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Biomedical subjects

J C Stanley

Publications and source records attributed to J C Stanley.

At least 109 records · Page 6Linked to original sources

Clinical characteristics and surgical management of vascular complications in patients undergoing cardiac catheterization: interventional versus diagnostic procedures.

The purpose of this report is to define the clinical characteristics and outcome of surgical management of vascular complications after interventional cardiac catheterization and to contrast them to those after diagnostic cardiac catheterization. From October 1985 to December 1989, 101 patients were treated for 106 vascular complications after 1866 interventional and 5046 diagnostic cardiac catheterizations at the University of Michigan Medical Center. Interventional catheterizations resulted in 69 vascular complications in 64 patients (frequency 3.4%). The most common interventions included coronary angioplasty (34), of which 10 required percutaneous partial cardiopulmonary bypass, intraaortic balloon pump placement (14), and aortic valvuloplasty (11). Interventional catheter-related complications included hemorrhage (33), arterial thrombosis (18), pseudoaneurysm formation (12), catheter embolization (2), thromboembolism (2), as well as arteriovenous fistula, pseudoaneurysm, and arterial dissection (1 each). Fifteen of these 69 patients (24%) had suffered acute myocardial infarction just before their catheterization. Surgical repair was performed under local anesthesia in 70% of patients. Major vascular reconstructions were required in 9% of patients. Three percent of the involved lower extremities had to be amputated because of complications occurring after arterial puncture. Eight percent of the patients incurring vascular complications after interventional procedures died after operation. Diagnostic catheterizations resulted in 37 vascular complications in 37 patients (frequency 0.7%). In contrast to diagnostic cardiac catheterization, vascular complications after interventional cardiac catheterization occurred more frequently, were most often due to hemorrhage at the vascular access site, and occurred in high-risk, critically ill patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Comparison of the haemodynamic effects of pipecuronium and pancuronium during fentanyl anaesthesia.

Haemodynamic variables were measured following administration of pipecuronium 70 micrograms.kg-1 and pancuronium 90 micrograms.kg-1 (approximately equivalent to 1.5 x ED95) in patients anaesthetised with fentanyl 50 micrograms.kg-1 and scheduled to undergo coronary artery bypass grafting. There were significant increases in heart rate (22%), mean arterial pressure (10%), cardiac index (16%), and the rate pressure product (35%) following administration of pancuronium. The absolute values of these parameters were, however, within acceptable clinical limits. Administration of pipecuronium produced minimal and insignificant changes in these parameters. Other measured or derived indices showed only small changes with both agents and these were generally insignificant. There were no incidences of significant bradycardia following pipecuronium administration. The results from the present study suggest that pipecuronium would have advantages for use in patients with significant cardiovascular disease.

Androstane-3,17-diol↗

Neuromuscular effects of pipecuronium bromide.

The neuromuscular effects of pipecuronium bromide have been evaluated in 90 adult patients anaesthetized with thiopentone, nitrous oxide in oxygen and intravenous fentanyl with or without halothane. Eighty patients received pipecuronium 45 micrograms kg-1 and the remaining ten 70 micrograms kg-1. A separate group of 10 patients received pancuronium in a dose of 60 micrograms kg-1 (equipotent to pipecuronium 45 micrograms kg-1). Neuromuscular block was measured using a single-twitch or train-of-four mode of stimulation. The time to onset of maximum block with pipecuronium 45 micrograms kg-1 varied between 3.5 and 5.7 min depending on the mode of stimulation and the anaesthetic technique used. The time to 25% recovery of this dose varied between 41 and 54 min. The recovery index (time from 25 to 75% recovery) averaged 29 min. These values were generally similar in the group receiving pancuronium 60 micrograms kg-1. The time to onset of complete block with 70 micrograms kg-1 of pipecuronium averaged 2.5 min and the duration to 25% recovery 95 min. There were no significant changes in heart rate and arterial pressure with the use of pipecuronium. The results show pipecuronium to be a drug resembling pancuronium in its neuromuscular effects when used in equipotent doses.

Adult↗

Arterial aneurysms in children: clinicopathologic classification.

