Refinements in the surgical technique of liver transplantation.
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Aorta↗
Biomedical subjects
C O Esquivel
Publications and source records attributed to C O Esquivel.
Liver rejection and its differentiation from other causes of graft dysfunction.
Numerous causes can lead to hepatic dysfunction following orthotopic liver transplantation. The most common cause is rejection, which is usually nonpreventable. The clinical presentation, time of onset, and even treatment are variable. Other causes, such as perioperative ischemic injury, vascular thrombosis, and complications of bile duct reconstruction may be preventable with good surgical technique. Infections can also be minimized by careful adjustment of immunotherapy, avoidance overimmunosuppression, and the judicious use of antibiotics. Hepatic dysfunction following orthotopic liver transplantation requires rapid assessment and proper treatment in order to prevent serious and possibly fatal complications.
Bile Duct Diseases↗
Nephrotoxicity of cyclosporine in liver transplantation.
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Administration, Oral↗
Postoperative small bowel intussusception.
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Female↗
In vitro evaluation of a biologic graft surface. Effect of treatment with conventional and low molecular weight (LMW) heparin.
Human umbilical vein grafts were treated with either conventional or LMW heparin, followed by exposure to alcohol. The grafts were investigated for their ability to adsorb and inactivate thrombin, and comparison was made with non-heparinized and saline-alcohol treated grafts and grafts supplied with a covalently bonded layer of conventional heparin. In addition, the effect of protamine exposure to heparin-alcohol and LMW heparin-alcohol treated grafts as well as native human umbilical veins (HUV) was studied. Native HUV and heparin treated graft surfaces adsorbed and inactivated thrombin, whereas non-heparinized and saline-alcohol treated grafts inactivated surface-bound thrombin to only a small degree. Surface-bound LMW heparin exhibited a significantly lower ability to inactivate thrombin as compared with conventional heparin, but LMW heparin-alcohol surfaces were better than non-heparinized ones. Protamine treatment of "heparinized" surfaces impaired the thrombin inhibiting ability of the heparin-alcohol surface, whereas this property was totally abolished for the LMW heparin-alcohol surface. The findings indicate that LMW heparin, despite its weaker thrombin inhibiting capacity, may be an alternative to conventional heparin, for "heparinizing" the human umbilical vein graft. Protamine exposure may be potentially harmful for a heparin treated surface, although protamine concentrations used in the present in vitro study may not be reached in vivo. The native HUV was not at all affected by protamine exposure regarding its ability to inactivate thrombin.
Heparin↗
Thromboxane production in umbilical vein grafts.
Umbilical vein grafts were placed in the carotid arteries of sheep and removed after 10 or 90 days for determination of in vitro production of 6-keto-PGF1 alpha and thromboxane B2 (TxB2) in the anastomoses and in the middle of the grafts. At both intervals the grafts produced much more TxB2 than carotid arteries, but no significant difference in production of 6-keto-PGF1 alpha was found between grafts and carotid arteries. The strongly decreased 6-keto-PGF1 alpha/TxB2 ratio indicates a low resistance to platelet adhesion and aggregation, which may be a contributory cause of the thrombogenicity of vascular grafts and may possibly be involved in the pathogenesis of neointimal fibrous hyperplasia.
6-Ketoprostaglandin F1 alpha↗
Prostacyclin (PGI2) and plasminogen activator (PA) activity in umbilical vein grafts. An experimental study.
