Artery Of Dogs Research Articles

Molecular profile of vascular ion channels after experimental subarachnoid hemorrhage.

Cerebral vasospasm is a transient, delayed constriction of cerebral arteries that occurs after subarachnoid hemorrhage (SAH). Smooth muscle cells show impaired relaxation after SAH, which may be caused by a defect in the ionic mechanisms regulating smooth muscle membrane potential and Ca(2+) permeability. We tested this hypothesis by examining changes in expression of mRNA and protein for ion channels in the basilar arteries of dogs after SAH using quantitative real-time polymerase chain reaction (PCR) and western blotting. SAH was associated with a significant reduction in basilar artery diameter to 41 +/- 8% of pre-SAH diameter (P < 0.001) after 7 days. There was significant downregulation of the voltage-gated K(+) channel K(v) 2.2 (65% reduction in mRNA, P < 0.001; 49% reduction in protein, P < 0.05) and the beta1 subunit of the large-conductance, Ca(2+) - activated K(+) (BK) channel (53% reduction in mRNA, P < 0.02). There was no change in BK beta1 subunit protein. Changes in mRNA levels of K(v) 2.2 and the BK-beta1 subunit correlated with the degree of vasospasm (r(2) = 0.490 and 0.529 respectively, P < 0.05). The inwardly rectifying K(+) (K(ir)) channel K(ir) 2.1 was upregulated (234% increase in mRNA, P < 0.001; 350% increase in protein, P < 0.001). There was no significant change in mRNA expression of L- type Ca(2+) channels and the BK-alpha subunit. These data suggest that K(+) channel dysfunction may contribute to the pathogenesis of cerebral vasospasm.

Treatment of aneurysms with wires and electricity: a historical overview.

Endovascular treatment of aneurysms has only recently become an accepted therapeutic modality. Nonetheless, treatment of aneurysms with the aid of various foreign bodies such as needle and wire insertion with or without electrical current has been reported since the first half of the 19th century. In 1832 Phillips induced clot formation in the femoral and carotid arteries of dogs by leaving needles in the arteries for variable lengths of time. Simultaneously, in France, Velpeau had proposed using "l'acupuncture des arteres dans le traitement des anevrismes." Later, Phillips and Pelrequin connected the offending needles to a source of electrical current in an attempt to increase thrombus formation and aneurysm occlusion. Subsequently, Moore introduced the concept of packing the aneurysm with wire inserted through a needle transfixed to the vessel wall. To this method, Corradi added electrical current. Widely known as the Moore-Corradi technique, it was used in ensuing years with variable success. The early phase of endovascular aneurysm treatment culminated when Blakemore and Moore treated a case of symptomatic cavernous sinus aneurysm by passing wire through the patient's orbit. These pioneering cases combined with technological advances in the diagnosis of intracranial aneurysms paved the way for further refinements in coil embolization of aneurysms.

Endothelium-dependent relaxation of canine uterine artery in response to acetylcholine: the possible involvement of alternative pathways.

The effect of acetylcholine on the isolated, pre-contracted, uterine artery of non-pregnant dog was investigated. Acetylcholine-induced concentration-dependent relaxation of isolated canine uterine artery with endothelium (pEC50 = 6.48 +/-0.01, n = 37) and was without effect on arterial segments denuded of endothelium. Indomethacin, 4-aminopyridine (10-5 m) and pre-contraction with K+-rich Krebs-Ringer bicarbonate solution had no effect on acetylcholine-induced relaxation. NG-nitro-l-arginine (l-NOARG) (10-5 m) inhibited relaxation evoked by acetylcholine. Indomethacin applied with l-NOARG led to further inhibition of acetylcholine-induced relaxation. In the presence of both l-NOARG and indomethacin, 4-aminopiridine did not provoke further inhibition of acetylcholine-induced relaxation of canine uterine artery. It is concluded that the acetylcholine-induced relaxation of canine uterine artery is probably mediated by endothelial production of nitric oxide (NO). However, if NO-synthase is inhibited, acetylcholine-induced vasorelaxation may be, in part, mediated through activation of cyclooxygenase pathway.