Thirty-one arterial macroaneurysms in 23 pediatric-aged patients (16 boys and 7 girls) were treated at the University of Michigan. The average age at time of diagnosis was 10.2 years (range 6 months to 18 years). Vessels involved the aorta (4), as well as hepatic (1), splenic (2), gastroepiploic (1), renal (12), iliac (1), superficial femoral (4), popliteal (1), brachial (1), radial (2), and ulnar (2) arteries. Twelve children exhibited overt clinical manifestations including presence of a mass (7), local pain (3), hematemesis (1), and painless obstructive jaundice (1). Eleven children had asymptomatic lesions. Aneurysm existence was confirmed by arteriography or operation. All but one child underwent surgical therapy, with 20 long-term survivors (mean follow-up 3.5 years). One operative death occurred and one death occurred 6 years after surgery. This experience and a review of previously reported cases served as a basis for categorization of childhood aneurysmal disease as true aneurysms associated with (I) arterial infection, (II) giant-cell aortoarteritis, (III) autoimmune connective tissue disease, (IV) Kawasaki's disease, (V) Ehlers-Danlos syndrome or Marfan's syndrome, (VI) other forms of noninflammatory medial degeneration, (VII) arterial dysplasias, (VIII) congenital-idiopathic factors, as well as (IX) false aneurysms associated with extravascular events causing vessel wall injury or disruption. Knowledge of the varied clinicopathologic characteristics of arterial aneurysms in children is important in treating these patients.

Adolescent↗

Extracellular matrix preparation of expanded polytetrafluoroethylene grafts seeded with endothelial cells: influence on early platelet deposition, cellular growth, and luminal prostacyclin release.

The importance of blood and extracellular matrix precoating of expanded polytetrafluoroethylene (ePTFE) grafts on the effectiveness of endothelial cell (EC) seeding was assessed in a canine experimental model. Part I of the study documented ex vivo platelet deposition in 256 ePTFE grafts, 6 cm x 4 mm internal diameter, after implantation as femoral artery-femoral vein or carotid artery-jugular vein arteriovenous shunts. These conduits were precoated with blood, fibronectin, laminin, or collagen type IV with laminin, after which they were seeded with enzymatically derived and cultivated venous canine endothelium at a density of 30,000 to 40,000 EC/cm2 of graft surface. Luminal deposition of Indium 111-labeled platelets, expressed as 10(8) platelets/cm2, at 30 minutes (n = 176) and 24 hours (n = 80), respectively, was 2.29 and 0.30 for blood, 2.83 and 0.37 for fibronectin, 0.99 and 0.08 for laminin, and 0.98 and 0.11 for collagen type IV with laminin. Part II of the study documented in vivo luminal EC coverage at 14 days of 6 cm x 4 mm internal diameter ePTFE femoral or carotid arterial grafts (n = 8) prepared in the same manner as part I ex vivo shunt grafts. EC coverage with blood, fibronectin, laminin, and collagen type IV with laminin preparation was 42%, 49%, 44%, and 52%, respectively. The graft:carotid artery ratio of luminal 6-keto-PGF1 alpha release at 14 days with these same four preparations was 0.38, 0.31, 0.35, and 0.32, respectively. Precoatings of ePTFE prostheses with fibronectin, laminin, and collagen type IV are known to enhance the initial attachment of seeded EC. Fibronectin caused an insignificant increase in early platelet accumulation; laminin or laminin with collagen type IV preparations were associated with significantly less (p less than 0.005) deposition of platelets when compared to whole blood preparations. Most importantly, none of the four preparation techniques resulted in different in vivo rates of EC growth or luminal release of prostacyclin from conduits studied 14 days after implantation.

Animals↗

Effects of plasma on PGI2 release from prolonged perfused canine veins.

