Internal Vessel Diameter Research Articles

Remodelling and Enhanced Myogenic Tone in Cerebral Resistance Arteries Isolated from Genetically Hypertensive Brattleboro Rats

In this study, we examined the structural and functional properties of cerebral resistance arteries isolated from normotensive (Di/N), and hypertensive (Di/H), vasopressin-deficient rats. Di/H rats had a significantly higher mean arterial blood pressure (MAP, 159 ± 3 mm Hg) than Di/N rats (125 ± 2 mm Hg). Vessels were set up in a pressure myograph, and the internal diameter and wall thickness were determined at increasing intraluminal pressures under passive (calcium-free) conditions. Arteries were then pressurized to the MAP of the animal, from which they were isolated and fixed with glutaraldehyde, embedded in araldite, sectioned and examined histologically. Under passive conditions, the middle cerebral artery (MCA) from Di/H rats had a smaller internal diameter than the MCA isolated from Di/N rats at all distending pressures. This smaller internal diameter of vessels from hypertensive rats is characteristic of eutrophic inward remodelling, whereby a similar amount of wall material is organized around a smaller lumen, without vascular growth or an alteration in artery distensibility. We have previously shown that similar structural alterations occur in mesenteric resistance arteries isolated from Di/H rats. In the presence of extracellular calcium (1.6 mmol/l), the MCA isolated from Di/H rats had significantly more intrinsic tone than the MCA isolated from Di/N rats in the pressure range of 10–110 mm Hg, although arteries from both strains had a similar myogenic index. The increased intrinsic constriction was a specific enhancement of pressure-induced tone, since responses to the thromboxane mimetic, U46619, were decreased, rather than increased, in the MCA isolated from Di/H rats. Furthermore, it is unlikely that the increased intrinsic tone in arteries isolated from Di/H rats was due to an impaired endothelial function since responses to the endothelium-dependent vasodilator, bradykinin, were enhanced in these vessels compared to arteries isolated from Di/N rats.

Nitric Oxide Inhibition Simulates the Enhancement of α1Agonist-Induced Vasoconstriction in Diabetes

We have previously reported that endothelium-dependent, nitric oxide (NO)-mediated vasorelaxation is impaired in diabetic mesenteric arteries. We hypothesized that vasoconstrictor responses should therefore be enhanced. The purpose of this study was to determine whether diabetic mesenteric arteries exhibit increased vasoconstrictor responses, and to investigate if these changes are receptor and/or NO mediated. Thirty age-matched male Sprague–Dawley rats were divided into control (C) and diabetic (D, streptozotocin: 60 mg/kg) groups and studied after 4 weeks. Terminal branches of ileal mesenteric arteries (300 ± 9 μm) were isolated, pressurized, and superfused with modified Krebs solution. Changes in vessel internal diameter were measured and dose–response curves (DRC) for each vasoactive agent were determined. Each vessel was initially constricted with 40 mMof KCl to determine maximal vasoconstriction. Phenylephrine (Phe, 10−8–10−4M) and UK14304 (10−9–10−5M) were used to determine α1- and α2-receptor responses, respectively. Similar studies were performed in the presence ofNω-nitro-l-arginine methyl ester (l-NAME, 10−4M), a competitive inhibitor of NO synthase. Maximal response (Max), area under the curve (AUC), and vessel sensitivity (ED50) for each DRC were calculated. Comparisons among groups were made using analysis of variance and Student'sttest with Bonferroni correction. There were no differences in vasoconstrictor responses induced by KCl (C: 82 ± 2% vs D: 80 ± 1%). α1-vasoconstrictor responses to Phe were enhanced in diabetes with significantly higher Max (96 ± 2% vs 83 ± 3%), and AUC (1.92 ± 0.09 vs 1.56 ± 0.08), but no difference in ED50. The addition ofl-NAME enhanced only Phe-induced vasoconstrictor response significantly in control rats. Thus, differences in Phe-induced vasoconstrictor responses between C and D were abolished in the presence ofl-NAME. α2-vasodilator responses induced by UK14304 were similar between C and D and unaffected byl-NAME. α1-, but not α2-, vasoconstrictor responses are enhanced in streptozotocin-induced diabetic rats. These enhanced responses can be duplicated by treatment of control vessels withl-NAME.

