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G J Wilson

Publications and source records attributed to G J Wilson.

At least 55 records · Page 3Linked to original sources

The influence of musculotendinous stiffness on drop jump performance.

This study investigated the relationship between musculotendinous stiffness and the ability to perform dynamic stretch-shorten cycle actions involving a range of eccentric loads. Twenty trained male subjects performed a series of quasi-static muscular actions in a supine leg press position, during which a brief perturbation was applied. The resulting damped oscillations allowed the estimation of each subject's maximal musculotendinous stiffness (k) for the lower body musculature. All subjects also performed a countermovement jump (CMJ) and a series of drop jumps (DJs) from heights of 20, 40, 60, 80, and 100 cm. When the jump heights of the nine most compliant (mean k = 11.4 +/- 2.7 kNxm-1) and nine stiffest (mean k = 20.5 +/- 2.5 kNxm-1) subjects were compared the stiff subjects demonstrated significantly poorer capacity to perform under the highest (DJ80 and DJ100) eccentric loading conditions. It was hypothesised that the relatively greater forces transmitted from the skeletal system to the musculature of the stiff subjects reduced their ability to attenuate the higher eccentric loads due to less effective contractile dynamics and greater levels of reflex induced inhibition.

Adult↗

Metabolism of the human immunodeficiency virus type 1 reverse transcriptase inhibitor delavirdine in rats.

Delavirdine mesylate (U-90152T) is a highly specific nonnucleoside reverse transcriptase inhibitor currently under development for the treatment of AIDS. The excretion, disposition, and metabolism of delavirdine were investigated in Sprague-Dawley rats after oral administration of [14C]delavirdine mesylate at single doses ranging from 10 to 250 mg/kg and multiple doses ranging from 20 to 250 mg/kg/day. Excretion studies showed that feces was the major route of elimination, delavirdine was well absorbed (>80%) after a 10 mg/kg single dose, and excretion was dose-dependent. The metabolism of delavirdine in the rat was extensive. The following metabolites were identified (% of dose in rats given 10 and 100 mg/kg, respectively): 6'-hydroxy delavirdine (7.1% and 15.6%) and its glucuronide (12.2% and 6.2%) and sulfate (5.5% and 3.2%) conjugates, despyridinyl delavirdine (12.1% and 11.7%) and its conjugate (13.0% and 11.7%), desalkyl delavirdine (16.5% and 13.4%), and its N-sulfamate, 6'- and 4'-sulfate conjugates (2.9% and 3.9%). Cleavage of the amide bond in delavirdine to give N-isopropylpyridinepiperazine and indole carboxylic acid constituted a minor pathway. Degradation of 6'-hydroxy delavirdine generated despyridinyl delavirdine and the pyridine-ring opened MET-14. The metabolic pathway of delavirdine involved N-desalkylation, pyridine ring hydroxylation, pyridine ring cleavage, and amide bond cleavage.

Administration, Oral↗

Metabolism of the HIV-1 reverse transcriptase inhibitor delavirdine in mice.

Delavirdine mesylate (U-90152T) is a highly specific nonnucleoside HIV-1 reverse transcriptase inhibitor currently under development for the treatment of AIDS. The excretion, disposition, brain penetration, and metabolism of delavirdine were investigated in CD-1 mice after oral administration of [14C]delavirdine mesylate at single doses of 10 and/or 250 mg/kg and multiple doses of 200 mg/kg/day. Studies were conducted with 14C-carboxamide and 2-14C-pyridine labels, as well as 13C3-labeled drug to facilitate metabolite identification. Excretion was dose dependent with 57-70% of the radioactivity eliminated in feces and 25-36% in urine. Pharmacokinetic analyses of delavirdine and its N-desisopropyl metabolite (desalkyl delavirdine) in plasma showed that delavirdine was absorbed and metabolized rapidly, that it constituted a minor component in circulation, that its pharmacokinetics were nonlinear, and that its metabolism to desalkyl delavirdine was capacity limited or inhibitable. Delavirdine did not significantly cross the blood-brain barrier; however, its N-isopropylpyridinepiperazine metabolite arising from amide bond cleavage-was present in brain at levels 2- to 3-fold higher than in plasma. The metabolism of delavirdine in the mouse was extensive and involved amide bond cleavage, N-desalkylation, hydroxylation at the C-6' position of the pyridine ring, and pyridine ring-cleavage as determined by MS and/or 1H and 13C NMR spectroscopies. N-desalkylation and amide bond cleavage were the primary metabolic pathways at low drug doses and, as the biotransformation of delavirdine to desalkyl delavirdine reached saturation or inhibition, amide bond cleavage became the predominant pathway at higher doses and after multiple doses.