Prostacyclin release from endothelial cells in culture appears increased by the presence of plasma, but occurrence of a similar phenomenon in intact vessels has not been established. In the present investigation release of 6-keto-PGF1 alpha, the stable breakdown product of prostacyclin, was quantitated from canine veins perfused ex vivo for 15 minute periods, using three different perfusates: 1) Hank's balanced salt solution (HBSS), 2) 20% platelet poor plasma (PPP) derived from heparinized blood, in HBSS, and 3) 20% PPP in HBSS with added arachidonic acid (AA). No differences in initial 6-keto-PGF1 alpha release existed among the three perfusates. However, PPP and PPP + AA solutions were associated with lesser declines in release, than occurred with HBSS alone, these differences being statistically significant after 60 min of perfusion (p less than 0.05). When PPP derived from heparinized and citrated blood rather than from only heparinized blood was used, there was a significantly lower release of prostacyclin (p less than 0.05). The latter may be due to citrate binding of calcium. These data indicate that autologous plasma does not alter initial prostacyclin release from freshly harvested canine veins, but that it weakens the decline in release usually following prolonged periods of perfusion.

Animals↗

Small-caliber polyurethane and polytetrafluoroethylene grafts: a comparative study in a canine aortoiliac model.

In vivo stability of a new small-caliber polyurethane graft (n8) was assessed in a canine aortoiliac model and compared to that of a conventional expanded polytetrafluoroethylene (ePTFE) graft (n8). Six months following implantation, marked aneurysmal dilatation to 230 +/- 80% (mean +/- SD) of the original diameter occurred in polyurethane grafts, while dilatation to 110 +/- 8% of the original diameter occurred in ePTFE grafts (p less than 0.005). Interval patency was 75% for each graft type. Luminal thrombus affected 59% of polyurethane graft surfaces compared to 22% of ePTFE graft surfaces (p less than 0.01). Qualitative examination of representative sections of polyurethane conduits demonstrated thick inner capsules with numerous small islands of graft material surrounded by macrophages and bands of mature fibrous tissue, in contrast to the thinner neointima and limited anastomotic pannus ingrowth observed in ePTFE grafts.

Animals↗

Reversal of depressed oxygen consumption accompanying in vivo protamine sulphate-heparin interactions by the prostacyclin analogue, iloprost.

Oxygen consumption (VO2) is known to be depressed 50 to 60% during protamine sulphate reversal of heparin anticoagulation. Accompanying this event are systemic hypotension, pulmonary artery hypertension and thrombocytopaenia. The effect of a pro-stacyclin analogue, iloprost, on protamine-induced changes in VO2 was assessed in this investigation. Three groups of anaesthetised adult mongrel dogs were studied: Group I--control subjects received i.v. normal saline infusions (n = 10); Group II--subjects received low-dose i.v. iloprost infusions (25-50 ng/kg/min) over 30 min (n = 7); and Group III--subjects received high-dose i.v. iloprost infusions (175 ng/kg/min) over 30 min (n = 7). All dogs initially received sodium heparin, 150 IU/kg i.v. Protamine sulphate, 1.5 mg/kg i.v., was subsequently administered over 10 s following the first 20 min of saline or iloprost infusion. Continuous measurements included: mixed venous (SvO2) and arterial (SaO2) oxygen saturation, arterial blood pressure, pulmonary artery pressure, heart rate and carotid artery flow (CaQ). Thermodilution cardiac output (CO) allowed calculation of VO2. Platelet counts were performed before and 3 min after protamine infusion. The VO2 declines in Group II and III subjects compared to Group I controls were markedly less. Maximum VO2 declines in Group I control dogs of -38.2 +/- 26.7% and Group II dogs of -34.1 +/- 36.8% at 75 to 90 s post-reversal contrasted to -2.9 +/- 31.9% in Group III animals at the same time interval. VO2 increases occurred 3 to 10 min after protamine exposure in Group III animals, as did attenuation of systemic hypotensive and pulmonary hypertensive responses in this group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Impaired myocardial function and oxygen utilization due to protamine sulfate in an isolated rabbit heart preparation.

