Biomedical subjects

T W Wakefield

Publications and source records attributed to T W Wakefield.

At least 73 records · Page 4Linked to original sources

PubMed1993

Popliteal vein entrapment presenting as deep venous thrombosis and chronic venous insufficiency.

PURPOSE: This report describes popliteal vein entrapment in three patients and demonstrates that it may present with manifestations of typical venous disease. METHODS: This report was compiled from a review of inpatient and outpatient records. RESULTS: In the first case, a 28-year-old woman was seen with left leg popliteal and calf deep vein thrombosis without obvious cause. She described long-standing calf discomfort, and passive dorsiflexion of the left foot caused disappearance of arterial pulsations at the pedal level. She was given the anticoagulants heparin and sodium warfarin (Coumadin) followed by surgical exploration. The popliteal vein and artery were entrapped by a fibrous extension of the medial head of the gastrocnemius muscle attaching to the lateral femoral condyle. After band lysis, the patient has been symptom free for 6 years. The second patient, a 37-year-old man, was seen with bilateral chronic venous insufficiency (CVI). Passive dorsiflexion and active plantar flexion of the feet did not diminish the pedal pulses; impedance plethysmography suggested mild outflow obstruction. Ascending venography demonstrated entrapment at the midportion of duplicated popliteal veins with no postthrombotic changes. He was treated with compression stockings and has done well during an 18-month follow-up. The third patient, a 17-year-old male, was seen with severe symptoms of right leg CVI and venous obstruction since 3 years of age. Air plethysmography revealed ambulatory venous hypertension, whereas venography demonstrated reflux down to the knee with an extrinsic narrowing at the midpopliteal vein. During operation, an abnormal origin of the lesser saphenous vein (LSV) from the popliteal vein was found; the LSV took a medial route, compressed the tibial nerve, and caused severe distortion and narrowing of the popliteal vein. Division of the LSV resulted in release of popliteal venous compression and immediate relief of symptoms. CONCLUSIONS: The three cases presented demonstrate that popliteal venous entrapment may begin with symptoms of deep vein thrombosis and CVI. Popliteal venous entrapment must be considered in the differential diagnosis of venous disease in younger patients in whom common predisposing factors are absent.

Adolescent↗

PubMed1993

Diagnostic approaches and surgical treatment of deep venous thrombosis and pulmonary embolism.

Diagnostic approaches for thromboembolism include Doppler probe examination, impedance plethysmography, phleborheography, radio-labeled fibrinogen scanning, magnetic resonance imaging, duplex imaging, and venography. The two primary diagnostic approaches for pulmonary embolism include ventilation/perfusion lung scanning and pulmonary arteriography. Surgical options available for venous thromboembolism are generally limited to those condition in which limb viability is threatened from acute iliofemoral thrombosis. Vena caval interruption, performed in patients with a contraindication to anticoagulation, a complication during anticoagulant therapy, and recurrent pulmonary embolism in the presence of adequate anticoagulation (among other indications) is best accomplished with the Greenfield filter. Surgical approaches for pulmonary embolism, limited to patients with massive embolism with hypotension, include catheter pulmonary embolectomy and open pulmonary embolectomy.

Humans↗

PubMed1993

Long-term experience with transvenous catheter pulmonary embolectomy.