Direct observations of sympathetic cholinergic vasodilatation of skeletal muscle small arteries in the cat.

1. The aim of this study was to examine the actual changes of the internal diameter (i.d.) of arterial vessels of skeletal muscle evoked by activation of sympathetic cholinergic nerve fibres during stimulation of the hypothalamic defence area in anaesthetized cats. 2. For this purpose, we have used our novel X-ray TV system for visualizing small arteries (100-500 microm i.d.) of the triceps surae muscle and larger extramuscular arteries (500-1400 microm i.d.) of the hindlimb (the femoral (FA), popliteal (PA) and distal caudal femoral (DCFA) arteries). The passage of a contrast medium from the large extramuscular arteries to the smaller intramuscular arteries was serially measured before and during hypothalamic stimulation. 3. Hypothalamic stimulation increased mean arterial blood pressure, heart rate and femoral vascular conductance. The i.d. of FA, PA, and DCFA did not change during the hypothalamic stimulation, whereas the i.d. of small arteries in the triceps surae muscle increased by 48 +/- 2% (mean +/- S.E.M.) and the cross-sectional area increased concomitantly by 118%. The maximum increase in i.d. of 78 +/- 6%, was observed in arteries of 100-200 microm. These increases in diameter were markedly reduced by intra-arterial injection of atropine or by cutting the sciatic nerve, but not by phentolamine and propranolol given together. 4. The vasodilatation evoked by hypothalamic stimulation was seen in almost all the sections of the small arteries observed under control conditions and was distributed along the entire length of the vessel. In addition, the number of arterial vessels that could be detected increased by 42% during hypothalamic stimulation. The newly detected arterial branches, which ranged from 100 to 300 microm in diameter, mostly arose from the branching points. 5. It is concluded that stimulation of sympathetic cholinergic nerve fibres dilates the small arteries of skeletal muscle ranging from 100 to 500 microm, but not the larger extramuscular arteries.

Effects of diabetes and uremia on mesenteric vascular reactivity

Diabetes and uremia are comorbid conditions that have significant effects on cardiovascular physiology. These studies were designed to examine the effects of diabetes and uremia on vascular reactivity. Sprague-Dawley rats were divided into control (C), diabetic (D), uremic (U), and diabetic/uremic (D + U) groups. Diabetes (D, D + U groups) was induced with an injection of streptozotocin. Uremic (U, D + U groups) was produced by seven-eighths nephrectomy. Serum glucose, blood urea nitrogen, creatinine, creatinine clearance, and protein excretion were measured at baseline and before microvascular studies at 4 or 8 weeks after injection. Vascular reactivity was studied in isolated, pressurized, and superfused segments of mesenteric arterioles (300 microns). Changes in internal vessel diameter were measured in response to phenylephrine (10(-8) to 10(-4) mol/L), acetylcholine (10(-9) to 10(-5) mol/L), and nitroprusside (10(-9) to 10(-2) mol/L). Results at 4 and 8 weeks were similar in all groups. Vasoconstrictor responses to phenylephrine and endothelium-independent vasodilator responses to nitroprusside were not altered in any experimental group. Endothelium-dependent vasodilator responses to acetylcholine were significantly depressed in both diabetic groups (D and D + U, p < 0.01 versus control), and there were no differences between the two diabetic groups. Streptozotocin-induced diabetes results in impairment of endothelial-dependent (nitric oxide mediated) vasodilator responses in mesenteric resistance vessels, which are unaffected by coexisting uremia. Uremia has little effect on mesenteric vascular reactivity in this model.

Vascular and myocardial protective effects of converting enzyme inhibition in experimental heart failure