The myocardial effects of protamine, with and without heparin, were documented in this investigation. Isolated rabbit hearts (n = 30) were retrograde perfused with Krebs-Ringers bicarbonate solution aerated with 95% O2/5% CO2 through the aortic root (37 C, 80 mmHg). Developed left ventricular blood pressure, heart rate, coronary artery flow, contractility as reflected by peak +dp/dt, oxygen extraction (a-vO2), and oxygen consumption (VO2) were measured at baseline and continuously throughout the experiment. Protamine (25 micrograms, 50 micrograms, and 250 micrograms per mL of perfusate) was circulated in the Krebs-Ringers buffer to hearts perfused without heparin (groups I, II, and III) or hearts perfused with heparin added to the buffer solution, 0.1 IU/1.0 microgram protamine (groups IV, V, and VI). Blood pressure 4 minutes after protamine was less in groups III (-23 mmHg) and VI (-28 mmHg) than in groups I (-6 mmHg), II (-18 mmHg), IV (-1 mmHg), and V (-7 mmHg). Heart rate changes (beats/minute) at 4 minutes revealed similar dose-dependent reductions (III and VI: -51, -55; II and V: -36, -36; and I and IV: -20, -16, respectively). Coronary artery flow at 4 minutes was slightly increased in groups III (9 mL/minute) and VI (15 mL/minute), but was relatively unchanged in the other groups. Decreases in contractility were apparent in all groups 4 minutes after protamine was started: group I, -14%; II, -16%; III, -30%; IV, -7%; V, -15%; and VI, -34%. Similarly declines in oxygen extraction and consumption were noted in all groups at the same time period and were greater in groups III (-53%, -44%) and VI (-55%, -49%) than in groups I (-25%, -26%), II (-15%, -12%), IV (-48%, -49%) and V (-15%, -18%), with p less than or equal to 0.05 or p less than or equal to 0.01 compared to baseline. Three of ten hearts exposed to high-dose protamine stopped beating after 5 minutes. This investigation establishes, for the first time, that protamine has dose- and time-specific adverse effects on cardiac contractility. In addition protamine decreases myocardial a-vO2 and VO2. These changes may contribute to certain adverse events accompanying the clinical administration of protamine.

Animals↗

Artery, periarterial adipose tissue, and blood microbiology during vascular reconstructive surgery: perioperative and early postoperative observations.

The presence and clinical significance of bacteria in the arterial wall, periarterial adipose tissue, and blood samples acquired during elective vascular operations were assessed in this study. Specimens were obtained from a random series of 84 patients (56 men, 28 women) undergoing 75 primary and 9 secondary arterial reconstructions. Operations performed most frequently included abdominal aortic aneurysmectomy (42), aortofemoral bypass reconstruction (15), and lower extremity bypass surgery for occlusive disease (7). Perioperative antibiotics were administered to all but one patient. A sample of artery, adjacent adipose tissue, and blood were obtained for microbial analysis during the vascular anastomosis or arteriotomy. This yielded a total of 152 artery, 139 adipose tissue, and 129 blood samples for study. Each specimen was divided and placed in blood agar plates, thioglycolate broth, and brain-heart infusion broth. Tissues yielding growth of the same organism(s) in two or more different media were considered positive for the presence of bacteria. Bacteria were present in at least one of the three tissues studied in 32/84 patients (38%). The frequency of positive cultures in primary (29/75, 39%) and secondary procedures (3/9, 33%) were similar. One positive culture site occurred in 26/32 (81%) patients, two positive culture sites existed in 5/32 (16%) patients, and three positive sites were found in 1/22 (3%) patients. Eighteen individual artery (18/152, 12%) and 19 adipose tissue samples (19/139, 14%) harbored bacteria, whereas only two blood cultures were positive (2/129, 2%). Organisms identified included coagulase-negative staphylococci (71%), gamma-streptococci (7%), diphtheroids (7%), Micrococcus (5%), alpha-streptococci (5%), Staphylococcus aureus (2%), and Pseudomonas picketti (2%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Prostanoid release from ex vivo perfused canine arteries and veins: effects of prolonged perfusion, intermittent perfusion, as well as exposure to exogenous arachidonic acid, thrombin and bradykinin.

