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PubMedDate not supplied

Transcatheter thoracic duct embolization in the dog. An experimental study.

Thoracic duct embolization was created by injecting an isobutyl 2-cyanoacrylate/iophendylate (IBCA) mixture through a cannulated mesenteric lymphatic vessel in eight normal dogs. Aqueous contrast lymphangiography was repeated at minute 10 and week 6. Six dogs were euthanatized at week 6 and two dogs at month 6. Embolization with 1.5 to 3.9 ml of the mixture resulted in complete obstruction of the thoracic duct in all eight dogs. Results of lymphangiography in six dogs at week 6 showed a persistent, complete obstruction of the thoracic duct in six dogs and alternate lymphaticovenous anastomoses in four dogs. Histologically, there were a sclerosing granulomatous response surrounding the lymphatic embolus, mild congestive changes in the mesenteric lymph nodes, and mild lacteal dilatation in the jejunum. The procedure was well tolerated with only a few complications. One dog suffered partial thrombosis of the cranial vena cava by the injected material with later dislodgement and embolization of a pulmonary artery branch. Modifications have been made in the injection procedure to avoid this complication. This technique for occlusion of the thoracic duct shows potential for clinical use in the management of canine chylothorax. The obstruction appears to be complete and permanent, and surgical/anesthetic time is decreased greatly from previously described procedures.

Animals↗

PubMed1992

Guanethidine sympathectomy of mature rats leads to increases in calcitonin gene-related peptide and vasoactive intestinal polypeptide-containing nerves.

Changes in the innervation of the heart (right atrium), mesenteric blood vessels, vas deferens and superior cervical ganglia have been examined following long-term sympathectomy of the mature rat. Patterns of innervation were investigated by histochemical and immunohistochemical techniques, while levels of noradrenaline and neuropeptides were measured by neurochemical assays. Large doses of guanethidine (80 mg/kg) were given daily for four weeks to 12-14 week-old male rats which were killed at 18-20 weeks of age. Catecholamine-containing nerves were severely depleted or absent in all tissues, together with a reduction in noradrenaline content. Neuropeptide Y levels were depleted by 97% in vas deferens, 78% in mesenteric vein and 50% in right atrium and superior cervical ganglion. Increases in levels of calcitonin gene-related peptide were seen in the mesenteric vein (up seven-fold), superior cervical ganglia (up 11-fold) and vas deferens (prostatic portion up three-fold), which were also evident by assessment of immunolabelling of nerve fibres. Calcitonin gene-related peptide levels were not increased in the right atrium. In addition, an increase in vasoactive intestinal polypeptide-immunoreactive nerve fibre density was seen in the mesenteric artery and vas deferens, although no significant differences were observed in assays of vasoactive intestinal peptide levels in any tissue. No changes were seen in the innervation of any of the tissues by substance P-immunoreactive nerve fibres either by immunohistochemical or immunochemical assay assessment. This study indicates that there are selective changes in the mature nervous system in response to the loss of sympathetic nerves. Differences between these changes and the response of the developing nervous system to long-term sympathectomy are discussed.

Animals↗

PubMed1978

Intravital measurement of arteriolar pressure and tangential wall stress in normotensive and spontaneously hypertensive rats (established hypertension).

Under intravital conditions, intravascular pressures of mesenteric resistance vessels were measured in normotensive (NR, mean blood pressure 92 mm Hg) and spontaneously hypertensive rats (SHR, 161 mm Hg) being elevated over all by about 75%; the tangential wall stress (sigma = p.r/h; p represents the intravascular pressure and r/h the ratio of internal radius to wall thickness) was found to be increased by 120-140% in SHR.

Animals↗

PubMed2002

Changes in NOS activity and protein expression during acute and prolonged ANG II administration.