Systemic vasoconstriction due to stimulation of the sympathetic and renin-angiotensin-aldosterone systems is a hallmark of heart failure and this is accompanied by impaired endothelium-dependent relaxations at the level of large arteries. This study investigated, in a rat model of heart failure, whether such an endothelial dysfunction also exists at the level of the resistance artery, and whether this is associated with morphologic changes, as well as the effects of chronic treatment with the angiotensin-converting enzyme inhibitor perindopril (2 mg/kg/day). After 12 months, arterial pressure, left ventricular (LV) end diastolic pressure (LVEDP), and LV dP/dt were measured in anesthetized rats. Responses to acetylcholine and nitroprusside were determined in isolated and perfused mesenteric artery segments (diameter: 280 +/- 15 microns). After fixation, vessel diameter, media cross-sectional area, and media collagen and elastin densities were measured by image analysis. After 12 months, untreated rats showed signs of heart failure, i.e., reduced LV dP/dt, and increased LVEDP, heart weight/body weight, LV cavity circumference, and myocardial collagen density. In mesenteric vessels the endothelium-dependent vasodilator response to acetylcholine was impaired, whereas the response to the nitric oxide donor nitroprusside was unaffected. Heart failure did not affect vascular morphological parameters. Perindopril decreased blood pressure and LVEDP without any modification of LV dP/dt, and prevented cardiac remodeling. At the vascular level, perindopril improved the response to acetylcholine and reduced media cross-sectional area and collagen density without affecting internal vessel diameter or elastin density. Thus, heart failure decreases endothelium-dependent vasodilator response to acetylcholine without modification of vessel structure.(ABSTRACT TRUNCATED AT 250 WORDS)

Vascular and myocardial protective effects of converting enzyme inhibition in experimental heart failure

Systemic vasoconstriction due to stimulation of the sympathetic and renin-angiotensin-aldosterone systems is a hallmark of heart failure and this is accompanied by impaired endothelium-dependent relaxations at the level of large arteries. This study investigated, in a rat model of heart failure, whether such an endothelial dysfunction also exists at the level of the resistance artery, and whether this is associated with morphologic changes, as well as the effects of chronic treatment with the angiotensin-converting enzyme inhibitor perindopril (2 mg/kg/ day). After 12 months, arterial pressure, left ventricular (LV) end diastolic pressure (LVEDP), and LV dP dt were measured in anesthetized rats. Responses to acetylcholine and nitroprusside were determined in isolated and perfused mesenteric artery segments (diameter: 280 ± 15 μm). After fixation, vessel diameter, media cross-sectional area, and media collagen and elastin densities were measured by image analysis. After 12 months, untreated rats showed signs of heart failure, i.e., reduced LV dP dt , and increased LVEDP, heart weight/body weight, LV cavity circumference, and myocardial collagen density. In mesenferic vessels the endothelium-dependent vasodilator response to acetylcholine was impaired, whereas the response to the nitric oxide donor nitroprusside was unaffected. Heart failure did not affect vascular morphological parameters. Perindopril decreased blood pressure and LVEDP without any modification of LV dP dt , and prevented cardiac remodeling. At the vascular level, perindopril improved the response to acetylcholine and reduced media crosssectional area and collagen density without affecting internal vessel diameter or elastin density. Thus, heart failure decreases endothelium-dependent vasodilator response to acetylcholine without modification of vessel structure. The heart-failure induced endothelial dysfunction could be prevented by angiotensin-converting enzyme inhibition.

Volumetric blood flow measurement by simultaneous Doppler signal and B-mode image processing: A feasibility study

A system is described for the estimation of volumetric flow in arteries in real time by the simultaneous processing of the audio output of a commercial ultrasound scanner carrying the Doppler signal, and the video output carrying B-mode images of the lateral view of the artery. These images are processed to provide estimates of instantaneous internal vessel diameter. Combination with the relevant estimates of spatial mean velocity provides estimates of instantaneous volumetric flow. The major limitations of the system are the low rate of production of the B-mode images (17 Hz), the limited computing power and the need to tilt the transducer to produce an acceptably low Doppler angle. This tilting diminishes the quality of the imaging echoes from the arterial walls, making diameter measurement difficult. In principle, this approach to flow measurement represents an improvement on the conventional duplex technique where a single estimate of diameter is used. In practice, its value is limited by current transducer capabilities.

Diameter and flow velocity changes of feline small pulmonary vessels in response to sympathetic nerve stimulation.