The discovery of the antiplatelet effect of aspirin: a personal reminiscence

The discovery of the antiplatelet effect of aspirin: a personal reminiscence

An experimental study on the pharmacokinetics of 5-fluorouracil regional chemotherapy for pancreatic cancer.

Recently a few centers reported promising results of regional intra-arterial chemotherapy for pancreatic cancer. However, the detailed pharmacokinetics and the side effects of anticancer agents remain unclear. Catheters were introduced into the gastroduodenal artery and the splenic artery of dogs. In group I, arterial infusion of 5-fluorouracil (5-FU) was performed over 10 minutes. In group II, 5-FU was infused systemically. In group III, an intra-arterial infusion was repeated weekly three times. Blood samples and liver and pancreas tissue samples were obtained to determine 5-FU levels. In a subset of each group, the pancreas, duodenum, and liver were excised for histological analyses. Immediately after the infusion of 5-FU, the portal level in group I was higher than that in group II. However, the mean systemic level in group I was lower than in group II. The mean tissue concentration in the pancreas in group I was significantly higher than that of group II. Histological examination revealed no microscopic alterations after treatment in all groups, including group III. This fundamental study suggested that intra-arterial chemotherapy of 5-FU for pancreatic cancer allows higher regional drug delivery without adverse effects on normal regions of the pancreas, the duodenum, and the liver.

The effect of an L-type calcium channel blocker on the hemodynamics of orbital arteries in dogs.

(1) To determine the effect of the l-type calcium channel blocker amlodipine on color Doppler ultrasound-determined vascular resistance and blood flow velocities in the distal retrobulbar arteries of dogs; (2) to determine any effect of blood pressure and PCO2 rate on such color Doppler-determined circulatory measurements. Color Doppler imaging measurements of the short posterior ciliary artery, long posterior ciliary artery, and ophthalmic artery of normal eyes of 10 dogs were obtained under isofluorane anesthesia before and 1 week after oral amlodipine administration. Mean systemic arterial blood pressure and PCO2 were monitored. The mean resistive index decreased significantly in the short posterior ciliary artery (P = 0.0347), in the long posterior ciliary artery (P = 0.0092), and ophthalmic artery (P = 0.0004) following systemic amlodipine administration. The end diastolic velocity increased significantly in the long posterior ciliary artery (P = 0.0368) and ophthalmic artery (P < 0.0001). The peak systolic velocity increased significantly in the ophthalmic artery (P = 0.0256). Mean systemic arterial blood pressure was significantly negatively associated with resistive index (P < 0.0001) and significantly associated with the log of the end diastolic velocity (P < 0.0001). Systemically administered amlodipine increases color Doppler imaging-determined blood flow velocity and decreases vascular resistive index in the ophthalmic artery, short posterior ciliary artery and long posterior ciliary artery of normal dogs. Changes in systemic arterial blood pressure can significantly affect the measurement of color Doppler imaging parameters.

Therapeutic angiogenesis induced by human hepatocyte growth factor gene in hindlimb ischemia of dogs

A preclinical study of treating peripheral artery occlusive disease (PAD) was performed by using a hepatocyte growth factor (HGF) gene-expressing vector, plasmid pUDKH, in a dog model with complete ischemia of one hindlimb. After ligation of femoral artery of one hindlimb, pUDKH was transferred directly into the ischemic limb muscles. The angiogenic activity of the plasmid pUDKH was evaluated. On D 30 after injecting once of pUDKH at different doses into local muscles immediately after operation, the degree of augmentation of collateral vessel formation was significantly greater than that treated by blank vector. In addition, the blood flow rate of femoral artery in dogs treated with pUDKH was recovered on D 90, while the flow rate was only 1/5 to 1/3 in control dogs. The pulse amplitude of pUDKH-treated dogs was recovered on D 90, but it was hardly detectable in most of the control dogs. The side effects of intramuscular transfection of pUDKH were also investigated, and no significant positive change was found. It is suggested that angiogenesis induced by HGF gene has the potential for clinical use in the treatment of peripheral arterial diseases.