Animals↗

Elafin, a serine elastase inhibitor, attenuates post-cardiac transplant coronary arteriopathy and reduces myocardial necrosis in rabbits afer heterotopic cardiac transplantation.

We have related experimentally induced post-cardiac transplant coronary arteriopathy to increased elastolytic activity, IL-1beta, fibronectin-mediated inflammatory and smooth muscle cell (SMC) migration, and SMC proliferation. Since our in vitro studies show that a serine elastase releases SMC mitogens and facilitates IL-lbeta induction of fibronectin, we hypothesized that administration in vivo of the specific serine elastase inhibitor, elafin, would decrease the post-cardiac transplant coronary arteriopathy. Cholesterol-fed rabbits underwent a heterotopic cardiac transplant without immunosuppression and received elafin (1.79 mg/kg per d continuous infusion after a 9 mg bolus, n = 6) or vehicle (n = 6). 1 wk later, hearts were harvested for morphometric, immunohistochemical, and biochemical analyses. A > 70% decrease in the total number of coronary arteries with intimal thickening in elafin-treated compared to control donor hearts (P < 0.002) was associated with reduced vascular elastolytic activity judged by fewer breaks in the internal elastic lamina (P < 0.03), less accumulation of immunoreactive fibronectin (P < 0.02), and reduced cell proliferation quantified by proliferating cell nuclear antigen (P < 0.0001). Despite myocardial lymphocytic infiltration, wet weight of elafin-treated donor hearts was reduced by 50% compared to untreated controls (P < 0.002) and associated with relative preservation of myocyte integrity, instead of extensive myocardial necrosis (P < 0.004). This protective effect correlated with decreased myocardial elastolytic activity (P < 0.0001) and inflammatory cell proliferation (P < 0.0001) and with an elafin-inhibitable elastase in lymphocytes. Serine elastase activity thus appears an important therapeutic target for post-cardiac transplant coronary arteriopathy and myocardial necrosis induced by rejection.

Animals↗

The validity and reliability of a test of lower body musculotendinous stiffness.

The aim of this study was to investigate the validity and reliability of an in vivo test of lower body musculotendinous stiffness. Male subjects (n = 23) with at least 12 months of weight training experience performed a series of quasi-static muscular actions in a supine leg press position during which a brief perturbation was applied. The resulting damped oscillations enabled each subject's maximal musculotendinous stiffness for the lower body musculature to be estimated. To assess the individual's capacity to benefit from active stretch, subjects also performed both a static jump and a countermovement jump. Statistical analysis revealed no significant different between day 1 and day 2 stiffness values (P < 0.01), an interday reliability of r = 0.94 and a coefficient of variance of 8%. It was further demonstrated that maximal stiffness was significantly correlated to both isometric and concentric rate of force development (r = 0.50 and r = 0.54, respectively), and inversely related to the percentage difference between vertical jumps with and without prior stretch (r = -0.54). Such results tend to suggest that the test is valid and are discussed with reference to the restitution of elastic strain energy, muscle potentiation and the interaction effects of elastic recoil on dynamic muscular function. It was concluded that the assessment of stiffness of the lower body using the oscillation technique is a valid and reliable in vivo measure of musculotendinous stiffness.

Adolescent↗

The specificity of strength training: the effect of posture.

There is a paucity of research into the importance of performing strength training exercises in postures specific to the movements they are attempting to facilitate. In addressing this question, 27 previously trained subjects were randomly allocated into heavy weight training and control groups. The weight training group performed 4-6 sets of 6-10 repetitions of the squat and bench press lifts twice a week for 8 weeks. Prior to and after the training period the following tests were conducted: bench press throw at 30% of maximal load, vertical jump, maximal squat and bench press lifts, push-up test performed over a force platform, 40-m sprint, 6-s cycle, and isokinetic tests assessing upper and lower body musculature in varying actions. The results supported the concept that posture is important in training as those exercises conducted in similar postures to the training recorded the greatest improvement in performance. For example, after completion of the training the weight training subjects significantly increased by approximately 12% the maximal load lifted in the bench press exercise and the peak torque in the isokinetic bench press test. However, performance in the isokinetic horizontal arm adduction test was not significantly changed. We speculate that the phenomenon of posture specificity may, at least in part, be caused by the differing postures altering the neural input to the musculature. The results stress the importance of selecting exercises in which the posture closely resembles that of the movements they are attempting to facilitate.