PURPOSE: Massive pulmonary embolism (PE), defined by systemic hypotension and need for inotropic support, has a high mortality rate. Transvenous catheter pulmonary embolectomy performed with the patient receiving local anesthetic provides an expeditious alternative to lytic therapy or open embolectomy on cardiopulmonary bypass. METHODS: The indication for embolectomy in this series of 46 patients was hypotension despite inotropic support in all but four patients (91%); the latter sustained major embolism and were respirator dependent. In the first 10 patients treated from 1970 to 1974, a metal cup attached to a straight catheter was used. RESULTS: Hemodynamic improvement occurred in nine of 10 initial patients, but recurrent PE and a mortality rate of 50% prompted addition of a vena caval filter and directional control to the catheter. Subsequently 36 patients were treated with this combination from 1975 to 1992. Emboli were extracted in 76% (35 of 46) of the total series with a 30-day survival rate of 70% (32 of 46). Hemodynamic data showed an average reduction in mean pulmonary artery pressure of 8 mm Hg and a significant increase in mean cardiac output from 2.59 L/min to 4.47 L/min (p = 0.003) after embolectomy. Complications included wound hematoma (15%), pulmonary infarct (11%), recurrent deep venous thrombosis (6%), pleural effusion (4%), and myocardial infarction (4%). CONCLUSIONS: Successful embolectomy was most likely for categories of major PE (4 of 4, 100%) and massive PE (27 of 33, 82%) and least likely for chronic PE (5 of 9, 56%) (p < 0.03). Successful embolectomy also predicted long-term survival (p < 0.01), which was 89 months for the series (range 1 to 237 months). Catheter pulmonary embolectomy by surgeon and radiologist is of maximal benefit for major or massive PE but less likely to benefit patients with chronic recurrent PE.

Adolescent↗

PubMed1993

Effects of lumbar sympathectomy on canine transcutaneous oxygen tension.

Augmentation of cutaneous blood flow by postganglionic lumbar sympathectomy may not reflect an increase in nutritive vascular supply to the dermal tissues. Transcutaneous oxygen tension (TcPO2) was compared with radionuclide microsphere determination of dermal microcirculation in a hind limb sympathectomy model in 20 dogs. After 90 minutes the TcPO2 was greater in the sympathectomized limbs than in the contralateral limbs (125 mm Hg versus 114 mm Hg, p < or = 0.05). In contrast, microsphere-determined paw dermal capillary flow declined in sympathectomized limbs (4.9 ml/min/100 gm versus 11.8 ml/min/100 gm, p < or = 0.05). Decreases in the TcPO2/venous PO2 ratio correlated with sympathectomy-induced increases in total limb blood flow (r = 0.60; p < or = 0.001), reflecting less efficient oxygen extraction. These observations confirm the lack of enhancement of tissue oxygen delivery by sympathectomy because of the associated dilation of cutaneous arteriovenous shunts.

Animals↗

PubMed1992

Time-related effects of heparin sulfate on regional and systemic anticoagulation.

Optimal timing of vascular clamping to anticoagulation during cardiovascular surgical procedures is poorly defined. This study uses a canine model to determine the effectiveness of three different methods of heparin administration. Heparin sulfate (150 IU/kg) was administered by: injection into the jugular vein 5 minutes before infrarenal aortic clamping (Group 1), injection into the terminal aorta immediately after infrarenal aortic clamping (Group 2), and injection into the jugular vein immediately after infrarenal aortic clamping (Group 3). Thrombin clotting times and partial thromboplastin times were measured in venous blood from the upper and lower extremities before (baseline) heparin administration, and 1, 3, and 5 minutes following heparin administration. Activated clotting times were assessed in lower extremity blood at baseline, and at 1 and 5 minutes after heparin injection. Significant differences existed between groups in both upper and lower extremities. Systemic anticoagulation occurred within 1 minute after intravenous heparin administration in Groups 1 and 2 in the lower extremity, and Groups 1 and 3 in the upper extremity. Delayed anticoagulation in the lower extremity was noted with systemic injection after aortic clamping in Group 3, and after regional intra-aortic administration in the upper extremity of Group 2 subjects. Complete anticoagulation was noted by 5 minutes in all groups in both the upper and lower extremities. These results suggest that the safe time period between heparin administration and vascular clamping varies with the route and the timing of its administration. Intravenous administration prior to aortic cross-clamping provided adequate anticoagulation in this canine model in both the upper and lower extremity blood after 1 minute of heparin circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Heparin-mediated reductions of the toxic effects of protamine sulfate on rabbit myocardium.