Using an X-ray television system, we measured directly changes in the internal diameter (ID), flow velocity, and volume flow of the small pulmonary vessels (100-500 microns ID) in response to electrical sympathetic nerve stimulation (SNS) in anaesthetized cats before and after adrenergic receptor blockade. Flow velocity was obtained by measuring the distance that the leading edge of the contrast medium moved per 0.1 s in the small arteries. Volume flow was obtained from the product of flow velocity and cross-sectional area calculated from the ID of the small arteries. SNS was accomplished with 10- to 15-V square-wave pulses of 2-ms duration at 20-30 Hz for 20-s periods. In response to SNS, arterial ID decreased significantly by 8-13% in the 200- to 500-microns vessels but not in the 100- to 200-microns vessels. In the veins, on the other hand, there was no significant ID decrease in any of the 100- to 500-microns vessels. After alpha-receptor blockade (phentolamine, 2 mg/kg i.v.), there were significant ID increases (4-9%) in the 100- to 500-microns arteries in response to SNS, the maximum increases being in the 100- to 200-microns arteries. After beta-blockade (propranolol, 2 mg/kg i.v.), the ID decrease due to SNS in the 200- to 500-microns arteries was enhanced (24-27%) and, in addition, the 100- to 200-microns arteries exhibited a significant ID decrease (18%). Combined alpha- and beta-blockade completely abolished the ID decrease due to SNS. In the veins, on the other hand, no ID change occurred even after alpha- or beta-blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Responses of the fetal cerebral vasculature to prenatal cytotoxic brain damage

Prenatal exposure to the drug methylazoxymethanol acetate (MAM Ac) has been commonly used as an experimental model of prenatal cytotoxic brain damage. We have examined the effects of this prenatal brain damage on the development of vasculature in the fetal neocortex, because vasculature is likely to play an important role in fetal brain repair. Pregnant Wistar strain rats received either MAM Ac (25 mg/kg) or saline on embryonic day (E) 13 by IP injection. At E15, E17, E19, and E21, the rats were overdosed with pentobarbitone (100 mg/kg) and fetuses removed for paraffin embedding, lectin histochemistry, and electron microscopy. For lectin histochemistry, sections were exposed to a horseradish peroxidase-conjugated B4 isolectin from Griffonia simplicifolia. Fetuses exposed to MAM Ac showed significant deficits in cortical vessel branch point density at E15 and E17 (46% and 20%, respectively). There were also significant reductions in stem vessel density at these ages (34% and 26%, respectively) among MAM Ac exposed animals, but there were no differences in growing tip density, capillary internal diameter, or stem vessel internal diameter. The only consistent differences between the two groups at the electron microscope level were an increase in vacuolisation and an irregular luminal surface in MAM Ac animals at E15. Tight junction formation, basement membrane formation, and loss of fenestrations were not delayed in experimental animals. The results indicate that there is no increase in angiogenic activity coincident with the fetal neocortical repair that follows MAM Ac induced damage.

Selective constriction of small cutaneous arteries by NPY matches distribution of NPY in sympathetic axons

This study has begun to investigate some functional implications of the differential localization of neuropeptide Y (NPY) in sympathetic neurons supplying different arterial segments in the cutaneous circulation of the guinea-pig ear. Responses of the main ear artery to exogenous NPY and norepinephrine (NE) were examined in vitro by measuring isometric tension. Responses of smaller arterial vessels to application of exogenous NPY or NE to the adventitial surface were examined in anaesthetized, ventilated guinea-pigs, by measuring changes in internal vessel diameter using video microscopy. Some arterial segments subsequently were examined for the presence of immunoreactivity (IR) to tyrosine hydroxylase (TH) and NPY. NPY (1 nM–10 μM) contracted the main ear artery (EC 50 = 10 nM; max. contraction = 30% KCl), and 1 nM NPY produced slight potentiation of contractions produced by NE. In vivo, local applications of NPY (1–10 μM) constricted only a subpopulation of arterial vessels (23 of 41). All vessels constricted by NPY were innervated by axons containing IR to both TH and NPY, and as a population, were more proximal in the arterial tree (branch orders 3 to 6) than were vessels insensitive to NPY (branch orders 4 to 8). Most vessels insensitive to NPY were arterioles and arterio-venous anastomoses <40 μm in diameter, which were innervated by axons containing TH-IR but not NPY-IR. In contrast, local application of NE (1–30 μM) constricted all vessels examined in vivo. When present, NPY constrictions had a longer latency (15–45 s) and duration (3–4 min) than NE constrictions of the same vessel segments. In vivo, NPY sometimes potentiated the peak amplitude of NE constrictions (2 of 7 vessels), but only in vessels where NPY also produced direct constriction. These results reveal an excellent correlation between the localization of NPY in sympathetic axons, and the location of postsynaptic NPY receptors throughout the cutaneous arterial system. Any NPY released in response to strong activation of cutaneous sympathetic neurons is likely to act preferentially on the proximal cutaneous arteries, and to lead to a more prolonged constriction of these arteries than of more distal arterioles and arterio-venous anastomoses.