The aim of this study was to assess the effects of acute or prolonged increases of ANG II on nitric oxide synthase (NOS) activities and protein expression in mesenteric resistance vessels, left ventricle, renal cortex, and renal medulla. The response of NOS activities to ANG II is compared with that induced by phenylephrine. ANG II or phenylephrine were infused over either 3 h or 3 days to conscious rats. NOS activity was examined by measuring the rate of conversion of L-[14C]arginine to L-[14C]citrulline. Protein levels of endothelial (e) and neuronal (n) NOS were determined by Western blot analysis. Arterial pressure (AP) increased (P < 0.05) during acute and prolonged ANG II infusion. Ca2+-dependent NOS activity values (pmol of citrulline x min(-1) x g wet wt(-1)) for control rats were 21 +/- 9 in mesenteric arteries, 13 +/- 7 in left ventricle, 14 +/- 8 in renal cortex, and 411 +/- 70 in renal medulla. Acute ANG II infusion increased (P < 0.05) Ca2+-dependent NOS activity in renal cortex and renal medulla (81 +/- 18 and 611 +/- 48, respectively), but no differences were found in mesenteric arteries and left ventricle with respect to control rats. In contrast to the renal changes in NOS activity, acute ANG II infusion did not modify eNOS or nNOS expression in any of the tissues examined. Prolonged ANG II infusion increased (P < 0.05) Ca2+-dependent NOS activity in mesenteric arteries (70 +/- 17), renal cortex (104 +/- 31), and left ventricle (49 +/- 8) and did not elicit changes in renal medulla. After a prolonged ANG II infusion, eNOS and nNOS levels increased in all tissues examined with the exception of eNOS in the mesenteric arteries and nNOS in the left ventricle, which were not altered. Acute and prolonged phenylephrine infusion elevated AP to a similar extent as ANG II but only elicited significant increments of Ca2+-dependent NOS activity in renal cortex. These data indicate that acute and prolonged elevations in ANG II upregulate Ca2+-dependent NOS activity and protein expression in different tissues related to the control of blood pressure. However, these ANG II effects are heterogeneous with respect to the tissue implicated, the time course of the stimulation, and the NOS isoform involved. Phenylephrine only induces a significant elevation of Ca2+-dependent NOS activity in renal cortex.

Angiotensin II↗

PubMed2002

Liver-derived insulin-like growth factor-I is involved in the regulation of blood pressure in mice.

IGF-I has been suggested to be of importance for cardiovascular structure and function, but the relative role of locally produced and liver-derived endocrine IGF-I remains unclear. Using the Cre-LoxP recombination system, we have previously created transgenic mice with a liver-specific, inducible IGF-I knockout (LI-IGF-I-/-). To examine the role of liver-derived IGF-I in cardiovascular physiology, liver-derived IGF-I was inactivated at 4 wk of age, resulting in a 79% reduction of serum IGF-I levels. At 4 months of age, systolic blood pressure (BP) was increased in LI-IGF-I-/- mice. Echocardiography showed increased posterior wall thickness in combination with decreased stroke volume and cardiac output, whereas other systolic variables were unchanged, suggesting that these cardiac effects were secondary to increased peripheral resistance. Acute nitric oxide-synthase inhibition increased systolic BP more in LI-IGF-I-/- mice than in control mice. LI-IGF-I-/- mice showed impaired acetylcholine-induced vasorelaxation in mesenteric resistance vessels and increased levels of endothelin-1 mRNA in aorta. Thus, the increased peripheral resistance in LI-IGF-I-/- mice might be attributable to endothelial dysfunction associated with increased expression of endothelin-1 and impaired vasorelaxation of resistance vessels. In conclusion, our findings suggest that liver-derived IGF-I is involved in the regulation of BP in mice.

Acetylcholine↗

PubMed2006

Abnormal renovascular parathyroid hormone-1 receptor in hypertension: Primary defect or secondary to angiotensin ii type 1 receptor activation?

We previously reported that PTHrP-induced renal vasodilation is impaired in mature spontaneously hypertensive rats (SHR) through down-regulation of the type 1 PTH/PTHrP receptor (PTH1R), a feature that contributes to the high renal vascular resistance in SHR. Here we asked whether this defect represents a prime determinant in genetic hypertension or whether it is secondary to angiotensin II (Ang II) and/or the mechanical forces exerted on the vascular wall. We found that the treatment of SHR with established hypertension by the Ang II type 1 receptor antagonist, losartan, reversed the down-regulation of PTH1R expression in intrarenal small arteries and restored PTHrP-induced vasodilation in ex vivo perfused kidneys. In contrast, the PTH1R deregulation was not found in intrarenal arteries isolated from prehypertensive SHR. Moreover, this defect, which is not seen in extrarenal vessels (aorta, mesenteric arteries) from mature SHR appeared kidney specific in accordance with the acknowledged enrichment of interstitial Ang II in this organ and its enhancement in SHR. In deoxycorticosterone-acetate-salt rats, an Ang II-independent model of hypertension, renovascular PTH1R expression and related vasodilation were not altered. In SHR-derived renovascular smooth muscle cells (RvSMCs), the PTH1R was spontaneously down-regulated and its transcript destabilized, compared with Wistar RvSMCs, both effects being antagonized by losartan. Exogenous Ang II elicited down-regulation of PTH1R mRNA in RvSMCs from Wistar rats. Together, these data demonstrate that Ang II acts via the Ang II type 1 receptor to destabilize PTH1R mRNA in the renal vessel in the SHR model of genetic hypertension. This process is kidney specific and independent from blood pressure increase.

