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Biomedical subjects

D E Chambers

Publications and source records attributed to D E Chambers.

15 recordsLinked to original sources
PubMed2001

Filler-coupling agent-matrix interactions in silica/polymethylmethacrylate composites.

The interactions of the silane coupling agent methacryloxypropyltrimethoxysilane (MPS) with both fumed silica and a polymethylmethacrylate (PMMA) resin matrix were investigated using thermogravimetric analysis and Fourier transform infrared spectroscopy. OX 50 fumed silica was silanated with MPS at concentrations of 1% and 5% in aqueous ethanol (95%), acetone, and anhydrous toluene. Methyl methacrylate was polymerized with the silanated fumed silica (5% wt/wt) to form composites. The amount of MPS adsorption on the fumed silica and the amount of PMMA attached to the silanated fumed silica were determined by thermogravimetric analysis. MPS could be removed from the fumed silica after washing with methanol, but not after it underwent a drying process at 25 degrees C under vacuum. After vacuum drying at 25 degrees C, two types of adsorbed silane were found, i.e., firmly adsorbed and loosely adsorbed silane. The loosely adsorbed silane could desorb from silica and be incorporated into the polymer matrix through copolymerization with monomeric methyl methacrylate, resulting in crosslinking of the matrix. When the silanated silica was dried at 110 degrees C for 2 h, the loosely adsorbed silane was removed and the amount of firmly adsorbed silane increased. There was a positive correlation between the amount of firmly adsorbed MPS and the amount of PMMA attachment. The highest efficiency for PMMA attachment was found when MPS was adsorbed as a monolayer, because the loosely adsorbed silane did not contribute to the bonding of PMMA, and this suggested that not all of the double bonds of the MPS were accessible for reaction with the methacrylate monomer. Drying at 110 degrees C may also decrease the number of unsaturated double bonds of MPS.

Absorption↗
PubMed1991

Effects of inhibition of nitric oxide formation on basal vasomotion and endothelium-dependent responses of the coronary arteries in awake dogs.

The role of nitric oxide in basal vasomotor tone and stimulated endothelium-dependent dilations in the coronary arteries in chronically instrumented awake dogs was studied by examining the consequences of inhibiting endogenous nitric oxide formation with the specific inhibitor of nitric oxide formation, NG-monomethyl-L-arginine (L-NMMA). In four awake dogs, coronary dimension crystals were chronically implanted on the circumflex artery for the measurement of epicardial coronary diameter, and Doppler flow probes were implanted for quantitation of phasic coronary blood flow (vasomotion of distal regulatory resistance vessels). Basal epicardial coronary diameter, acetylcholine-stimulated endothelium-dependent dilation, and flow-induced endothelium-dependent dilation of the epicardial arteries and phasic blood flow were recorded before, and after 5, 15, 50, and 120 mg/kg of L-NMMA. L-NMMA induced a dose-related increase in basal epicardial coronary vasomotor tone. There was an accompanying increase in aortic pressure and a decrease in heart rate. At doses greater than or equal to 50 mg/kg, rest phasic coronary blood flow was also decreased. Left ventricular end-diastolic pressure and contractility were not significantly changed. In contrast, the flow-induced or acetylcholine-stimulated endothelium-dependent responses were attenuated only after infusion of the highest does of L-NMMA (120 mg/kg). The changes in the basal vasomotor tone and acetylcholine-stimulated endothelium-dependent responses returned towards the control states in the presence of L-arginine (660 mg/kg). These data support the view that nitric oxide plays a significant role in modulating basal vasomotion and endothelial-dependent dilation stimulated by acetylcholine or increase in blood flow in epicardial coronary arteries and also influence the regulation of coronary blood flow during physiologic conditions.

Acetylcholine↗
PubMed1990

Nitric oxide modulates epicardial coronary basal vasomotor tone in awake dogs.