Glutaraldehyde-tanned human umbilical cord vein grafts (Dardik Biograft, Meadox) (HUV) measuring 6 cm in length and 5-6 mm in diameter were placed in the carotid arteries (CA) or jugular veins (JV) of sheep and the anastomoses were made end-to-end. Sections from the anastomotic sites and mid-graft were submitted to prostacyclin (PGI2) (radioimmunoassay) and plasminogen activator, PA, (histochemical) assays. Anastomotic PGI2 production from 6 grafts placed in the CA and removed 10 days later was similar to that of control arteries. The midgraft PGI2 synthesis tended to be less but the difference was not statistically significant. Anastomotic PGI2 from 11 grafts placed in the CA and removed 90 days later was also similar but the midgraft production was significantly less (p less than 0.025). From the distal anastomoses and mid portion of grafts placed in the jugular veins and removed 10 days later PGI2 synthesis was significantly less than that of control veins (p less than 0.025 and p less than 0.005 respectively) but no difference between the proximal anastomosis and control veins was observed. In none of 11 HUV removed on the 10th postoperative day was there any PA in the neointima; however, in 6 out of the 9 HUV removed on the 90th postoperative day, PA was demonstrated in the neointima. In conclusion, PGI2 synthesis similar to that of control vessels but less from the mid-graft regions. Neointima gained the ability to produce plasminogen activator.
Animals↗
Reduced thrombogenic characteristics of expanded polytetrafluoroethylene and polyurethane arterial grafts after heparin bonding.
The effect of bonding of heparin, via a glutaraldehyde-stabilized ionic complex, on the early thrombogenicity of polyurethane (PU) and expanded polytetrafluoroethylene (PTFE) (Gore-tex) as well as covalent bonding of heparin on PTFE was studied in vivo. Grafts 6 cm long and 4 mm in diameter were placed in the carotid arteries of sheep and perfused for 4 hours at 25 ml/min in order to accelerate thrombus formation. The thrombogenicity was determined by calculation of the percent of the luminal surface free of thrombus and patency. In addition, 32P-labelled platelet accumulation was determined in some of the grafts. The stabilized ionic bonding of heparin significantly reduced the early thrombogenicity of PU but had little effect on PTFE grafts; but the thrombogenicity of the latter was markedly decreased following covalent bonding of heparin. A regional distribution of platelet accumulation was found with the distal anastomoses showing the highest platelet deposition. By choice of an appropriate method of heparinization, a significant reduction of the thrombogenicity of PU and PTFE grafts was achieved.
Animals↗
The effect of serotonin inhibition on initial microvessel hemostasis and platelet aggregation in vivo.
The role of serotonin (5-HT) in initial microvascular hemostasis is not fully understood. This study was made to evaluate the effect on hemostatic plug formation and laser-induced arteriolar microembolism of different substances which counteract the effect of 5-HT. Hemostatic plug formation time and stability was measured in the rabbit mesenteric microcirculation and laser-induced embolism in the rabbit ear chamber. Ketanserine, a selective 5-HT2-receptor blocker shortened arteriolar hemostatic plug formation time. Dihydroergotamine, an unselective blocker (with 5-HT-and alpha-adrenergic receptor affinity) increased venular hemostatic plug formation time and also decreased the hemostatic plug stability. Laser-induced platelet embolism was unaltered after both ketanserine and dihydroergotamine administration. The magnitude of these changes seems to exclude an important effect of 5-HT in initial microvessel hemostasis or on platelet activity.
Animals↗
Decreased acute thrombogenicity of human umbilical veins after heparin and alcohol treatment.
Nine glutaraldehyde-tanned human umbilical veins (GAUV) were incubated in heparin followed by storage in ethyl alcohol 50% (HAUV). These grafts were compared to five GAUV flushed with a heparinized solution without subsequent treatment in alcohol (HsAUV) and four nonheparinized GAUV (NHUV) placed in the contralateral carotid arteries of dogs for approximately 3 h. The thrombogenicity was evaluated by measuring the platelet adhesion and aggregation (51Cr), fibrinogen accumulation (125I-fibrinogen), the thrombus-free surface and the thrombus weight. The HAUV had the lowest 51Cr radioactivity. The means of thrombus-free surface and thrombus weight for the grafts were as follows: HAUV, 82% and 0.3 g (n = 9); HsAUV, 53% and 0.6 g (n = 5); NHUV, 13% and 1.2 g (n = 4). The HAUV showed a lower thrombogenicity than both the NHUV and the HsAUV grafts.