Angiotensin II↗

PubMed1979

Study on the fixation method of microcirculation system for electron microscopy.

1) Although glutaraldehyde solution was injected into the superior mesenteric artery, vessels and blood cells were not fixed immediately. 2) Glutaraldehyde was considered not to be suitable for the fixation of vessels and blood cells. 3) To observe the physiological and topographical correlation of vessels and blood contents, drop osmium fixation method was better to fix the microcirculatory units immediately. 4) The perfusion of glutaraldehyde was supposed to be necessary for the fixation of the solid tissue in which microcirculatory systems exist in deeper places like liver. However, the findings observed by the perfusion method might reflex microcirculatory disturbances occured by the perfusion of glutaraldehyde itself.

Animals↗

PubMed1985

Pontamine sky blue: a counterstain for background autofluorescence in fluorescence and immunofluorescence histochemistry.

The stain pontamine sky blue (PSB) has been shown to reduce background autofluorescence in catecholamine fluorescence and immunofluorescence histochemical preparations. Using PSB as a counterstain on whole-mount stretch preparations of human mesenteric blood vessels, a medium dense noradrenergic nerve plexus is clearly revealed, which previously had been only partially visible because of background autofluorescence. Image analysis of nerve densities in whole-mount stretch preparations of guinea-pig arteries containing noradrenergic, substance P-, and vasoactive intestinal polypeptide (VIP)-positive nerve plexuses shows that PSB staining does not alter the specific neuronal fluorescence and that it improves image definition.

Animals↗

PubMed2000

5-HT inhibits spontaneous contractility of isolated sheep mesenteric lymphatics via activation of 5-HT(4) receptors.

Spontaneous isometric contractions were measured in rings of sheep mesenteric lymphatic vessels in vitro. 5-Hydroxytryptamine (5-HT) produced a concentration-dependent decrease in spontaneous contraction frequency and force which was not antagonised by either the nonspecific 5-HT(1)/5-HT(2) receptor antagonist methysergide (1 microM) or the 5-HT(3) receptor antagonist ondansetron (1 microM). The 5-HT(4) receptor agonist BIMU-8 mimicked the inhibitory effect of 5-HT and its effects were abolished by the 5-HT(4) receptor antagonist DAU 6285 (1 microM). DAU-6285 also abolished the inhibitory effect of 5-HT and unmasked a weak excitatory response, which was mimicked by the 5-HT(2) receptor agonist alpha-methyl-5-hydroxytryptamine maleate. This excitatory response was, in turn, blocked by the 5-HT(2) receptor antagonist pirenperone (1 microM). The results of this study suggest that sheep mesenteric lymphatics possess both 5-HT(4) receptors and 5-HT(2) receptors. The inhibitory 5-HT(4) receptor appeared to be the predominant subtype since the excitatory response to 5-HT could only be observed in the presence of the 5-HT(4) receptor antagonist DAU 6285.

Animals↗

PubMed1993

Effects of acetylcholine on spontaneous contractions in isolated bovine mesenteric lymphatics.