Catheter-Implanted Prosthetic Heart Valves

A new expandable artificial heart valve was developed for implantation by a transluminal catheter technique without using thoracotomy or extracorporeal circulation. The aim of this study was to implant the valve in isolated vessels of the descending thoracic aorta as well as in closed chest pigs, and furthermore to study the prosthesis' mechanical stability and the valve function. The artificial valve was made by mounting a porcine aortic valve on an expandable stent. Before implantation, the stent-valve was compressed on a deflated balloon catheter and mounted inside an introducer sheath. After intravascular introduction to the descending thoracic aorta the stent-valve was discharged from the sheath. Implantation was performed by balloon inflation which expanded the stent-valve to a diameter exceeding the internal vessel's diameter. After balloon deflation the stent-valve maintained an expanded configuration ensuring a stable fixation against the vessel wall. In vitro implantations were performed in 36 isolated descending thoracic aorta specimens obtained from 80 kg pigs. Mechanical stability was evaluated by applying a downing load to the prosthesis. No displacement occurred at loads < or = 1 kg when a large balloon (31 mm) was used for implantation. Transvalvular pressure differences between 11-47 mmHg (median) were obtained at antegrade flowrates between 5-8 l/min. Furthermore, only moderate leakage flows were measured during retrograde perfusion. In vivo implantations were performed in six 80 kg pigs. Implantation was safe and easy, and angiograph and haemodynamic evaluations revealed essentially no stenosis or regurgitation. No complications in migration, perforation, hemorrhage or thrombosis were observed. This study indicates a good mechanical stability and valve function of the new expandable artificial valves.

Effect of chronic hypoxia on rat pulmonary resistance vessels: vasodilatation by atrial natriuretic peptide.

1. We have investigated the vasoreactivity of isolated pulmonary resistance vessels of rats after acclimatization to chronic hypoxia in a normobaric, hypoxic chamber. Vasoconstriction, in response to KCl and prostaglandin F2 alpha, and vasodilation, in response to atrial natriuretic peptide, were studied isometrically in a small-vessel myograph. Resting tensions were set to simulate transmural pressures of 17.5 mmHg or 35 mmHg. 2. There were no significant differences between intergroup internal vessel diameters or maximal contractile responses to either agonist. Both control and chronically hypoxic vessels generated significantly greater active contractions at 35 mmHg than at 17.5 mmHg. There were significant positive correlations between vessel diameter and maximum contractility for both control and chronically hypoxic vessels, but when contraction was expressed as equivalent transmural pressure no correlation existed. 3. There was a significant increase in potency (as measured by the concentration necessary to produce 50% of the maximum response) of KCl in chronically hypoxic vessels compared with control vessels at 35 mmHg, but not at 17.5 mmHg. In contrast, the potency of prostaglandin F2 alpha was significantly increased in chronically hypoxic vessels at 17.5 mmHg, but not at 35 mmHg. Thus the change in contractile responses of vessels from chronically hypoxic animals, in terms of maximal response and potency, is dependent on both resting pressure and agonist used. 4. After exposure to chronic hypoxia, atrial natriuretic peptide induced significantly greater maximal relaxation of pulmonary resistance vessels at both resting pressures, but its potency was unaffected.

Determinants of smooth muscle injury during balloon angioplasty.