Differences in coupling interval‐dependent effects of sotalol on infarcted and noninfarcted areas of dog hearts after myocardial infarction

AbstractWe examined the coupling interval‐dependence of the effects of sotalol (dl‐sotalol) on effective refractory periods (ERPs) and epicardial activation in ventricles of dog hearts after myocardial infarction, and clarified their differences between infarcted and noninfarcted areas. Myocardial infarction was produced by the two‐stage ligation of left anterior descending coronary artery in dogs. At 7 to 9 days after ligation, bipolar electrodes were sutured on the ventricular surface of the noninfarcted and the infarcted areas. Single (S1) or double (S1/S2) electrical stimulations with various coupling intervals were applied on the ventricle during atrial pacing. S1 was triggered by a prior R wave of pacing rhythm with coupling interval of 300 ms (S1[300]) or 180 ms (S1[180]). Coupling intervals of S1 and S2 were between 250 and 130 ms. ERPs, activation delay, and functional refractory periods (FREPs) in ventricles were measured after S1(180) or S1(300). Ventricular activation delay was a time interval from the artifact of S1 or S2 to the most delayed measurable wave. The coupling interval of S1–S2 was 170 or 160 ms. RT intervals were measured in the bipolar ECGs after S1(300) or S1(180). Sotalol was administered intravenously in dosages of 2, 4, and 8 mg/kg. Sotalol prolonged the ERPs in noninfarcted areas in a lesser extent after S1(180) than after S1(300), whereas in infarcted areas the ERP prolongation was in a similar extent after S1(180) and S1(300). Sotalol prolonged the RT intervals in a lesser extent after S1(180) than after S1(300) in noninfarcted areas, but in a similar extent after S1(180) and after S1(300) in infarcted areas. FERPs were also prolonged by sotalol in infarcted areas in a similar extent after S1(180) and after S1(300). Sotalol prolonged ventricular activation delay after S1/S2 in the infarcted areas, which was greater after S1/S2(180/170) than after (300/170). Delayed activation was blocked more frequently after the S1/S2(180/160) than after S1/S2(300/160). These results indicate that the effects of sotalol on ventricular activation delay are reverse‐use dependent in noninfarcted areas but use‐dependent in infarcted areas, which may contribute to suppression of ventricular tachyarrhythmias in patients with coronary heart disease. Drug Dev. Res. 58:258–267, 2003. © 2003 Wiley‐Liss, Inc.

Intraarterial Infusion of Lipiodol CDDP Suspension into the Internal Iliac Artery-Pre Clinical Dose Escalation Study Using Canine Model-

Background and Aims : To investigate the usefulness of intraarterial chemotherapy (IAC) with CDDP powder and lipiodol suspension (LCS) for invasive bladder cancer as a dose escalation modality of conventional IAC, we administered LCS into the internal iliac artery of dogs and evaluated pharmacokinetics of CDDP. Methods : An angiographic catheter was inserted to the internal iliac artery of an anesthetized dog under fluoroscopic guidance. CDDP solution, LCS, or a combination of CDDP solution and LCS were intra-arterially infused. For comparison, CDDP solution was also intravenously infused. The dose of CDDP ranged from 1 to 3 mg/kg. For combination study, the dose of CDDP ranged from 3 to 5 mg/kg. In all groups, blood samples were collected 5, 15, 30, 60, 120, and 180 minutes after administration, and serum Pt levels were measured. Results : In the LCS group, the serum Pt level was lower than those after intravenous or intraarterial infusion of CDDP solution. In the combination therapy group, the serum Pt level increased with the total dose of CDDP. Conclusions : Intraarterial infusion of LCS showed a lower systemic CDDP level. This method may reduce the incidence of side effects, suggesting the usefulness of intraarterial infusion therapy with LCS for invasive bladder cancer.