Protamine sulfate causes direct myocardial suppression when used to reverse heparin anticoagulation. Protamine's excessive positive charge accompanying its surface arginine groups appears to be responsible for this toxicity. This study was designed to assess the hypothesis that negatively charged heparin given after protamine exposure may enhance the recovery of protamine-induced myocardial dysfunction. Isolated rabbit hearts (n = 20) were perfused with physiologic saline solution at 80 to 90 mm Hg containing high dose protamine, 250 micrograms/ml, until heart contraction essentially ceased (baseline). Hearts were then randomly reperfused for 15 minutes with either physiologic saline solution (group I, n = 10) or heparin plus physiologic saline solution (group II, n = 10) at a dose of 0.1 IU/1.0 microgram of previously administered protamine. Developed left ventricular blood pressure, heart rate, pulmonary artery PaO2, contractility (+dp/dt), oxygen extraction (AvO2), oxygen consumption (VO2), and rate x pressure product were assessed. A protective, beneficial response accompanied heparin administration (group II) in all functions assessed except blood pressure. Maximum changes, comparing group I with II, were heart rate (beats/min) -72 versus -1, p less than 0.001; +dp/dt -64% versus -51%, p less than 0.01; PaO2 +86% versus +9%, p less than 0.001; AvO2 -37% versus -4%, p less than 0.001; VO2 -50% versus -28%, p less than 0.008; and rate x pressure product -73% versus -51%, p less than 0.001. These data suggest a separation of protamine's hemodynamic effects (blood pressure) and metabolic effects (VO2). Furthermore, these data support the tenet that heparin is able to markedly lessen the toxic myocardial effects of protamine.

Animals↗

PubMed1991

Increased prostacyclin and adverse hemodynamic responses to protamine sulfate in an experimental canine model.

Prostanoid activity was correlated with the hemodynamic effects of protamine sulfate reversal of heparin in 24 dogs undergoing three different pretreatment regimens: Group I (n = 8) received saline, Group II (n = 8) received the thromboxane synthetase inhibitor U63,557A (30 mg/kg), and Group III (n = 8) received indomethacin (10 mg/kg). Pretreatment substances were administered as 5-min intravenous infusions 20 min before anticoagulation with intravenous heparin (150 IU/kg). Protamine sulfate (1.5 mg/kg) was subsequently given as a 10-sec intravenous infusion 30 min after heparin had been administered. Hemodynamic data, as well as prostacyclin (PGI2) and thromboxane (TxA2) activity in aortic, venous, and pulmonary artery blood samples, were assessed over a 30-min time period following protamine administration. Group III indomethacin pretreatment provided the most protection from declines in blood pressure, heart rate, cardiac output, venous oxygen saturation, oxygen consumption, and elevations in pulmonary pressures and was accompanied with actual declines in PGI2. Group II U63,557A pretreatment was associated with the most severe hemodynamic changes and the greatest increase in PGI2 (+576%). Elevated PGI2 correlated with hypotension at 1 and 3 min (P less than 0.01), as well as pulmonary artery pressure declines at all times following protamine reversal. TxA2 changes did not correlate with hemodynamic changes. Protamine's adverse hemodynamic responses were attenuated with cyclooxygenase blockade by indomethacin, but were worsened with selective TxA2 blockade with U63,557A. Excess arachadonic acid precursors in the latter setting may increase PGI2 production. This study, for the first time, raises the possibility that PGI2 contributes to the adverse effects accompanying protamine reversal of heparin anticoagulation.

Animals↗

PubMed1991

Absence of complement-mediated events after protamine reversal of heparin anticoagulation.