Animals↗
Heparinized human umbilical vein grafts. Delayed heparin desorption after alcohol treatment.
Tanned human umbilical vein grafts (Dardik Biograft, Meadox) were heparinized with tritium-labelled heparin. Two methods of heparinization were undertaken: (1) incubation with heparin followed by ethyl alcohol 50% treatment, and (2) incubation with heparin without alcohol. Grafts were placed in the carotid arteries of sheep and removed 10 and 90 days later. Heparin was lost in contact with blood but the alcohol treatment delayed heparin desorption significantly.
Animals↗
Coarctation of the abdominal aorta associated with renal hypertension.
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Adolescent↗
Comparison between commercial heparin, low molecular weight heparin and pentosan polysulfate on hemostasis and platelets in vivo.
The effect of commercial heparin (MW 15000; 60 U/kg), low molecular weight heparin (MW 4500, 60 U/kg), sodium pentosan polysulfate (PZ-68) in doses of 0.5, 1, 2 and 5 mg/kg and 1 mg/kg combined with dextran 70 (0.5 g/kg) on microvascular hemostasis and platelet activity in vivo was investigated in the microcirculation of rabbit mesentery and ear chamber, respectively. Low molecular weight heparin did not alter the hemostasis: nonetheless, commercial heparin and PZ-68 interfered with the hemostatic mechanism by decreasing the stability of the hemostatic plug. This abnormality was more apparent in the venular than in the arteriolar system. Both heparins exhibited a trend towards an increase in platelet reactivity and the reverse was observed following the administration of PZ-68.
Animals↗
Assessment of antithrombotic properties of sodium ibuprofen.
The effect of sodium ibuprofen on platelet activity in vivo and the lysability of ex vivo thrombi was investigated. The formation of a hemostatic platelet plug in the rabbit mesentery and platelet embolism as a response to a laser-induced injury in the ear chamber of rabbits were used as models for determining platelet activity. Ibuprofen at a dose of 25 mg/kg i.v. was found to increase the primary (PHT) and the total hemostatic plug formation time (THT). The same dose decreased the number of cumulative emboli over a 10 min period after a laser injury to arterioles. A dose of 10 mg/kg i.v. did not affect the formation of the hemostatic platelet plug. In dogs, doses of 10, 25 und 50 mg/kg did not enhance the release of 125I-FDP from the thrombi after incubation in plasmin, but the largest dose which is approximately five times the recommended dose in humans, did significantly decrease the thrombus weight 90 and 180 min after the drug administration. In conclusion, sodium ibuprofen was shown to have an inhibitory effect on platelet function in vivo and in large doses was also found to diminish the thrombus weight.
Animals↗
Effect of volume expanders on the lysability of ex vivo thrombi in the rabbit.
The lysability of ex vivo thrombi before and after the infusion of dextran 70 (0.5 g/kg, 1.5 g/kg and 2 g/kg), dextran 40 (1.5 g/kg), albumin 5% (1.5 g/kg) and normal saline (0.3 g/kg) was studied in rabbits. All rabbits received 125I fibrinogen before the experiment. The thrombi were treated with plasmin or sodium chloride and the radioactivity released in the supernatant by the thrombus was determined. The thrombus weight was also recorded. A gradual increase in the lysability of thrombi after dextran 70 administration was observed and the maximum effect occurred 24 hours later. Increasing dose of dextran 70 did not potentiate the release of 125I fibrin degradation products in the supernatant, but did significantly decrease the thrombus weight during the first hours postinfusion, Dextran 40 was found to have a similar action but the effect was shorter and the lysability at 24 hours was similar to the preinfusion values. Albumin 5% and normal saline increase the radioactivity released from the thrombi to the supernatant but no change in the thrombus weight was observed. A similar result was obtained in the control group. The present investigation demonstrated that increasing doses of dextran 70 potentiate the effect on thrombolysis demonstrated by statistically significant decrease in the thrombus weight. Furthermore, albumin 5% and normal saline increase the release of 125I fibrin split products in the supernatant but did not have any effect on the thrombus weight and finally, the rabbit showed a marked spontaneous fibrinolysis probably related to the stress, anesthetic agent and surgical manipulation.