An automated coronary artery occlusion device for stimulating collateral development in vivo

Introduction: Repetitive, brief coronary artery occlusions produce collateral development in experimental animals. This model causes coronary collateralization in a highly reproducible fashion, but the process is very labor intensive. We report the design and use of a fully automated hydraulic coronary occlusion device capable of producing repetitive coronary occlusions and enhancement of coronary collateral development in dogs. Methods: The device consists of analog electronics that allow adjustment of occlusion number, frequency, pressure and duration, and mechanical components responsible for the coronary occlusion. The motor and piston of the device are coupled to a chronically implanted hydraulic vascular occluder placed around the left anterior descending coronary artery (LAD) of dogs instrumented for measurement of systemic and coronary hemodynamics. One group of dogs ( n=6) underwent brief (2 min) LAD occlusions once per hour, eight times per day, 5 days/week for 3 weeks to stimulate collateral development (measured using radioactive microspheres). Another group of dogs ( n=6) that did not receive repetitive occlusions served as controls. Results: The device reproducibly produced repetitive LAD occlusions for the duration, frequency, and time interval initially programmed. A time-dependent increase in transmural collateral blood flow was observed in dogs undergoing repetitive occlusions using the device. Collateral blood flow was unchanged in dogs that did not undergo occlusions. Discussion: The automated occluder device reliably produces repetitive coronary occlusions and may facilitate further study of coronary collateral development in response to chronic myocardial ischemia.

Usefulness of polyurethane for small-caliber vascular prostheses in comparison with autologous vein graft

For long-term patency of small-caliber vascular prostheses, antithrombogenicity and microporous structure are very important. We have developed a new technique to give a microporous structure to a polyurethane vascular prosthesis that has favorable antithrombogenicity. A solution of tetrahydrofuran/dimethylformamide (1 : 1) containing 13 wt% of segmented polyurethane (PTMG + MDI) and calcium carbonate (mean particle size, 8 μm) was dipcoated on a glass mandrel 3 mm in diameter and placed into distilled water. After the glass mandrel was removed, the polyurethane tube was placed into hydrochloric acid, and a microporous polyurethane vascular prosthesis was produced. Prostheses made in this fashion, and autologous jugular vein grafts were implanted into the femoral artery and the carotid artery of mongrel dogs. Patency was recognized on the arteriogram and duplex scanning (ultrasonography), and the removed grafts were inspected macroscopically and microscopically. This prosthesis was similar in elasticity to a vein graft. Patency was defined 8 weeks after implantation, and this prosthesis showed less intimal hyperplasia than the autologous vein graft. The new polyurethane prosthesis might be useful for small-caliber vascular reconstruction.

Nipradilol induces vasodilation of canine isolated posterior ciliary artery via stimulation of the guanylyl cyclase-cGMP pathway

We examined the effect of nipradilol on contraction of the posterior ciliary artery induced by high potassium or norepinephrine and on cyclic GMP (cGMP) levels in the posterior ciliary artery of dogs. Nipradilol caused dose-dependent relaxation of KCl-and norepinephrine-induced contractions of posterior ciliary artery. The relaxant effect of nipradilol on norepinephrine-contracted ciliary artery was significantly greater than that on KCl-contracted ciliary artery. In KCl-contracted ciliary artery, N G-nitro-L-arginine methyl ester hydrochloride (L-NAME, 10 −4 M) did not alter the relaxant effect of nipradilol, whereas 1H-1,2,4-oxadiazolo-4,3-a-quinoxalin-1-one (ODQ, 10 −6 M) significantly inhibited this effect. Ethacrynic acid at 10 −5 M, sulfasalazine at 10 −4 M and S-decylglutathione at 10 −4 M (glutathione S-transferase inhibitors) did not inhibit the relaxant effect of nipradilol. In addition, nipradilol produced dose-dependent increases in cGMP levels in the canine posterior ciliary artery. These findings indicate that nipradilol-induced vasorelaxation in the canine posterior ciliary artery occurs via stimulation of the guanylyl cyclase-cGMP pathway.

