but only marginally affected those in response to PE (27 +/- 2% maximal inhibition). At 1 micromol/L, Y-27632 also significantly enhanced relaxations to sodium nitroprusside (SNP; 0.0001-1 micromol/L). 4. At 1 micromol/L, SNP (but not 1 micromol/L Y-27632) significantly elevated the cGMP content above basal levels. Coincubation with SNP and Y-27632 increased cGMP levels, but the results were not significantly different from those in the presence of SNP alone. 5. Western blot analysis revealed the protein expression of RhoA, ROKalpha and ROKbeta. The PDZ-RhoGEF, p115RhoGEF and leukaemia-associated RhoGEF (LARG) mRNA expression in coeliac artery was visualized by electrophoresis on agarose gels. 6. The results clearly demonstrate a role for the RhoA/ROK signalling pathway in the regulation of rat coeliac artery smooth muscle contraction. The findings of the present study suggest that endogenous nitric oxide-induced relaxation is mediated, in part, by inhibition of RhoA/ROK signalling in this tissue.

Spontaneous isolated dissection of the superior mesenteric artery.

A case of a 63-year-old man with isolated dissection of the superior mesenteric artery (SMA), demonstrated by enhanced computed tomography (CT) and abdominal angiography, was admitted to our hospital. The severity of this disease varies from mild to severe; the severe cases require surgery. But the mild cases, like the one presented here, only need conservative therapy. This case demonstrated the usefulness of anticoagulation therapy and the indications for surgical and radiological intervention.

Caffeine impairs cerebral and intestinal blood flow velocity in preterm infants.

OBJECTIVE: In adults, a single dose of 250 mg of caffeine may decrease cerebral blood flow by 30%. In preterm infants, caffeine is commonly used for the treatment and prophylaxis of apnea. The purpose of this investigation was to assess effects of caffeine on circulatory parameters in preterm infants. METHODS: We studied 16 preterm neonates with a mean gestational age (mean +/- standard deviation) of 31 +/- 1.2 weeks (range: 29-33 weeks), birth weight of 1400 +/- 380 g (range: 625-2060 g), and postnatal age of 24 to 72 hours before and 1 and 2 hours after an oral loading dose of 25 mg/kg pure caffeine. We investigated left ventricular output (LVO), cerebral blood flow velocity (BFV) of the internal carotid artery (ICA) and the anterior cerebral artery, and intestinal BFV of the celiac artery and superior mesenteric artery by Doppler sonography. RESULTS: Mean BFV in the ICA decreased significantly 1 (17%) and 2 hours (22%) after caffeine administration. Mean BFV in the anterior cerebral artery showed a reduction of 14% after 2 hours. The mean BFV in the superior mesenteric artery decreased significantly 1 and 2 hours after caffeine administration (30%). Mean BFV in the celiac artery showed a significant reduction of 14% 1 hour after caffeine. No changes were observed in LVO, blood pressure, and heart rate. CONCLUSION: Oral administration of a high loading dose of caffeine results in marked reduction of cerebral and intestinal BFV, without changing LVO, blood pressure, and heart rate.

Neuropeptide Y effects on vasorelaxation and intestinal contraction in the Atlantic cod Gadus morhua.

Neuropeptide Y (NPY) has prominent cardiovascular effects in mammals and sharks, but no such effect has previously been demonstrated in any teleost fish. In the Atlantic cod, we found that cod NPY (10(-10)-10(-6) M) relaxed celiac arteries precontracted with epinephrine, and weak contractions were elicited in intestinal ring preparations. A few NPY-immunoreactive nerve fibers were present along small gut arteries. The results suggest that cod NPY produces vasorelaxation both by a direct action on smooth muscle and by release of prostaglandins, but with no involvement of nitric oxide, leukotrienes, or endothelium-derived relaxing factors. An additional indirect effect involving another neurotransmitter may occur. Cod NPY (10(-7) M) and human NPY (10(-7) M) had identical effects on the vessels. Small differences only in the effects of porcine [Leu(31),Pro(34)]NPY, NPY-(13-36), and cod NPY suggest the presence of a Y(1) subfamily receptor, similar to the zebrafish Ya receptor. A physiological role for NPY in teleost vasculature is concluded, but surprisingly the effect, a vasodilation, is opposite to that in mammals and is mediated by prostaglandins.