This study evaluates the role of endogenous nitric oxide in the modulation of basal coronary vasomotor tone by studying the effects of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide formation from L-arginine, on resting epicardial coronary diameter and coronary flow. L-NMMA (5 mg/kg) was infused in seven awake dogs chronically instrumented with coronary dimension crystals for measurement of epicardial coronary diameter, and Doppler flow probes for quantitation of phasic coronary flow (vasomotion of distal regulatory resistance coronary vessels). Epicardial coronary diameter decreased 5.5% from 3.47 +/- 0.17 to 3.28 +/- 0.15 mm (mean +/- SE). The diameter change was gradual, reaching a maximum at 13 +/- 2 min after infusion, and persistent, lasting greater than 90 min. Phasic coronary flow did not change. Mean aortic pressure significantly increased from 99 +/- 3 to 111 +/- 3 mmHg and heart rate decreased from 56 +/- 4 to 46 +/- 3 beats/min. Left ventricular end-diastolic pressure and contractility were not significantly altered. L-Arginine (66 mg/kg) but not D-arginine reversed all hemodynamic parameters. These data support an important role of nitric oxide in modulating basal epicardial coronary vasomotor tone and systemic vascular resistance.

Animals↗
PubMed1990

Ischemia-induced epicardial vasoconstriction. A potential mechanism for distant myocardial ischemia.

This study evaluated the effects of transient coronary occlusion on the diameter of a nonischemic vessel or a nonischemic coronary segment proximal to the site of occlusion. Awake mongrel dogs chronically instrumented with dimension crystals, Doppler flow probes, and distal pneumatic occluders on the circumflex coronary arteries were subjected to transient 2-minute circumflex occlusions (n = 9) under constant heart rate (120 beats/min). Left ventricular end-diastolic pressure increased by 60% (from 10 +/- 1 to 16 +/- 2 mm Hg), and dP/dt decreased by 8% (from 2,048 +/- 130 to 1,885 +/- 110 mm Hg/sec); systemic hemodynamics were unaltered. Epicardial coronary diameter proximal to the site of occlusion decreased by 4.37% (from 3.62 +/- 0.25 to 3.46 +/- 0.29 mm, p less than 0.05). Constriction began 15-20 seconds after the onset of ischemia and progressed to maximum in 1-2 minutes. Combined alpha- and beta-receptor blockade (n = 8) with phentolamine (2 mg/kg) and propranolol (1 mg/kg) or cyclooxygenase inhibition (n = 5) with indomethacin (7.5 mg/kg) did not attenuate the ischemia-induced vasoconstriction response. Transient 2-minute occlusion of the left anterior descending coronary artery (n = 6) also elicited significant epicardial vasoconstriction in the circumflex coronary artery in the first minute (from 3.88 +/- 0.31 to 3.81 +/- 0.31 mm, p less than 0.05); the constriction was attenuated subsequently by an increase (25.5%) in circumflex flow. When left anterior descending occlusion was repeated (n = 6) with circumflex flow held constant, the ischemia-induced circumflex constriction was augmented; diameter decreased 3.7% (from 3.83 +/- 0.29 to 3.69 +/- 0.29 mm, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1987

Xanthine oxidase is not a source of free radicals in the ischemic rabbit heart.

The xanthine oxidase pathway has been proposed as a source of oxygen-derived free radicals in ischemic and reperfused myocardium. A spectrophotometric assay was employed to measure the xanthine oxidase activity of rat and rabbit hearts exposed to varying durations of global ischemia. In the rat 24.6 +/- 4.8 mIU/g wet wt of xanthine dehydrogenase + xanthine oxidase activity were detected in both ischemic and normally perfused myocardium. In the non-ischemic state only 6% of this activity was associated with the free radical-producing oxidase form. After 5 min of ischemia however about 25% of the enzyme was in the oxidase form, a value which remained unchanged over the following 25 min. Neither xanthine dehydrogenase nor xanthine oxidase could be detected in the rabbit heart. Failure of allopurinol, an inhibitor of xanthine oxidase, to limit infarct size in a rabbit model of ischemia/reperfusion provides further evidence that this species has insignificant amounts of xanthine oxidase in its heart. Anesthetized rabbits were subjected to coronary artery ligation for 45 min and 3 h of reperfusion. The volume of the zone of underperfusion was assessed with fluorescent microspheres and infarct size was assessed by tetrazolium staining. In control animals 67.5 +/- 3.8% of the zone of underperfusion became necrotic. In rabbits given superoxide dismutase (15000 IU/kg) + catalase (50,000 IU/kg) for 90 min starting 15 min before occlusion, infarct size was only 35.4 +/- 3.3% of the zone of underperfusion. However, in rabbits pretreated with allopurinol (75 mg p.o. 24 h before study + 30 mg/kg 5 min before occlusion) infarct size was 65.8 +/- 8.7%.(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1985

Xanthine oxidase as a source of free radical damage in myocardial ischemia.