Pathomechanism of shock wave injuries on femoral artery, vein and nerve: An experimental study in dogs

Purpose: To study the pathomechanism of shock wave injuries to the femoral artery, vein and nerve in dogs. Materials and methods: High-energy shock wave (0.47 mJ/mm 2 energy flux density) were applied to the right femoral artery, vein and nerve in nine mongrels, and the left side was used as control. Macroscopic examinations including structure integrity, edema, discolouration and extravasation; and microscopic examinations including detachment of the intima layer, disruption of the medium layer, capillary congestion, neutrophil margination and extravasation of the outer layer and the surrounding tissues were performed in 2 h, and in 4 days, respectively, after shock wave application. Results: The most serious injuries included disruption of the medium layer with separation from the adventitia layer of the femoral artery. The injuries to the femoral vein and nerve predominantly involved the outer adventitia layer and the surrounding tissues. Mild nerve bundle swelling was noted in most cases. There were capillary congestion, neutrophil margination and extravasation indicative of inflammatory tissue reaction after shock wave application. Conclusion: High-energy shock waves caused serious injuries to the femoral artery, vein and nerve, especially the femoral artery and inflammatory reaction to the surrounding tissues.

Influence of Isoflurane Anesthesia on Pulsatility Index and Peak Systolic Velocity of Basilar Artery in Dogs by Doppler Ultrasonography

This study was performed to examine the influence of isoflurane anesthesia on the pulsatility index (PI) and the peak systolic velocity (PSV) of the blood flow in the basilar artery of dogs by duplex Doppler ultrasonography. Twelve healthy dogs were used to measure the PI and the PSV under the conscious state and isoflurane anesthesia. The pulsatility index (PI) and the peak systolic velocity (PSV) in the basilar artery were measured five times with random intervals. The blood pressure was measured. The PI and PSV values in dogs under isoflurane anesthesia were 1.37 +/- 0.32 and 72 +/- 19 cm/sec, whereas those in the conscious dogs were 1.37 +/- 0.13 and 81 +/- 16 cm/sec, respectively. The indirect mean arterial systolic and diastolic pressures under isoflurane anesthesia were 107 and 51 mmHg, whereas those in the conscious dogs were 133 and 74 mmHg. Though the isoflurane is generally known to induce hypotension, there were no significant differences in the PI and PSV between the isoflurane-anesthetized and the conscious dogs. In conclusion, the isoflurane anesthesia did not influence the PI and PSV in the basilar artery of dogs.

The Effect of Low Dose Nitroglycerin on Hemodynamics and Local Liver Perfusion Following an Occlusion and Reperfusion of the Hepatic Artery and Portal Vein in Experimental Dogs

Background: To reduce massive blood loss during a hepatectomy, many anesthesiologists have used the technique of low central venous pressure maintenance by administration of low dose nitroglycerin (NTG) and/or intravenous fluid reduction. However, so far there have been no studies about local liver perfusion (LLP) changes after hepatic artery (HA) or portal vein (PV) reperfusion in patients receiving nitroglycerin administration. In this study, the changes in hemodynamics and LLP following HA and PV reperfusion along with low dose (2/kg/min) NTG administration in dogs were observed. Methods: A total of 20 mongrel dogs were divided into four groups; HA occlusion and reperfusion group (H, n = 5), NTG administration group during the reperfusion on H (H-NTG, n = 5), PV occlusion and reperfusion group (P, n = 5), NTG administration group during the reperfusion on P (P-NTG, n = 5). After femoral and pulmonary arterial catheterization, a midline abdominal incision was made. HA and PV were exposed to clamp and declamp. A thermal diffusion microprobe was inserted in the liver parenchyme to measure LLP. Results: The PV blood flow was not changed after HA occlusion, but HA blood flow increased after PV occlusion. The LLP decreased after HA and PV occlusion. The LLP recovered to the baseline level in group H-NTG after HA reperfusion, but the LLP was more increased compared to the baseline level in group H. In group P, the LLP did not recover after PV reperfusion, but the LLP in group P-NTG recovered to the baseline level after PV reperfusion. Conclusions: In conclusion, it was observed that the LLP recovered to the baseline level by administration of NTG after PV reperfusion. However, the LLP did not increase after HA reperfusion by administration of low dose NTG.