The effects of acetylcholine (ACh) on spontaneous contractions in isolated bovine mesenteric lymph vessels were investigated. ACh ranging from 3 x 10(-8) M to 10(-5) M produced dose-dependent negative chronotropic and inotropic effects on the spontaneous contractions. In the lymph vessels without endothelium, ACh at the same concentration range had no significant effect on the spontaneous contractions. Atropine (10(-9) and 10(-8) M) caused a parallel shift to the right of the dose-chronotropic response curve for ACh. The pA2 value of atropine to ACh in the negative chronotropic effect was 8.90 +/- 0.20 (n = 6). Aspirin (10(-5) M) produced no significant inhibition of the ACh-induced negative chronotropic and inotropic effects. NG-monomethyl-L-arginine (L-NMMA; 3 x 10(-5) M) significantly suppressed the ACh-induced negative responses on spontaneous contractions. In the same lymphatic segments, L-arginine (10(-4) M) reversed completely the inhibition by L-NMMA of the ACh-induced responses. These results suggest that low concentrations of ACh produce negative chronotropic and inotropic effects on spontaneous contractions in bovine mesenteric lymphatics and that the responses may be mediated by nitric oxide or its related compound released from the endothelial cells through activation of low-affinity muscarinic receptors.

Acetylcholine↗

PubMed2000

Beneficial insulin-sensitizing and vascular effects of S15261 in the insulin-resistant JCR:LA-cp rat.

S15261, a compound developed for the oral treatment of type II diabetes, is cleaved by esterases to the fragments Y415 and S15511. The aim was to define the insulin-sensitizing effects of S15261, the cleavage products, and troglitazone and metformin in the JCR:LA-cp rat, an animal model of the obesity/insulin resistance syndrome that exhibits an associated vasculopathy and cardiovascular disease. Treatment of the animals from 8 to 12 weeks of age with S15261 or S15511 resulted in reductions in food intake and body weights, whereas Y415 had no effect. Troglitazone caused a small increase in food intake (P <.05). Treatment with S15261 or S15511 decreased plasma insulin levels in fed rats and prevented the postprandial peak in insulin levels in a meal tolerance test. Y415 had no effect on insulin levels. Troglitazone halved the insulin response to the test meal, but metformin gave no improvement. S15261 decreased the expression of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase and stimulated the expression of acetyl-CoA carboxylase and acyl-CoA synthase. S15261 also reduced the expression of carnitine palmitoyltransferase I and hydroxymethyl-glutaryl-CoA synthase. S15261, but not troglitazone, reduced the exaggerated contractile response of mesenteric resistance vessels to norepinephrine, and increased the maximal nitric oxide-mediated relaxation. S15261, through S15511, increased insulin sensitivity, decreased insulin levels, and reduced the vasculopathy of the JCR:LA-cp rat. S15261 may thus offer effective treatment for the insulin resistance syndrome and its associated vascular complications.

Animals↗

PubMed1981

The rat mesenteric artery-intestinal loop preparation. Noradrenaline outflow and vascular responses to nerve stimulation and drugs.

A new preparation, intestine-mesenteric blood vessels of the rat, was tested for simultaneous measure of noradrenaline (NA) overflow and vasoconstrictor response (delta p) induced by electric stimulations. Control experiments showed that this preparation could be used within a wide range of frequencies and repeatedly stimulated without any important decrease of response. The effects of phenoxybenzamine, dihydroergotoxine mesylate, imipramine and pargyline were investigated. All the drugs inhibited delta p and, except for dihydroergotoxine mesylate, increased NA outflow. The results were discussed in the light of the present knowledge. It is concluded that this preparation can be profitably used to study drug effects at pre- and post-synaptic level.

Adrenergic alpha-Antagonists↗

PubMed1993

Changes of intracellular pH in rat mesenteric vascular smooth muscle with high-K+ depolarization.

1. In mesenteric vascular smooth muscle cells changes in extracellular pH are rapidly transmitted to the cytoplasm. The mechanism involved is unknown, but it may be due to a high proton permeability of the surface membrane, in which case changes in membrane potential would alter the driving force for proton entry. We have therefore examined the voltage sensitivity of intracellular pH (pHi) in these cells. 2. Strips of mesenteric resistance vessels were loaded with SNARF-1 to monitor pHi and tension was simultaneously measured. Tissues were superfused with oxygenated solutions at 37 degrees C and pH 7.4. Isosmotic substitution of K+ for Na+ was used to depolarize the preparations. 3. pHi was found to be sensitive to alteration of [K+]. Depolarization of the tissue with K+ caused contraction and produced transient increases in pHi. When pHi regulation was blocked there was no significant change in the size of the alkalinization induced by high K+, thus it is unlikely that the results can be explained by voltage sensitivity of pHi regulating mechanisms. 4. In nominally Ca(2+)-free solution, the tissue does not contract and the alkalinization with high K+ was significantly greater than that occurring in 3 mM Ca2+. 5. There was a rapid acidification, when pHi regulation was blocked, which is consistent with a high proton permeability. 6. The effects of membrane potential on pHi have been modelled and show that they can be accounted for by effects of voltage on H+ influx through a proton channel. The effects of changing external pH on H+ influx also fit the model. Estimation of the proton permeability gave a high value (0.4 cm s-1). 7. The results presented demonstrate (i) a voltage sensitivity of pHi in mesenteric vascular smooth muscle cells and (ii) a particularly high permeability of the membrane to protons. The physiological significance of these findings is discussed.