Adolescent↗

Poor correlations between isometric tests and dynamic performance: relationship to muscle activation.

The purpose of this research was to perform isometric tests at two joint angles and examine their relationship to dynamic performance. In addition, electromyograph data were collected from the triceps brachii and pectoralis major muscles to compare underlying neural characteristics between the isometric tests and dynamic movement. A group of 24 healthy male subjects performed two isometric tests in a bench press position, at elbow angles of 90 and 120 degrees. From these data, the maximal force and rate of force development were determined. In addition, each subject performed a seated medicine ball throw as a measure of dynamic upper body performance. Correlations showed that isometric measurements of force (r = 0.47-0.55) and rate of force development (r = 0.08-0.31) were poor predictors of dynamic performance. The angle of isometric assessment had little effect on the relationship between the tests and measurements of performance. The myo-electric data was processed in terms of the integrated electromyogram and the Fourier transformed frequency spectrum. These data demonstrated differences in the neural activation patterns of the musculature, between the isometric 90 degrees test and the medicine ball throw. The poor relationship between isometric tests and medicine ball performance was consequently, at least partially, attributed to differing motor unit activation patterns between isometric and dynamic movement. The results of this research strongly suggest that isometric tests have limited value when assessing dynamic upper body performance.

Adult↗

Human pediatric and adult ventricular cardiomyocytes in culture: assessment of phenotypic changes with passaging.

OBJECTIVES: The purpose of this study was to assess morphologically and biochemically the phenotypic changes which occur in vitro with passaging of human pediatric and adult ventricular cardiomyocytes. METHODS: Human ventricular cardiomyocytes from 3 children (1 to 2 years of age) and an adult patient (65 years of age) undergoing open heart surgery and an adult heart transplant patient (55 years of age) were isolated, cultured, purified, and passaged. Growth curves and 3H-thymidine uptake studies were performed. Characterization of the cells was done by light microscopy, transmission electron microscopy, immunofluorescent staining for myoglobin, CK-MB, and cardiac-specific troponin I isoform, human ventricular myosin heavy chain (HVMHC) and light chain 1 (HVMLC1), Northern blot analysis of HVMHC, and CK-MB activity and mass measurements. Passage 3 cardiomyocyte and pediatric myocardial phospholipids were analysed by gas chromatography. RESULTS: Pediatric cells were smaller (P < 0.01) and divided faster (P < 0.001, ANOCOVA) than adult cells. The cardiomyocytes showed phenotypic changes in primary culture with essentially complete loss of sarcomeres by 10 days and a gradual loss of myofilaments with passaging. The cells were identified as cardiomyocytes by immunohistochemistry for myoglobin, CK-MB, cardiac-specific troponin I isoform, HVMHC and HVMLC1, and by Northern blot analysis for the 3'-end of HVMHC mRNA. The composition of phospholipid fatty acids in the cultured pediatric cells was similar to that found in the pediatric myocardium. CK-MB activity and mass could be measured in the cardiomyocytes. The adult cardiomyocytes were more difficult to maintain than the pediatric cells which could be cultured for as long as 6 months. CONCLUSIONS: Primary cultures of human pediatric and adult partially differentiated ventricular cardiomyocytes can be passaged. Although rapid disorganization of the myofibrils occurs, the non-contractile cells can be identified as cardiomyocytes by morphological appearance, immunofluorescent staining, Northern blot analysis for HVMHC, and CK-MB activity.

Actin Cytoskeleton↗

Strength diagnosis: the use of test data to determine specific strength training.

The aim of this study was to determine if pre-training strength and power tests could provide data that effectively discriminated between subjects whose cycling performance improved considerably from training, from those who did not. Twenty active healthy male subjects performed 10 weeks of plyometric or weight training. Prior to and at the completion of the training, the following tests were performed: (1) a 6-s cycle ride; (2) isokinetic leg extension at 1.05 and 5.24 rads s-1; and (3) a maximum isometric squat. The subjects in the two training groups were separated into those whose cycling performance improved significantly as a result of the training (good) and those who did not (poor). The pre-training muscular function tests of the good versus poor achievers were then compared, individually for each form of training, to determine if they could be used to discriminate between the two subject groups. The pre-training isometric data effectively discriminated between those individuals who improved their cycling performance significantly as a consequence of training and those who did not. While this finding has practical implications for the exercise science field, further research is required before generally useful normative data can be used with confidence to prescribe individual specific training programmes.