Albumins↗
Experimental carotid stenosis due to fibrous intimal hyperplasia.
Although fibrous intimal hyperplasia has been reported to be involved in up to one-third of recurrences of carotid restenosis following endarterectomy, little is known of its origin. This prompted us to attempt to produce it experimentally. Fibrous intimal hyperplasia could not be induced in the canine carotid model using simple endarterectomy or endarterectomy with an autogenous vein patch angioplasty. Polytetrafluoroethylene graft angioplasties in the same model produced this lesion readily and usually led to stenosis or occlusion. The experimental and clinical lesion of fibrous intimal hyperplasia of the carotid artery and the lesion of intimal fibrous hyperplasia that occurs when prosthetic arterial grafts are placed into small and medium size arteries appear histologically similar and may be due to a common factor. A review of the factors available in our series, as well as those of others, leads us to believe that the common denominator is hemodynamic in nature. The experimental data showing stenotic fibrous intimal hyperplasia occurring with polytetrafluoroethylene patch angioplasties has been previously reported. These data indicate that polytetrafluoroethylene should cautiously be used for small and medium diameter arterial patch angioplasties.
Animals↗
Aspirin failure in symptomatic atherosclerotic carotid artery disease.
Over a 26-month period 27 urgent carotid endarterectomies were performed on patients who had been taking antiplatelet aggregating drugs for 6 months to 2 years. Angiography confirmed an original diagnosis of symptomatic extracranial carotid artery stenosis and ulceration in all patients. Nineteen had been started on dosages of aspirin from 325 to 1,300 mg/day, and eight started on aspirin plus persantine. Compliance to aspirin use appeared high. All had partial or total resolution of the ischemic symptoms after aspirin therapy was instituted. On readmission three patients had early stroke in evolution, and 24 had crescendo transient ischemic attacks. Reevaluation included cerebral angiography which confirmed progression of carotid artery disease to 90% or greater stenosis in each instance. All patients underwent successful carotid endarterectomies. A review of history of these 27 in the urgent group as opposed to the 45 symptomatic carotid patients who were electively operated on in the same time period revealed no significant (P greater than 0.10) differences in incidence of risk factors for atherosclerosis. However, none of the elective group had regularly taken aspirin. It would appear that aspirin decreased ischemic symptoms in the patients who underwent urgent operation by its antithromboxane effect, inhibiting platelet aggregation and embolization. However, aspirin appeared to have a deleterious effect on these patients by allowing their carotid disease to progress to a dangerous state by eliminating the symptoms of progressive carotid artery atherosclerosis or by accentuating the process of atherosclerosis possibly by inhibition of arterial prostacyclin.
Aged↗
Adenoviral infections in pediatric liver transplant recipients.
Over a 5 1/2-year period, 22 of 262 children receiving liver transplants developed adenoviral infections. Five had adenoviral hepatitis in the allograft, caused by serotype 5. All five were treated for rejection, either just before or at the time of infection. Liver biopsy specimens had characteristic histological appearance, and diagnosis of adenoviral infection was confirmed with monoclonal antiadenoviral antibodies, electron microscopy, and by culture of liver tissue. In the remaining 17 patients, adenovirus was isolated from urine, stool, throat secretions, and/or blood samples, but none had any detectable visceral infection. Serotypes 1 and 2 predominated, similar to children not receiving transplants during the same time period. Three of the patients with hepatitis are alive and well; two died of liver failure. Adenoviral hepatitis did not recur in the second allograft of a patient who underwent retransplantation for combined rejection and adenoviral hepatitis, and appears, therefore, not to be a contraindication to retransplantation when liver failure ensues.
Adenoviridae Infections↗