Experiments were performed to determine if xanthine oxidase is a source of free radicals during myocardial ischemia. Open chest dogs were subjected to 1 h of total occlusion of the left anterior descending coronary artery followed by 4 h of reperfusion. Directly after coronary artery occlusion, Ce141 microspheres were injected into the left atrium to mark the ischemic bed. At the end of reperfusion, the hearts were removed and sectioned. Autoradiography determined the ischemic myocardium at risk, and the necrotic zone was determined by triphenyl-tetrazolium staining. Animals were divided into three groups: control, allopurinol (24-h oral pretreatment 400 mg, then 50 mg/kg IV bolus on occlusion); and superoxide dismutase starting with occlusion (15 000 U/kg). The size of the infarct as a percentage of the tissue at risk was: 23.1 +/- 4.1 for the control; 8.7 +/- 1.2 for the allopurinol group; and 5.4 +/- 1.2 for the superoxide dismutase group. The infarcts in the allopurinol and superoxide dismutase groups were significantly smaller than those in the control groups. In a second series of experiments we determined the xanthine oxidase/xanthine dehydrogenase content of dog myocardium. The left anterior descending branch was ligated for 30 min and then biopsies were removed from both the normal and the ischemic regions. Total enzyme content did not differ between the two regions averaging 0.259 U/g protein for the ischemic tissue and 0.225 U/g protein for the normal region. Only 9.8% of the enzyme was in the oxidase form in the normal region while 32.8% was in the oxidase form in the ischemic zone.(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1985

Infarct size limitation by the xanthine oxidase inhibitor, allopurinol, in closed-chest dogs with small infarcts.

The present study was designed to evaluate the ability of allopurinol to limit infarct size following permanent coronary occlusion in the greyhound. Coronary occlusion was produced by injecting 2.5 mm plastic beads into the coronary artery of the closed chest dog. Non-perfused myocardium, the area at risk, was visualised by autoradiography of 141Cerium labelled microspheres which were infused immediately following coronary embolization. The treated dogs (n = 12) received 400 mg of allopurinol orally one day before surgery. A 25 mg . kg-1 bolus was administered (iv) immediately before occlusion, and repeated every 8 h. 11 dogs served as controls. After 24 h, the dogs were killed and the hearts were sliced into 5.0 mm transverse sections. The infarcted myocardium was visualised by triphenyl tetrazolium chloride staining. The percentage of the risk zone which evolved to infarct was calculated. This percentage was 18.1 +/- 3.95% in the allopurinol group vs 58.4 +/- 2.81% in the control group (p less than 0.001). We conclude that allopurinol is a potent drug for the limitation of infarct size in the dog with permanent coronary occlusion.

Allopurinol↗
PubMed1984

The role of vascular capacitance in the coronary arteries.

When the left coronary artery was perfused with nonpulsatile pressure, the onset of diastole was accompanied by a capacitance overshoot in flow with an exponential decay back to a steady state. Time constant for that decay ranged from 55 msec when tone was present to 105 msec with maximal dilation. Since the transient resulted from a fall in tissue pressure, this represents an estimation of intramural arterial capacitance only. Transients in perfusion pressure, which would also affect epicardial arteries, yielded similar time constants. We concluded that most of the coronary capacitance resides in the small intramural vessels. Analysis of transients yielded a value for capacitance of between 0.01 and 0.05 ml/mm Hg per 100 g. We then used the data from the transients to construct coronary pressure flow curves which were free of any back flow from capacitance. When coronary tone was present, the curves indicated that flow ceased at 30 mm Hg. With maximal dilation, flow ceased at only 18 mm Hg. Long diastoles in those same hearts indicated that flow ceased at about 10 mm Hg higher pressure. Although capacitance causes critical closing pressure as determined by a long diastole to be artifactually high, critical closing pressure is still appreciable in the heart, and tone dependent. Finally, three computer models were built, one of which included only small vessel capacitances, the second, only vascular waterfalls, and the third, both of the above. Only model 3 was capable of reproducing the flow patterns which were actually seen.

Animals↗
PubMed1983

Sustained limitation of myocardial necrosis 24 hours after coronary artery occlusion: verapamil infusion in dogs with small myocardial infarcts.