Effects of cod bradykinin and its analogs on vascular and intestinal smooth muscle of the Atlantic cod, Gadus morhua.

The effects of [Arg(0),Trp(5),Leu(8)]-BK (cod [Arg(0)]BK) on vascular preparations from branches of the cod celiac artery and on longitudinal smooth muscle preparations from the cod intestine were investigated. Cod [Arg(0)]BK (3 x 10(-8) M) caused a relaxation of the celiac artery precontracted with adrenaline. The relaxation was abolished by the cyclooxygenase inhibitor indomethacin, suggesting that the effect is mediated through the release of prostaglandins, but there was no evidence for the involvement of leukotrienes or nitric oxide in the response. In the intestinal preparations, cod [Arg(0)]BK produced concentration-dependent contractions (pD(2) = 8.28 +/- 0.16). Experiments with N-terminally and C-terminally truncated analogs and with alanine-substituted analogs of cod [Arg(0)]BK demonstrate that the central amino acid Gly(4) and the C-terminal amino acids Leu(8) and Arg(9) are the most important in determining the conformation of the peptide that interacts with the receptor. The results indicate that the ligand binding properties of the cod BK receptor are considerably different from the receptor present in trout tissues and may resemble those of the mammalian B(2) receptor more closely.

[The effects of Xuezhikang on neointimal proliferation and C-myc gene expression after angioplasty in rabbits].

OBJECTIVE: To investigate the effects of Xuezhikang (XZhK) on the neointimal proliferation and C-myc gene expression after angioplasty in rabbits. METHODS: Angioplasty for atherosclerotic stenosis of celiac arteries was performed in 30 male white rabbits after being fed with cholesterol-supplemented diet for 8 weeks, which were then randomized to control group, high-cholesterol group and XZhK group. After 4 weeks, the local vessels were collected for morphological observation. C-myc mRNA level was measured with RT-PCR and C-myc protein with immunohistochemical analysis. RESULTS: Morphological observation showed that the neointimal area in the XZhK group were less than the control group (P < 0.05), and that in control group were less than that in the high-cholesterol group (P < 0.05). The levels of C-myc mRNA measured with RT-PCR and the percentage of C-myc protein positive cell by immunohistochemical analysis were lower in the XZhK group than in the control and high-cholesterol group (P < 0.05), The levels in the latter two groups showed no difference (P > 0.05). CONCLUSION: XZhK can inhibit the neointimal proliferation and the expression of C-myc gene after angioplasty in rabbits.

Peptidergic control of gastrointestinal blood flow in the estuarine crocodile, Crocodylus porosus.

Peptidergic mechanisms influencing the resistance of the gastrointestinal vascular bed of the estuarine crocodile, Crocodylus porosus, were investigated. The gut was perfused in situ via the mesenteric and the celiac arteries, and the effects of different neuropeptides were tested using bolus injections. Effects on vascular resistance were recorded as changes in inflow pressures. Peptides found in sensory neurons [substance P, neurokinin A, and calcitonin gene-related peptide (CGRP)] all caused significant relaxation of the celiac vascular bed, as did vasoactive intestinal polypeptide (VIP), another well-known vasodilator. Except for VIP, the peptides also induced transitory gut contractions. Somatostatin and neuropeptide Y (NPY), which coexist in adrenergic neurons of the C. porosus, induced vasoconstriction in the celiac vascular bed without affecting the gut motility. Galanin caused vasoconstriction and occasionally activated the gut wall. To elucidate direct effects on individual vessels, the different peptides were tested on isolated ring preparations of the mesenteric and celiac arteries. Only CGRP and VIP relaxed the epinephrine-precontracted celiac artery, whereas the effects on the mesenteric artery were variable. Somatostatin and NPY did not affect the resting tonus of these vessels, but somatostatin potentiated the epinephrine-induced contraction of the celiac artery. Immunohistochemistry revealed the existence and localization of the above-mentioned peptides in nerve fibers innervating vessels of different sizes in the gut region. These data support the hypothesis of an important role for neuropeptides in the control of the vascular bed of the gastrointestinal tract in C. porosus.