Regulation of prostanoid release from ex vivo perfused vessel segments is not fully understood. A series of perfusion experiments were performed with canine arteries and veins to define certain regulatory phenomena. Arteries were perfused with pulsatile flow of 90 ml/min at a pressure of 100 mmHg, and veins with nonpulsatile flow of 90 ml/min at a pressure of 7 mmHg. Segments were perfused with Hanks' balanced salt solution for five 15-min periods with the perfusate exchanged after each study period. With onset of perfusion, there was an initial burst of prostacyclin release to 127 +/- 40 pg/mm2, declining to 32 +/- 10 pg/mm2 after 60 minutes (p less than 0.005). If perfusion continued for 5.5 hours, there was a stable release period between 1 and 3 hours, followed by a very slow decline. At that time addition of arachidonic acid (AA) increased prostacyclin release six-fold (p less than 0.01). Vessels perfused for 1 hour and then rested for another hour, responded to reperfusion at the second onset of flow with a two-fold increase in prostacyclin release (p less than 0.01). Vessels perfused with thrombin, bradykinin or AA (either added to each perfusate or only to the last perfusate) exhibited greater prostacyclin release than did control segments. Release of thromboxane steadily declined with time in all parts of the study, and only increased with the addition of AA to the perfusate.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

Recombinant gene expression in vivo within endothelial cells of the arterial wall.

A technique for the transfer of endothelial cells and expression of recombinant genes in vivo could allow the introduction of proteins of therapeutic value in the management of cardiovascular diseases. Porcine endothelial cells expressing recombinant beta-galactosidase from a murine amphotropic retroviral vector were introduced with a catheter into denuded iliofemoral arteries of syngeneic animals. Arterial segments explanted 2 to 4 weeks later contained endothelial cells expressing beta-galactosidase, an indication that they were successfully implanted on the vessel wall.

Animals↗

Effect of preexcisional heparin anticoagulation on excised canine vein and artery prostanoid production.

The effect of heparin, administered prior to vessel dissection and excision, on the luminal release of prostanoids from an excised vessel was assessed. Eight adult mongrel dogs underwent removal of the jugular vein and carotid artery on one side, followed by intravenous administration of heparin sodium (150 IU/kg) and subsequent removal of these same vessels from the contralateral neck. The excised vessels were perfused in an ex vivo system with Hanks' balanced salt solution for five consecutive 15-min periods. Prostacyclin release (measured as 6-keto-PGF1 alpha) and thromboxane A2 (measured as thromboxane B2) release into the perfusate were quantitated by radioimmunoassay. Vessel segments were studied with and without first period thrombin stimulation (2 U/ml) and with arachidonic acid (4 micrograms/ml) stimulation during the last perfusion period. Vein segments following heparin administration exhibited greater prostacyclin production than veins not exposed to heparin. This effect did not occur in arteries. Heparin did not influence thromboxane A2 release. Luminal endothelial cell coverage was not affected by the presence or absence of heparin. Thus heparin anticoagulation prior to dissection and excision of a vein, may enhance early preservation of its endothelial cell function as evident by increased luminal release of prostacyclin.

6-Ketoprostaglandin F1 alpha↗

Effects of thromboxane synthetase inhibition on patency and anastomotic hyperplasia of vascular grafts.

The efficacy of a thromboxane synthetase inhibitor (U-63,557A, Upjohn) in promoting early patency and inhibiting anastomotic intimal hyperplasia in ePTFE grafts was compared to that of acetylsalicylic acid (ASA) in a canine model. Animals were started on ASA 5 gr po qd (Group I, n = 12) or U-63,557A 10 mg/kg po bid (Group II, n = 12) 1 day before placement of bilateral 5-mm-i.d., 13- to 16.5-cm-long ePTFE aortoiliac grafts and continued on the medication for the 16-week study. Six dogs in each group received autologous endothelial cell-seeded grafts, while the other six received unseeded grafts. Patency was determined weekly by assessment of femoral pulses. At the conclusion of the study anastomotic intimal hyperplasia was measured on serial sections through the distal anastomosis using a computer-linked digitizer. In Group I the patencies of seeded and unseeded grafts were not significantly different, being 100 and 83%, respectively. Furthermore, luminal narrowing due to intimal hyperplasia was not significantly different being 9.1 +/- 7.6% (chi +/- SD) in seeded grafts and 8.8 +/- 8.1% in unseeded grafts. On the other hand, in Group II the seeded grafts had significantly improved patency when compared to the unseeded grafts (83% vs 33%, P less than 0.05) and less luminal narrowing (11.4 +/- 11.1% vs 21.9 +/- 19.5%, P less than 0.01). Although U-63,557A administration promoted patency of unseeded grafts compared to no antiplatelet medication (0% patency), it was significantly less effective than ASA in improving patency (P less than 0.05) and inhibiting luminal narrowing (P less than 0.01).