To study the determinants of smooth muscle injury during balloon angioplasty, we conducted a series of experiments to examine the effects of degree of arterial stretching, duration of balloon inflation, and arterial precontraction on smooth muscle injury after balloon angioplasty in isolated, perfused whole-vessel segments of rabbit aortas and dog carotid arteries. Freshly dissected rabbit thoracic aortas and dog carotid arteries were mounted in a muscle bath-perfusion chamber and perfused at 80 mm Hg. The proximal half of each aorta was dilated with a 5-mm (41 +/- 6% stretch), 6-mm (64 +/- 6% stretch), or 8-mm (97 +/- 9% stretch) balloon angioplasty catheter, and the uninjured half of each vessel served as the control. The vasoconstrictor behavior of the dilated segment was then assessed by dose-response testing; long-axis, ultrasonic imaging combined with computerized edge-detection image processing was used to measure changes in segmental internal vessel diameters that were induced by phenylephrine. A similar series of experiments was performed in dog carotid arteries with 5-mm balloon catheters (42 +/- 2% stretch) to compare the susceptibility to smooth muscle injury between elastic (aortic) and muscular (carotid) arteries. Additional experiments were performed to determine the roles of prolonged (30 minutes) balloon inflation and arterial precontraction on smooth muscle injury after balloon angioplasty. In rabbit aortas, the dilated arterial segments demonstrated normal reactivity to phenylephrine after dilatation with 5- and 6-mm balloons (p = NS versus control). Severe smooth muscle injury (histopathologically) with "arterial paralysis" was observed after severe stretch (8-mm balloon) and after 5-mm balloon dilatation (46 +/- 5% stretch) in precontracted vessels. Prolonged balloon inflations did not impair aortic vasoconstrictor behavior. Dog carotid (muscular) arteries demonstrated angioplasty-induced smooth muscle injury with less severe degrees of stretch (47-52% stretch). Geometric modeling suggests that medial stretching during balloon angioplasty of diseased vessels in vivo is in the range of 15-41%.(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of Percutaneous Transcatheter Embolization on Pulmonary Function, Right-to-Left Shunt, and Arterial Oxygenation in Patients with Pulmonary Arteriovenous Malformations

The effects of percutaneous transcatheter embolization on pulmonary function and exercise capacity were assessed in 15 patients with pulmonary arteriovenous malformations (PAVM). Vital capacity (VC), FEV1, DLCO, SaO2, exercise performance, and right-to-left shunt (100% oxygen method) were measured before and 2 to 6 months after treatment. Surgical correction had been attempted in 9 patients prior to referral, and 11 had associated hereditary hemorrhagic telangiectasia (HHT). Lung function tests before intervention showed normal VC and FEV1/VC ratios, reduced DLCO (mean 71% predicted, range 36 to 123%), a resting supine SaO2 of 86% (range 67 to 95%) and mean shunt fraction of 33% (range 15 to 47%). Despite further marked falls in SaO2 on exertion, exercise capacity was well preserved. Following steel coil embolization of all PAVM with a feed vessel internal diameter greater than 3 mm (one to four sessions per patient), mean shunt fraction improved from 33 to 19% and resting SaO2 from 86 to 92% with no change in VC. A consistent improvement in diffusing capacity was seen only in patients with coexisting HHT. Exercise capacity increased in the majority (unchanged in 6), and SaO2 during maximal exercise improved in all except one patient. There were no long-term complications following embolization. These findings indicate that embolization of all macroscopic PAVM, undertaken primarily to reduce the risk of paradoxical embolization, is safe and results in substantial improvements in resting and exercise SaO2 without evidence of loss of normal lung. The right-to-left shunts remaining following embolization may reflect the presence of numerous microscopic PAVM in these patients.

Angiographic and Histologic Course after Implantation of Balloon Expandable Intravascular Stents in Miniswine Coronary Arteries: Short‐ and Mid‐Term Observations