Animals↗

PubMed1997

The direct effects of thyroid hormones on rat mesenteric resistance arteries.

The direct relaxant effects of thyroid hormones on mesenteric resistance vessels were investigated using an isometric wire myograph. Both the L- and the D-isomers of thyroxine (T4) and triiodothyronine (T3) were studied. In contrast with the long-term effects of thyroid hormones, both T4 enantiomers proved more potent in inducing vascular relaxation than the two T3 enantiomers. The interaction between thyroid hormones and calcium-induced contractions was studied. T4 concentration dependently inhibited the Ca2+ induced contractions, showing noncompetitive interaction. Furthermore, we investigated whether the endothelium was involved in the relaxant effect to L-T4. The T4 induced relaxation proved impaired by prior incubation with the nitric oxide (NO) inhibitor N-omega-nitro-L-arginine methylester HCl (L-NAME, 0.1 microM), indicating that T4 is able to stimulate the production of endothelium-derived NO. L-T4-induced relaxation was enhanced by prior incubation with indomethacin (10 microM), whereas in endothelium-denuded preparations an unaltered response was found. The present results indicate that L-T4-induced relaxation is established by an indirect effect via the endothelium and by a direct effect on vascular smooth muscle cells, possibly by influencing calcium fluxes. Because vascular relaxation is established at supraphysiologic concentrations (approximately 100 times the basal level) of thyroid hormone, it is concluded that the direct effect of thyroid hormone on mesenteric vascular smooth muscle cells are not relevant for the in vivo situation.

Animals↗

PubMed1996

The influence of hyperthyroidism on beta-adrenoceptor-mediated relaxation of isolated small mesenteric arteries.

We investigated the influence of hyperthyroidism on relaxant responses of small mesenteric resistance arteries to beta-adrenoceptor agonists and to compounds stimulating the corresponding second-messenger system. Hyperthyroidism was induced by feeding rats for 28 days with 5 mg/kg L-thyroxine (T4)-containing rat chow. This treatment produced a stable hyperthyroid state, as indicated by several biochemical/metabolic and haemodynamic parameters. Preparations of small mesenteric arteries were mounted in an isometric wire myograph. Subsequently, concentration-effect curves were determined for isoproterenol, noradrenaline and salbutamol as well as for forskolin, dibutyryl-cAMP and theophylline. We also determined concentration-effect curves to the beta-adrenoceptor agonists in the presence of ICI 118,551 and CGP 20712A (i.e., in the presence of a selective beta 2- and beta 1-adrenoceptor antagonist, respectively). Apparent pA2-values were calculated to determine which beta-adrenoceptor subtype causes vasodilation. These experiments indicate that beta-adrenoceptor-mediated vasodilation involves both beta 1- and beta 2-adrenoceptors in mesenteric resistance vessels of both hyperthyroid and control rats. In our experiments hyperthyroidism has a sensitizing influence on vascular responses induced by the beta-adrenoceptor agonist isoproterenol and the selective beta 2-adrenoceptor agonist salbutamol. Sensitization to isoproterenol was abolished in the presence of ICI 118,551, whereas it was emphasized in the presence of CGP 20712A. Although this was not fully supported by the results obtained with noradrenaline, these results indicate that the sensitization to beta-adrenoceptor agonists is probably limited to the beta 2-adrenoceptor/G-protein complex and not associated with alterations of the corresponding second messenger system.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1985

Interaction between prejunctional alpha 2-receptors and neuronal transmitter reuptake in small mesenteric arteries from the rat.