Anastomosis, Surgical↗

Arterial 6-keto-PGF1 alpha and TxB2 release in ex vivo perfused canine vessels: effects of pulserate, pulsatility, altered pressure and flow rate.

Certain experimental conditions are known to influence the release of prostacyclin and thromboxane from the vessel wall. The specific effects of altered pulsatility, pressure, and flow rate on intraluminal release of 6-keto-PGF1 alpha and thromboxane B2 were assessed in canine arteries perfused ex vivo for five 15 min periods with arachidonic acid (AA) added during the last period. Control arteries were perfused at 100 mmHg with pulsatile flow of 90 ml/min. Experimental arteries were perfused at 7, 50 and 200 mmHg with pulsatile flow of 90 ml/min, and at 100 mmHg pressure with pulsatile flow of 20, 60, 130 and 180 ml/min, as well as at 100 mmHg with 90 ml/min nonpulsatile flow. Perfusion pump rates of 44 and 96 beats/min were also assessed. The lowest perfusion pressure, 7 mmHg, resulted in a lesser initial release of prostacyclin compared to higher pressures, and there was a tendency to a higher release of prostacyclin with increasing pressures. There was also a tendency for a lesser response to AA in arteries perfused at 200 mmHg, perhaps due to endothelial cell damage. Nonpulsatile flow was associated with a decreased initial release of prostacyclin, and diminished release following addition of AA when compared to pulsatile flow. Altered flow rate elicited no difference in prostacyclin release, although there was a tendency towards a lesser release when perfused at 20 ml/min compared to 130 ml/min or 180 ml/min. Thromboxane release was decreased by nonpulsatile flow but was otherwise unaffected by the experimental conditions tested. It is concluded that pulsatility enhances release of prostacyclin from arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

Platelet reactivity in human aortic grafts: a prospective, randomized midterm study of platelet adherence and release products in Dacron and polytetrafluoroethylene conduits.

Platelet-related phenomena at the blood-surface interface of randomly placed knitted Dacron (n = 6) and polytetrafluoroethylene (ePTFE) (n = 6) interposition aortic grafts were studied in patients undergoing abdominal aortic aneurysmectomy. Luminal accumulation of platelets was assessed by infusing indium-111-oxine (400 microCi) labeled autologous platelets and imaging grafts at 1 week, 3 months, and 6 months after surgery. Image analysis included an indium ratio technique (comparing aortic graft radioactivity to that of an iliac artery) and a red blood cell technetium subtraction technique (excluding blood pool radioactivity from graft radioactivity, with the heart or iliac artery serving as reference regions). Plasma levels of beta-thromboglobulin and platelet factor 4 were correlated with platelet accumulations on the aortic prostheses. Differences in graft radioactivity or platelet-release products were not evident 1 week after surgery. Three months after implantation, Dacron and ePTFE conduits exhibited 87% and 47% (p less than 0.05) more radioactivity with the indium ratio technique than the iliac artery. Similarly, increased Dacron compared with ePTFE graft radioactivity was noted using technetium subtraction techniques: 71% vs 30% with a heart reference and 26% vs 11% with an iliac artery reference, respectively. Increases in graft radioactivity correlated with increases in both plasma beta-thromboglobulin and platelet factor 4 at 3 months (r = 0.6 to 0.9; p less than 0.05 to 0.001 depending on the imaging technique used). At 6 months, differences did not persist. In fact, technetium subtraction techniques suggested less Dacron conduit reactivity. It is speculated that differences in platelet accumulation and activation associated with different graft substrates may prove clinically important.

Adult↗

Comparative potency of pipecuronium bromide and pancuronium bromide.

Cumulative dose-response curves were constructed to determine the comparative potency of pipecuronium and pancuronium. From these, the ED50 and ED95 values were calculated. These were 24.96 micrograms kg-1 and 44.96 micrograms kg-1, respectively, for pipecuronium and 30.42 micrograms kg-1 and 61.12 micrograms kg-1, respectively, for pancuronium.

Adult↗