Studies were undertaken to ascertain whether verapamil infusion affords a sustained limitation of myocardial injury in the dog after a 24-hour period of coronary artery occlusion. Regional myocardial ischemia was induced by an embolization procedure which did not involve thoracotomy. Immediately after embolization radioactive microspheres were administered intraventricularly to define any area of myocardial underperfusion (zone at risk of infarction). Verapamil (0.005 mg/kg/min) was then administered and maintained for 24 hours during which time the dogs were allowed to recover from anesthesia. The control group received a corresponding infusion of saline solution. After 24 hours the dogs were killed and transverse myocardial sections (3 mm) were prepared. The resulting area of necrosis was visualized by tetrazolium staining, and risk zones were visualized by autoradiography. In the control heart, 62 +/- 7% of the zone at risk deteriorated to necrotic tissue, whereas in the verapamil-treated group only 18 +/- 4% of the tissue in the zone at risk became necrotic. Verapamil appeared to exert a significant (p less than 0.001) tissue-sparing effect that was sustained for at least 24 hours after the onset of ischemia.

Animals↗
PubMed1983

Effects of flurbiprofen in altering the size of myocardial infarcts in dogs: reduction or delay?

Anti-inflammatory agents such as flurbiprofen have been claimed to reduce infarct size in a number of models of coronary artery occlusion. However, several of the studies are controversial and also do not allow the critical distinction between reducing and delaying injury. In the present study, a closed chest method of coronary occlusion was used to generate small areas of regional myocardial ischemia in dogs. The method involved cannulation of the coronary ostium by way of the carotid artery and coronary embolization with 2.5 mm diameter beads. Flurbiprofen (1 mg/kg) was given immediately after occlusion and thereafter every 6 hours. Groups of dogs were subjected to either 6 or 24 hours of elapsed ischemia, after which time the hearts were removed and sectioned. Frozen-tissue slices were stained with triphenyl tetrazolium in order to delineate infarct size. After staining the tissue slices were subjected to autoradiography in which microspheres given immediately after occlusion were visualized to delineate the perfusion bed served by the occluded coronary artery (zone at risk). Risk zone to infarct size ratios for drug treated and control animals revealed that flurbiprofen treatment had no effect upon infarct size as determined 24 hours after occlusion. Despite significant residual coronary flow in the ischemic area, virtually all of the risk zone deteriorated to necrotic tissue. By contrast, after 6 hours of elapsed ischemia, infarct size was considerably reduced in the flurbiprofen-treated group. With the proviso that the drug might have affected only the sensitivity to tetrazolium staining, these results indicate that in severe ischemia, flurbiprofen can greatly delay but not prevent tissue necrosis.

Animals↗
PubMed1983

Reduction of myocardial ischemic injury with oxygen-derived free radical scavengers.

Experimental data suggesting that oxygen-derived free radicals may play a role in the myocardial injury associated with ischemia and reperfusion are presented. In several studies of prolonged global myocardial ischemia, the administration of free radical scavenging agents, such as superoxide dismutase, catalase, and mannitol, resulted in significantly better recovery of left ventricular function following reperfusion. In a region-at-risk model of localized myocardial ischemia, both superoxide dismutase and allopurinol significantly reduced the extent of myocardial necrosis that developed following reversible coronary arterial branch occlusion. The manner in which oxygen-derived free radicals may be harmful is examined. In particular, the possibility that these toxic species are involved in the exacerbation of the ischemic injury that develops upon reflow and reoxygenation is examined.

Animals↗
PubMedDate not supplied

Nifedipine limits infarct size for 24 hours in closed chest coronary embolized dogs.

We studied the ability of nifedipine, a calcium antagonist, to limit infarct size in the closed chest, coronary embolized dog. Immediately after embolization 141Ce labelled microspheres were administered into the left ventricle. Myocardium not receiving microspheres was considered to be the region at risk. The nifedipine group (10 dogs) received a bolus (16 micrograms/kg i.v. over 8 minutes as a loading dose) followed by continuous infusion (1,000 micrograms/24 hours) 10 min after embolization. The control group (9 dogs) received an equal volume of saline. Twenty-four hours after embolization the dogs were sacrificed, the heart sectioned into 4-mm slices and the slices were stained with tetrazolium to reveal the infarct. The region at risk was determined by autoradiography of the microspheres in the heart slices. Infarct and risk zone volume were determined by planimetric methods. The nifedipine group had a significantly smaller infarct volume to risk zone volume ratio than the control group (38.7 +/- 4.7% vs. 79.5 +/- 4.3%, p less than 0.001). We conclude that nifedipine produces a sustained limitation of infarct size following permanent occlusion of a dog's coronary artery.

Animals↗