Sixteen balloon expandable Medtronic Wiktor tantalum stents were implanted in the major coronary arteries of six minipigs, which were maintained on a normal diet and given 500 mg aspirin per day. Angiographic and histologic examinations were performed 6 and 26 weeks after implantation. Angiographically reviewed, stenting increased the inner diameter of the coronary arteries from 2.61 ± 0.44 to 3.02 ± 0.34 mm (n = 16, P ≤ 0.001). Six weeks later, this value was reduced from 2.98 ± 0.35 to 2.33 ± 0.46 mm (n = 9, P ≤ 0.05), and between 6 and 26 weeks, an increase from 2.17 ± 0.44 to 2.93 ± 0.40 mm occurred (n = 6, P ≤ 0.05). Histologic evaluation at 26 weeks after stent implantation revealed an increase of the cross‐sectional area of the total vessel from 4.30 ± 1.09 to 5.50 ± 1.67 mm2 (n = 9; P ≤ 0.01). This was due to widening of the total vessel and intimal proliferation, which amounted to 1.19 ± 0.46 mm2 within the stented segment, as compared to 0.03 ± 0.03 mm2 in control sections (P ≤ 0.01). The areas of free vessel lumen, media muscularis, and adventitia remained unchanged. In 15 of the 16 hislologically examined coronary arteries, the internal elastica was fractured at the site of stent implantation. Twelve stents had also penetrated through the external elastica without evidence of wall hemorrhage. Thirteen out of 16 stents were angiographically followed, of which 12 were patent at the final reangiography. In one animal, acute thrombosis of the stented vessel after guidewire induced coronary artery spasm caused chronic right heart failure due to right ventricular myocardial infarction. Sudden death occurred in another pig 2 hours after successful implantation of three grossly oversized stents (inner vessel diameter: 2.4 ± 0.2 mm, stent diameter 3.2 ± 0.5 mm). Autopsy revealed extensive dissections of the media with subsequent vessel occlusion. It is concluded that Medtronic Wiktor stents can be placed easily, even in more distal or curved coronary arteries. Despite antiaggregational medication, intimal proliferation is observed early after implantation, reaches a maximum at about 6 weeks, and is followed by a regression 26 weeks poststenting. At 26 weeks follow‐up, the free vessel lumen at the stent site was not significantly reduced as compared to control segments. Proper adjustment of internal vessel diameter and stent diameter is necessary to prevent major dissections and thrombotic occlusions.

Endothelium-dependent arterial vasoconstriction after balloon angioplasty.

To determine whether balloon angioplasty can provoke arterial vasoconstriction independent of platelet aggregation and neurogenic input, we studied the spontaneous vasomotor effects of balloon dilatation in isolated, perfused whole-vessel segments of rabbit aorta and pig carotid artery. Freshly dissected rabbit thoracic aortas were mounted in a muscle bath-perfusion chamber, perfused with physiologic saline solution at 70 mm Hg, and allowed to equilibrate. The proximal or distal half of the aortas were dilated with either a "large" (5 mm, 31-51% stretch beyond relaxed diameter) or a "small" (4 mm, 5-16% stretch) balloon angioplasty catheter with the other half of the vessel serving as the control. A similar series of experiments were performed in pig carotid arteries using "large" (6 or 8 mm, 48-90% stretch) balloon catheters. The spontaneous vasomotor effects of balloon angioplasty were examined with long-axis, high-frequency ultrasonic imaging combined with computerized edge detection image processing to measure changes in segmental internal vessel diameters. Additional experiments were carried out in rabbit aortas to determine the roles of the endothelium, extracellular calcium, indomethacin, ibuprofen, and calcium-channel blockade in modulating angioplasty-induced vasoconstriction. Significant arterial vasoconstriction was observed in the balloon angioplasty segments after dilatation with 5-mm balloons but not with 4-mm balloons. After dilatation with 5-mm balloons, the angioplasty segments' cross-sectional areas decreased by an average of 31% versus 4% for the nondilated (control) segments (p less than 0.0001). Similar postangioplasty vasoconstriction was observed in the pig carotid arteries (decrease in minimal vessel cross-sectional area of 41% [angioplasty segment] versus 2% [control segment]) (p less than 0.005). This angioplasty-induced vasoconstriction was prevented by endothelial denudation before angioplasty, removal of extracellular calcium, and pretreatment with indomethacin or ibuprofen. The vasoconstriction was only partially inhibited by calcium channel blockade with verapamil. These findings demonstrate that stretch-pressure-induced arterial vasoconstriction may occur after balloon angioplasty, independent of platelet aggregation and neurogenic input. This angioplasty-induced vasoconstriction appears to be mediated by an endothelially derived cyclooxygenase product(s).

Assessment of coronary artery bypass graft flow by intraoperative Doppler ultrasound technique.

A high frequency (10 MHz) Doppler ultrasound pencil probe was used to estimate flow in coronary artery bypass grafts in vitro and during cardiac surgery. In vitro, increasing the angle of the Doppler transducer in relation to flow caused underestimation of the Doppler derived flow, and using the external rather than internal vessel diameter to calculate cross sectional area caused significant overestimation. This overestimation was considerably greater for the internal mammary artery. Accurate flow estimation was obtained in vitro by the Doppler technique, but considerable variation occurred in patients studied during coronary artery bypass surgery. In conclusion, intraoperative Doppler ultrasound provides a qualitative assessment of phasic flow in coronary artery bypass grafts but is less accurate in quantifying absolute flow in these patients.