Adult↗

Stretch shorten cycle performance: detrimental effects of not equating the natural and movement frequencies.

This study aimed to assess whether the benefits associated with stretch shorten cycle (SSC) movements required the movement frequency to be in resonance with the natural frequency of the elastic structures. Seventeen untrained participants performed SSC and concentric bench press throws. Further, quasi-static muscular actions were also performed in which a brief perturbation was applied to the bar with the resulting damped oscillations providing natural frequency data. It was observed that prior stretch did not facilitate concentric performance. Further, there were large significant differences between the natural frequency of the musculo-tendinous system and the frequency of the SSC movements. The authors hypothesize that the failure to achieve resonance contributed to the poor performance achieved in the SSC actions.

Adult↗

Persistent reovirus infections of L cells select mutations in viral attachment protein sigma1 that alter oligomer stability.

During maintenance of L-cell cultures persistently infected with reovirus, mutations are selected in viruses and cells. Cells cured of persistent infection support growth of viruses isolated from persistently infected cultures (PI viruses) significantly better than that of wild-type (wt) viruses. In a previous study, the capacity of PI virus strain L/C to grow better than wt strain type 1 Lang (T1L) in cured cells was mapped genetically to the S1 gene (R. S. Kauffman, R. Ahmed, and B. N. Fields, Virology 131:79-87, 1983), which encodes viral attachment protein sigma1. To investigate mechanisms by which mutations in S1 confer growth of PI viruses in cured cells, we determined the S1 gene nucleotide sequences of L/C virus and six additional PI viruses isolated from independent persistently infected L-cell cultures. The S1 sequences of these viruses contained from one to three mutations, and with the exception of PI 2A1 mutations in each S1 gene resulted in changes in the deduced amino acid sequence of sigma1 protein. Using electrophoresis conditions that favor migration of sigma1 oligomers, we found that sigma1 proteins of L/C, PI 1A1, PI 3-1, and PI 5-1 migrated as monomers, whereas sigma1 proteins of wt reovirus and PI 2A1 migrated as oligomers. These findings suggest that mutations in sigma1 protein affecting stability of sigma1 oligomers are important for the capacity of PI viruses to infect mutant cells selected during persistent infection. Since no mutation was found in the deduced amino acid sequence of PI 2A1 sigma1 protein, we used T1L X PI 2A1 reassortant viruses to identify viral genes associated with the capacity of this PI virus to grow better than wt in cured cells. The capacity of PI 2A1 to grow better than T1L in cured cells was mapped to the S4 gene, which encodes outer-capsid protein sigma3. This finding suggests that in some cases, mutations in sigma3 protein in the absence of sigma1 mutations confer growth of PI viruses in mutant cells. To confirm the importance of the S1 gene in PI virus growth in cured cells, we used T1L X PI 3-1 reassortant viruses to genetically map the capacity of this PI virus to grow better than wt in cured cells. In contrast to our results using PI 2A1, we found that growth of PI 3-1 in cured cells was determined by the sigma1-encoding S1 gene. Given that the sigma1 and sigma3 proteins play important roles in reovirus disassembly, findings made in this study suggest that stability of the viral outer capsid is an important determinant of the capacity of reoviruses to adapt to host cells during persistent infection.

Animals↗

Weight and plyometric training: effects on eccentric and concentric force production.

The study was performed in an effort to gain greater insights into the adaptations invoked by plyometric and weight training. Forty-one previously trained males were randomly allocated in either a control, plyometric, or weight-training group. The experimental groups trained for 8 weeks, performing either heavy lifts or dynamic plyometric exercises. The following test items were performed prior to and at the completion of the training period: (a) vertical jump, (b) a series of isoinertial concentric and eccentric tests, (c) push-up tests, and (d) maximal bench press and squat lifts. Plyometric training significantly enhanced the rate of eccentric lower body force production. The weight-training group primarily enhanced concentric function. These results were attributed to the specific stresses imposed by the differing forms of training and are discussed with reference to methods of enhancing training induced adaptations and the types of movements such training would tend to facilitate.