Light and electron microscopic analyses of autologous pericardial tissue used as a small-diameter arterial graft in dogs.

As a form of small-diameter arterial graft, we implanted fresh autologous pericardium and pericardium treated with 0.6% glutaraldehyde in the bilateral carotid arteries of dogs and then compared the time-related changes of the grafts explanted after the predetermined periods. The pericardial grafts were implanted in 1 animal each for scheduled periods of 3 days, 2 weeks, 1 month, 3 months, and 6 months. The retrieved grafts were processed for light and electron microscopic analyses following gross observation. The glutaraldehyde-treated small-diameter pericardial vascular grafts showed a better endothelialization of the blood-contacting surface and a slower fragmentation of the collagen layers than the fresh grafts although it has yet to be proven whether these differences are so significant as to affect the patency results between the groups.

Efficacy of azimilide and dofetilide in the dog right atrial enlargement model of atrial flutter.

Azimilide dihydrochloride blocks both the rapid (I(Kr)) and slow (I(Ks)) components of the delayed rectified K+ current; dofetilide blocks only I(Kr). Their efficacies were assessed on atrial flutter reentrant circuits in dogs with surgically induced right atrial enlargement. Multiple biopsies of the tricuspid valve and banding of the pulmonary artery in male mongrel dogs made them susceptible, about 3 weeks postoperatively, to stimulation-induced sustained (5 min or longer) atrial flutter. Azimilide 3 mg/kg administered intravenously (i.v.) terminated flutter in 8 of 8 dogs, but a slower, nonsustained arrhythmia could be reinduced in 5. In these 5 dogs, azimilide 10 mg/kg terminated flutter and prevented reinduction. This dose increased effective refractory period significantly more in the slow conduction zone (25%) than in the normal zone (17%) and increased flutter cycle length (37%). Termination followed progressive conduction delay in the slow zone of the reentrant circuit. Dofetilide 1 microg/kg i.v. terminated flutter in 6 of 6 dogs, but the arrhythmia could be reinduced. At 3 microg/kg, flutter terminated in all dogs and could not be reinduced. Dofetilide also increased the effective refractory period significantly more in the slow zone (17%) than in the normal zone (12%) and increased cycle length (33%), leading to interruption of the arrhythmia circuit. In the canine right atrial enlargement model of circus movement atrial flutter, both azimilide 10 mg/kg i.v. and dofetilide 3 microg/kg i.v. were 100% effective in terminating flutter and preventing reinduction. Efficacy relied on a similar mechanism of differentially prolonged refractoriness in the slow conduction component of the reentrant circuit where drug-induced termination occurred.