Protamine reversal of heparin anticoagulation is associated with adverse hemodynamic effects that may be attenuated with protamine pretreatment (PP). This study assesses the role of complement activation during these phenomena in adult cardiac surgery patients. Sixteen individuals undergoing cardiopulmonary bypass were given intravenous normal saline or protamine (2 mg/kg) as a randomized pretreatment prior to undergoing heparin anticoagulation (400 IU/kg), coronary artery revascularization, and subsequent reversal of the anticoagulated state with protamine (4 mg/kg). Blood pressure, pulmonary artery diastolic pressure (PAD), heart rate, and cardiac output (CO) were measured during and after pretreatment, prior to heparin reversal by protamine, and for 10 min after reversal. Total hemolytic complement (CH50), C3 conversion to C3b, C3a/C5a, platelet count, and white blood cell count (WBC) were also measured at the same time periods. No significant correlation existed between complement activation and hemodynamic events, as might have been evident by decreased CH50, increased C3 conversion to C3b, or elevations in C3a/C5a levels. PP significantly prevented the CO decrease occurring at 1 and 3 min following heparin reversal by protamine (-0.8 and -1.4 liters/min vs 0.1 and -0.2 liters/min, P less than 0.05 and P less than 0.01, respectively). Reversal hypotension was less with PP, although PAD fell equally in both groups. WBC decreases after heparin reversal were less after PP (-25% vs -7%, P = 0.06). These data support the conclusion that, contrary to earlier reports, adverse hemodynamic and hematologic responses accompanying protamine reversal of heparin anticoagulation do not appear to be correlated with activation of complement. In fact, those patients having the greatest C3a generation exhibited the least hemodynamic changes.

Adult↗

PubMed1991

Effect of controlled hemorrhage on tissue and serum cefazolin clearance.

Effects of blood loss on tissue and serum antibiotic levels were investigated in 30 New Zealand white rabbits. Studies were conducted over a 3.5-hr period after intravenous administration of cefazolin, 30 mg/kg, in control animals (Groups I and IV, n = 5 each) and animals having 50% (Groups II and V, n = 5 each) or 100% (Groups III and VI, n = 5 each) of their blood volume removed and replaced with either Ringer's solution (Groups I, II, and III) or rabbit whole blood (Groups IV, V, and VI) sufficient to maintain central venous pressures at baseline levels. Periodic samples of retroperitoneal fat, iliac artery, and serum were assayed for cefazolin concentration by disc diffusion. Decreased tissue antibiotic levels were observed in animals undergoing 100% blood replacement (Groups III and VI) compared to controls (Groups I and IV) in both fat (P less than or equal to 0.01) and artery (P less than or equal to 0.01) at 90 min. Decreased antibiotic serum half-life accompanying hemorrhage existed when comparing Group II to I (P less than or equal to 0.05), Group III to I (P less than or equal to 0.01), and Group IV to V (P less than or equal to 0.01). The increased antibiotic clearance related to blood loss in this study justifies reassessment of intraoperative dosing intervals. More frequent dosing may be required to maintain stable tissue and serum antibiotic levels during substantial operative hemorrhage.

Animals↗

PubMed1991

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↗

PubMed1991

Deep venous thrombosis in the baboon: an experimental model.

Experimental models of deep venous thrombosis, heretofore, have not been available for laboratory studies. This investigation establishes a novel model of venous thrombosis by inhibiting the protein C system combined with venous stasis and subtle venous injury. Ten adolescent baboons were studied in pairs, with one animal receiving saline solution (B2, B4, B6, B8, B10) and one being exposed to thrombogenic reagents (B1, B3, B5, B7, B9). These reagents represented a combination of a monoclonal antibody (HPC4) to protein C, 1 to 4 mg/kg administered over 5 minutes, and tumor necrosis factor administered over 3 minutes at a dose of 150 micrograms/kg through a catheter placed into the left superficial femoral vein with distal ligation. To encourage stasis, a pediatric size blood pressure cuff was inflated to 40 mm Hg on the right thigh for 50 minutes of every hour during the first experimental day (day 1) in B5 to B10. The animals were observed for a 6-hour period on day 1 and then for an 11- to 15-day period until sacrifice. Hemodynamic and hematologic parameters were recorded along with duplex imaging of the iliac veins and inferior vena cava on a daily basis. Venography was performed on day 1, day 4, and the day of sacrifice. At sacrifice the entire iliac and vena caval system was carefully dissected, opened, and photographed. Experimental animals given the HPC4 and tumor necrosis factor developed left iliac vein thrombosis extending into the inferior vena cava. Duplex imaging, venography, and autopsy revealed that control animals receiving saline solution never developed comparable thrombus. Experimental subjects exhibited thrombus on duplex imaging by day 4 (B1), day 3 (B3), day 2 (B5), 120 minutes (B7), and 360 minutes (B9) after receiving HPC4 and tumor necrosis factor. Venograms performed on day 1 exhibited thrombus in B5, B7, and B9. The extent of thrombus, the timing of its occurrence, and its effect on the animals' left leg followed a dose-dependent relationship for the animals in which the occlusive blood pressure cuff was used. Significantly greater declines in blood pressure, white blood cell count, and platelet count were found in affected animals given HPC4 and tumor necrosis factor reagents as compared to control subjects. All affected animals demonstrated the appearance of fibrin split products and a markedly prolonged prothrombin time. This investigation, for the first time, establishes a reproducible model of deep venous thrombosis involving inhibition of protein C that will facilitate further laboratory studies on venous thrombosis.