Adaptation, Physiological↗

Effect of ischemic preconditioning of the myocardium on cAMP.

Reduction of cAMP has been implicated in the protection of ischemic preconditioning (IP), but until now, this possibility has not been directly addressed. In this study, we found that in the in vivo rabbit heart 10 to 30 minutes of sustained regional ischemia was accompanied by a nearly twofold rise in cAMP levels. This increase in cAMP was attenuated when sustained ischemia was preceded by IP induced with a single cycle of transient ischemia and reperfusion (TI/R) and prevented when ischemia was preceded by three cycles of TI/R. The mechanism of cAMP reduction by IP does not involve activation of protein kinase C (PKC), since the PKC inhibitor polymyxin B (24 mg/kg) did not raise cAMP levels during sustained ischemia in IP hearts. Furthermore, this effect is also not mediated by reduced responsiveness of the beta-adrenergic effector pathway, since both nonischemic hearts and hearts subjected to three cycles of TI/R exhibited similar increases in cAMP in response to 5 micrograms/kg isoproterenol. However, propranolol (0.75 mg/kg) abolished the rise in cAMP levels observed during sustained ischemia in control hearts but did not reduce cAMP levels further in IP hearts. These data indicate that the ischemia-induced rise in cAMP levels in control hearts was mediated by activation of the beta-adrenergic receptor. Taken together with data demonstrating that beta-adrenergic responsiveness was not affected by IP, these data support the conclusion that the lack of elevation in cAMP levels observed during sustained ischemia in IP hearts is mediated by an attenuation of norepinephrine release. To examine whether the protection of IP against necrosis was mediated by the lack of elevation in cAmp levels, we determined whether the infarct size-limiting effect of IP could be blocked by NKH477, an activator of adenylyl cyclase. Four groups or rabbits were subjected to 30 minutes of in vivo regional ischemia and 90 minutes of reperfusion. Control hearts (n = 10) had 53.6 +/- 5.5% infarction of the area at risk. IP with three cycles of transient ischemia limited infarct size to 3.2 +/- 1.3% (N = 13, p < .0001). NKH477 (45 micrograms/kg) increased average cAMP levels in IP hearts during sustained ischemia to levels similar to those in untreated control hearts. However, NKH477 did not block IP (50.2 +/- 7.7% of the area at risk was infarcted in the control +NKH477 group [n = 10] versus 10.0 +/- 5.9% in the IP + NKH477 group [n = 7], P < .05). Therefore, we conclude that although IP lowers cAMP levels during sustained ischemia, this effect is not necessary for its protection against necrosis, since raising cAMP does not block this protection of IP.

Adenylyl Cyclases↗

The use of isometric tests of muscular function in athletic assessment.

Isometric assessment of muscular function is a popular form of testing which has been used in exercise science for over 40 years. It typically involves a maximal voluntary contraction performed at a specified joint angle against an unyielding resistance which is in series with a strain gauge, cable tensiometer, force platform or similar device whose transducer measures the applied force. Often both the maximum force and the rate of force development are recorded. These tests have generally shown high reliability in both single and multi-joint test protocols, although the maximum force is typically more reliable than rate of force development. This review outlines the reliability of isometric assessment and discusses a number of methodological considerations designed to enhance reliability and validity, including standardisation procedures, type of instructions, muscular pre-tension, testing position and joint angle. Currently, there appears to be considerable controversy as to the external validity of isometric assessment, particularly the ability of the tests to monitor changes in dynamic performance and their relationship to such performances. Indeed, a number of studies have recently shown that dynamic assessment modalities (isokinetic and isoinertial) are superior in terms of their relationship to dynamic performance and ability to discriminate between athletes of various performance levels compared with isometric assessment. This article reviews the use of isometric assessment in exercise science and consequently outlines a number of neural, mechanical and methodological factors which may have contributed to the contrasting research, and which may limit the ability of isometric assessment to relate to dynamic movement. Because of the large neural and mechanical differences between isometric and dynamic muscular actions, athletic assessment, which is dynamic in its nature, is generally most appropriately accomplished using dynamic muscular assessment methods, and in most instances isometric testing should be avoided.

Biomechanical Phenomena↗

The assessment of human dynamic muscular function: a comparison of isoinertial and isokinetic tests.