The role of the prejunctional alpha 2-receptors for the response to vaso-constrictor nerve stimulation has been examined before and after inhibition of neuronal transmitter reuptake in mesenteric resistance vessels from the rat. Small arteries (diameter about 200 micron) feeding the jejunum were mounted in a myograph for recording of their isometric wall tension during transmural field stimulation of the intramural nerves. Blockade of prejunctional alpha 2-receptors with 0.01 microM idazoxan (RX 781094) caused a marginal potentiation of the neurogenic response when neuronal reuptake was left intact. Also, inhibition of reuptake alone with 3 microM cocaine had little effect on the response. However, when both alpha 2-receptors and reuptake had been inhibited, a strong enhancement of the neurogenic vasoconstriction was observed. Similar findings were made when yohimbine and LU 3-010 instead were used for alpha 2-blockade and reuptake inhibition, respectively. The results thus indicate that in these resistance arteries the effector response is normally influenced by the combined activity of alpha 2-receptors and uptake, and that failure of one mechanism increases the activity of the other, so as to maintain a largely constant effector response.

Adrenergic alpha-Agonists↗

PubMed1993

Extracellular pH signals affect rat vascular tone by rapid transduction into intracellular pH changes.

1. Changes in extracellular pH (pHo) are known to produce large effects on vascular tone, but the mechanisms involved are not understood. As changes in intracellular pH (pHi) can also affect vascular tone, we have investigated the effects of changing pHo upon both pHi and tone. 2. Strips of rat mesenteric resistance vessels were loaded with the pH-sensitive fluorophore SNARF 1; thus tension and pHi could be simultaneously measured as pHo was altered. 3. Whenever pHo was altered there was a corresponding alteration of pHi. Furthermore, when pHo was changed the pHi change was more rapid than that reported to occur in other cells. The time to half-peak intracellular response was 38 +/- 4 s (n = 11). The induced pHi change was also less attenuated than in many other cells studied. Thus a ratio of 0.73 was obtained for the change in pHi per unit pHo change (n = 7). 4. An increase in pHi produced by an increase in pHo was accompanied by an increase in tension in the vascular strips. In other experiments pHi was increased at constant pHo by the addition of the weak base trimethylamine (40 mM). This also elevated tension in the strips. Conversely when pHo was changed while pHi was held at resting values, no change in vascular tone occurred. 5. It is concluded that the effects of pHo on vascular tone are due to the induced change in intracellular pH, and that the vascular smooth muscle cell is functionally well adapted to respond to changes in tissue pH, thereby allowing blood flow to a tissue to be rapidly altered to meet changing needs.

Animals↗

PubMed2002

Superselective mesenteric embolization with microcoils in a porcine model.

PURPOSE: There is a lack of data regarding the degree of ischemic change that may occur in small and large bowel after superselective arterial embolotherapy with platinum microcoils. The purpose of this study was to gain a clearer understanding of the ischemic complications of superselective embolization of peripheral mesenteric arteries with microcoils by gross and histologic examination of postembolectomy bowel specimens at several time intervals in an adult porcine model. METHODS: Two-millimeter platinum microcoils with fibrils were superselectively deployed into six isolated mesenteric branch vessels in each of nine adult pigs. The animals were observed for two days (n = 3), one month (n = 3), or three months (n = 3) and then killed. At necropsy, intestines were examined for gross abnormalities. Sections of bowel containing microcoils were identified under fluoroscopy, resected, and evaluated histologically. RESULTS: A total of 54 microcoils were deployed into the distal arterial mesentery supplying the jejunum (n = 14), ileum (n = 26), and colon (n = 14) of nine adult pigs. Each animal received six microcoils. There were no clinical complications, and all pigs gained weight during their observation periods. Gross examination of the intestines did not reveal any evidence of acute or chronic ischemia. The coils were found in the distal arterial vasculature of the intestine. Histologic examination revealed mild superficial necrosis of villous tips in several samples; however, this finding is likely related to a fixation artifact rather than ischemic injury. There was no other histologic evidence suggestive of ischemic injury. CONCLUSIONS: Gross and histologic findings after superselective arterial embolotherapy demonstrated minimal changes in the bowel, and there were no significant clinical consequences to the animals. We conclude that transcatheter arterial embolotherapy in pigs is safe and may be applicable in the control of massive lower gastrointestinal hemorrhage in humans.

Angiography↗