Efficacy of a New Angioplasty Catheter for Severely Narrowed Coronary Lesions

Conventional over the wire dilation catheters may be unsuccessful in crossing coronary lesions that are severely narrowed. Hence, a new, extremely low profile coronary angioplasty catheter specifically designed to dilate such lesions was investigated. The catheter features a 2.0, 2.5 or 3.0 mm (inflated diameter) balloon mounted on a guide wire. The deflated profile of the 2.0 mm balloon measures 0.020 +/- 0.001 in. (0.51 +/- 0.03 mm). The catheter can be used in conjunction with 7F angiographic or 8F guide catheters. The catheter was used in 61 patients, aged 43 to 86 years, with predominantly Canadian Cardiovascular Society class III-IV angina. Dilation was attempted in 77 lesions. Lesion length averaged 5.7 +/- 3.1 mm (mean +/- 1 SD), minimal diameter 0.51 +/- 0.25 mm and internal vessel diameter 2.27 +/- 0.43 mm. Sixty lesions (78%) were successfully dilated to less than 50% residual stenosis with this catheter alone; nine lesions were further dilated with a larger balloon catheter. The new catheter was unable to cross 13 lesions (17%); only 2 of these lesions were subsequently crossed with a conventional over the wire system. On the other hand, the catheter was used after failure of conventional dilating catheters in 21 lesions and was successful in 16. The new catheter was particularly valuable for distal lesions and those demonstrating 90 to 99% diameter reduction. For all lesions crossed, stenosis decreased from 76 +/- 11 to 29 +/- 12% after 2.9 +/- 2.7 inflations and peak inflation pressure of 8.0 +/- 2.9 bar. Complications were rare; coronary occlusion occurred in two lesions (3%) and dissection in three lesions (4%).(ABSTRACT TRUNCATED AT 250 WORDS)

A Doppler flowmeter for use in theatre

We have developed a Doppler flowmeter based on a 10 MHz pencil probe and mean frequency estimator which overcomes many of the limitations of existing electromagnetic and ultrasonic flowmeters. The output of the flowmeter, which is proportional to the first moment of the Doppler power spectrum and hence mean blood velocity is linear from 1.3 to over 50 cm s −1 for pulsatile flow. Variation in vessel diameter and angle of insonation, which are the common sources of error in Doppler flowmetry, are minimised by constraining the vessel in a plastic cuff which fixes the probe angle at 50°. A simple gauge is used to compress the vessel flat, before the cuff is applied, to measure the wall thickness to within 0.25 mm. The vessel internal diameter and hence blood flow can then be calculated using an experimentally determined calibration factor to compensate for non-even insonation. A range of sterilizable cuffs from 3–12 mm diameter have been built and the flowmeter is now being used routinely during all arterial reconstructive surgery. The accuracy and reproducibility of the system was tested for range of different sized silastic tubes on a hydraulic model and found to be <12% for vessels >2 mm internal diameter. Satisfactory signals were easily obtained from all prosthetic materials with the exception of PTFE. The instantaneous output was compared to an electromagnetic flowmeter using a fast Fourier transform algorithm; the moduli of the harmonics were virtually identical but the Doppler system produced a smaller phase shift with increasing harmonics. The Doppler flowmeter is easy to use because no electrical contact with the vessel or zeroing is required and there is no variation in sensitivity with different wall compositions or thicknesses. It can also be used on plastic tubing and is relatively inexpensive because only one transducer is required.

Dynamics and limitations of blood/muscle interface detection using Doppler power returns.

A new method that relies on backscattered Doppler power from red cells to locate and track blood/muscle interfaces is described. It allows current pulsed Doppler flowmeter systems to yield continuous information on internal vessel diameter and to evenly distribute range gates within the lumen. A smal signal model is fommulated that describes this feedback approach and indicates the relationships between system parameters (filter characteristics, gain settings, sampling rate, etc.) and tracking dynamics. Large signal nonlinear effects, problems of initial lock-in, potential loss of lock, and sources of tracking error are then outlined to provide a thorough description of this novel technique.