Oral administration of a specific chymase inhibitor, NK3201, inhibits vascular proliferation in grafted vein

Chymase may play an important role in vascular proliferation, as shown by in-vitro experiments, but the role of chymase in vivo has been unclear. In this study, we investigated the effect of a novel chymase inhibitor, NK3201, on this proliferation in dog grafted veins. NK3201 inhibited human and dog chymases, but not rabbit ACE. NK3201 suppressed the Ang I-induced vascular contraction in isolated dog arteries in the presence of an ACE inhibitor, and the IC 50 value of chymostatin and NK3201 in dog artery was 320 nM. In dog, the concentration of NK3201 in blood was about 10 μM at 24 h after oral administration of the drug (5 mg/kg). In the group treated with NK3201, each dog was administered orally 5 mg/kg per day from 5 days before to the day before the removal of the grafted veins. Each dog underwent right common carotid artery bypass grafting with the ipsilaterial external jugular vein. By 28 days after grafting, a significant vascular proliferation was observed in the grafted veins and the chymase activity was also increased significantly. Treatment with chymase inhibitor significantly suppressed the proliferation of the grafted veins and the increased chymase activity. In this study, we demonstrate for the first time that oral administration of a specific chymase inhibitor, NK3201, appears useful for preventing vascular proliferation.

Experimental Study of Small Arterial Anastomosis with Gelatin‐Resorcin‐Formaldehyde Glue and Collagen Sheet

In cardiovascular surgery, the manual continuous suture has often been used for microvascular anastomosis, but the luminal irregularity often causes thrombotic stenosis in the anastomosis sites. The purpose of this study was to examine the feasibility of the combined use of gelatin-resorcin-formaldehyde (GRF) glue and a collagen sheet for the anastomosis of small arteries 3 to 4 mm in diameter in experimental animals. End-to-end anastomoses of the carotid and femoral arteries of mongrel dogs were carried out with the combined use of GRF glue and collagen sheet. The physical strength of the anastomosis, the histopathologic condition of the vassels, and the absorptivity and the inflammatory response of the glue were evaluated. The physical strength of the anastomosis sites was good and their flexibility optimal, the smooth luminal surface appeared excellent for preventing thrombotic stenosis in all follow-up periods, and the glue was absorbed almost completely within 12 weeks postoperatively. The combined use of GRF glue and collagen sheet would be feasible for the anastomosis of small arteries 3 to 4 mm in diameter and could substitute for the conventional suture method.

A model for evaluation of arterial thrombosis following interventional procedures.

A model to assess thrombus formation following vascular injury was evaluated using various interventional systems. The model consisted of a 'stretchable' shunt box that served as an arteriovenous shunt between the carotid artery and jugular vein in dogs. Arterial homografts obtained from both carotid and femoral arteries were mounted between two plastic connectors attached to either side of the shunt box. The opposing walls of the shunt box were then stretched apart to achieve the original length of the arteries. The arterial side of the box was connected to the ipsilateral carotid artery and the venous side was connected to the contralateral jugular vein. Haemostasis valves were placed at the exit ports on the venous side of the shunt box. These were used as an access to the various interventional catheters into the lumens of the homografts. Interventions were performed prior to initiating blood flow. After the interventions, 111indium-labelled platelets were injected on the arterial side of the shunt box and arterial blood flow initiated across the shunt. After one hour of circulation through the shunt box, the blood flow was interrupted, and the homografts were perfusion-fixed with glutaraldehyde and segments removed for radioactive counts and processed for histology. This shunt box was then used to compare platelet adhesion and thrombus formation after balloon angioplasty (BA) to direct laser (LA) and laser-thermal angioplasty (LTA). A total of 28 arteries were used from seven dogs. In each experiment, one homograft was used as control, and three other homografts were treated with either BA, LA or LTA. Following the interventions, 111indium-labelled platelets were injected and circulated for one hour using the dog's native circulation. Labelled platelet counts for BA (19102+/-4869/cm2; mean +/- SE) were significantly greater than LA (7038+/-980/cm2), thermal LTA (5189+/-1961/cm2), and control (1575+/-541/cm2), respectively (p<0.05, ANOVA). Histology examination showed few platelets at LA, LTA and control sites whereas extensive platelet adhesion was noted at BA treated sites. The model provided a means to conduct simultaneous comparison of several interventions under similar conditions. In this case thermal treatment of the arterial homografts had the least amount of platelet adhesion.