Animals↗

PubMed1991

The use of immobilized protamine in removing heparin and preventing protamine-induced complications during extracorporeal blood circulation.

Heparin, currently used in extracorporeal blood circulation procedures, may lead to hemorrhagic complications. Protamine, used for reversal of heparin-induced anticoagulation at the end of such procedures, can cause adverse hemodynamic responses. To prevent both types of complications, we have developed a reactor device containing immobilized protamine (i.e., a protamine bio-reactor) that can be placed at the distal end of the circuit, thus providing simultaneous extracorporeal heparin removal and protamine treatment. In preliminary in vivo studies involving dogs at a blood flow of 100 ml/min, the bio-reactor removed about 50% of the administered dose of heparin (i.e., 100 units/kg) in 10 min. While rapid injection of protamine in dogs anticoagulated with heparin produced a transient and significant (P less than 0.005) decreases in systemic arterial blood pressure (-39.5 +/- 9.2 mmHg), cardiac output (-1.59 +/- 0.23 L/min), and mixed venous oxygen saturation (-7.5 +/- 1.3%) and increases in pulmonary artery systolic (+12.7 +/- 4.4 mmHg) and diastolic pressures (+10.0 +/- 3.6 mmHg), the use of the protamine bio-reactor did not elicit any statistically significant change in any of the variables measured. Hemolysis was not significant, as reflected by a statistically insignificant change of the animals' red blood cell counts, hematocrits, and total hemoglobin values. In addition, hemolytic complement was found to be reduced only by 10% in animals with the protamine bio-reactor, whereas it was reduced rapidly by 20% in animals receiving intravenous protamine administration and progressively by 20% in control animals with a sham reactor that contained no protamine. Furthermore, the use of the protamine bio-reactor also significantly reduced the protamine-induced transient thrombocytopenic and granulocytopenic responses. The white blood cell counts and platelet counts decreased to 87.7 +/- 7.5 and 83.3 +/- 5.0% of baseline, respectively, in dogs with the protamine bio-reactor compared to 35.5 +/- 14.3 and 32.1 +/- 8.1% of baseline in dogs receiving intravenous protamine. The protamine bio-reactor may provide a unique means to simultaneously control both heparin- and protamine-induced complications.

Animals↗

PubMed1991

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↗

PubMed1990

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↗

PubMed1990

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↗

PubMed1990

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↗

PubMed1989

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↗

PubMed1989

Prevention of venous thrombosis and pulmonary embolism.

Transvenous Greenfield filter insertion is a safe and efficient mechanical means of protection against recurrent pulmonary thromboembolism both in the infrarenal and suprarenal positions. Long-term follow-up to 12 years has demonstrated a consistently high patency rate of 96%, which is independent of concomitant anticoagulant therapy. The incidence of recurrent embolism in patients with filters has not changed over time, and there has been no significant filter migration over prolonged periods of observation.

Filtration↗