This investigation compared the relationship of isokinetic and isoinertial tests of muscular function to dynamic upper body performances. The electromiyographic activity of each of the tests of muscular function, as recorded by surface electrodes, were examined to determine whether neural differences underlie the ability of the test to relate to performance. Twenty four subjects performed isokinetic and isoinertial tests of muscular function in a bench press movement. The isokinetic tests were performed at velocities of 60, 90 and 120 deg/s while the isoinertial tests were performed at loads of 30%, 60% and 130% of the one repetition maximum. Subjects also performed the following tests of dynamic performance: a maximum one repetition bench press (1 RM), a seated shotput throw and two drop bench press throws from a height of 0.25 m at various loads. Forces/torques, displacement and electromyographic data were recorded from the isoinertial and isokinetic tests. Both the isoinertial and isokinetic parameters were related to the various measures of upper body performance (r = 0.33-0.94), however, neither was superior at predicting performance. Further, the relationship between the tests of muscular function were consistently high (r = 0.75-0.88). This was the case, even though the magnitude of the EMG signals were significantly higher in the isoinertial, as compared to the isokinetic tests. It is postulated that structural considerations, such as a specific testing position, rather than neural factors, underlie the observed results. These results support previous research which has reported the existence of a generality of strength across dynamic testing modalities.

Adult↗

Biomechanical and ultrastructural comparison of cryopreservation and a novel cellular extraction of porcine aortic valve leaflets.

Heart valve substitutes of biological origin often fail by degenerative mechanisms. Many authors have hypothesized that mechanical fatigue and structural degradation are instrumental to in vivo failure. Since the properties of the structural matrix at implantation may predetermine failure, we have examined the ultrastructure, fracture, mechanics, and uniaxial high-strain-rate viscoelastic properties of: (1) fresh, (2) cryopreserved, and (3) cellular extracted porcine aortic valve leaflets. The cellular extraction process is being developed in order to reduce immunological attack and calcification. Cryopreservation causes cellular disruption and necrotic changes throughout the tissue, whereas extraction removes all cells and lipid membranes. Both processes leave an intact collagen and elastin structural matrix and preserve the high-strain-rate viscoelastic characteristics of the fresh leaflets. Extraction does cause a 20% reduction in the fracture tension and increases tissue extensibility, with the percent strain at fracture rising to 45.3 +/- 4 (mean +/- SEM) from 31.5 +/- 3 for fresh leaflets. However, extraction does preserve matrix structure and mechanics over the physiological loading range. Glutaraldehyde fixation produces increased extensibility, increased elastic behavior, and, when applied to extracted leaflets, it causes a marked drop in fracture tension, to 50% of that for fresh leaflets. The combination of extraction and fixation may lead to early degenerative failure. The cellular extraction technique alone may be a useful alternative to glutaraldehyde fixation in preparing bioprosthetic heart valves.

Animals↗

Acellular matrix: a biomaterials approach for coronary artery bypass and heart valve replacement.

We have developed a multistep detergent-enzymatic extraction process (involving hypotonic and hypertonic solutions, the detergents octyl-phenoxy-polyethoxyethanol and sodium dodecyl sulfate, as well as DNAse and RNAse) which, while inhibiting autolysis, removes all cells from tissues and, with them, cellular antigens together with lipids and more soluble glycosaminoglycans. What remains is acellular matrix with the structural proteins well conserved and normally arranged. Canine arteries extracted to acellular matrix were implanted as coronary artery bypass allografts in a canine model, without the use of cardiopulmonary bypass, and compared with autogenous saphenous veins. Of nine pilot acellular matrix implants, four were patent, as compared with four of seven saphenous vein grafts. All occlusions in both graft types occurred acutely soon after implantation, with almost all patent grafts followed up for 6 months. The acellular matrix allografts showed no inflammation and only minimal cellular repopulation. This model needs further development, but appears promising for preclinical evaluation. Canine aortic and pulmonic valves extracted to acellular matrix using a modification of our extraction process, eliminating the detergent sodium dodecyl sulfate, were implanted heterotopically as allografts in the left main pulmonary artery in dogs, a location chosen to avoid the need for cardiopulmonary bypass. At 1 month, two-dimensional echocardiography of six implants showed leaflet motion and 3- to 5-mm Hg transvalvular gradients. Explant histology of four valves at 1 month showed no inflammation, cellular repopulation at the base of the valve, and partial endothelialization.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