The legacy of Dr. Alzheimer. Nearly a century after the disease got its name, the spotlight on care burns brighter than ever.
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Biomedical subjects
Publications and source records attributed to D D Buss.
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The results of the first sixty-nine consecutive patients who had had seventy arthroscopically assisted reconstructions of the anterior cruciate ligament with use of an autogenous patellar-ligament graft at our institution were reviewed retrospectively. Sixty-seven patients (sixty-eight knees) were available for evaluation after a minimum of two years. All patients had been managed with early, postoperative range-of-motion exercises and a standardized program of physical therapy. At the time of the most recent follow-up evaluation, the median ligament score, according to the rating system of The Hospital for Special Surgery, was 93 of a possible 100 points. Of the sixty-eight knees, forty-four were rated excellent; fifteen, good; six, fair; and three, poor. Eighteen knees had symptoms related to the patellofemoral joint and sixty-three had a full range of motion; two knees had had manipulation for loss of flexion. At the follow-up evaluation, KT-1000 arthrometric measurements were obtained for both knees of fifty-six patients. Eighty-four per cent of the patients had an increase of three millimeters or less in anterior-posterior displacement of the tibia on the reconstructed side compared with the normal side, while 93 per cent had an increase of four millimeters or less. Postoperatively, there was no apparent association between changes in the Insall-Salvati patellar ligament-to-patella ratios and pain in the patellofemoral joint. The results of the arthroscopically assisted reconstructions combined with use of early range-of-motion exercises were comparable with those reported after open reconstruction and immobilization of the limb in a plaster cast. The frequency of pain in the patellofemoral joint and the need for manipulation because of loss of motion were decreased after the arthroscopically assisted procedures.
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Previous studies in our laboratory have shown an effect of 12 weeks of hypoxia on the electrophysiology of the heart. This study was designed to determine the effects of hypoxia for shorter periods (1, 2, 3 and 6 weeks) on the neonatal heart as well as the chronotropic effects of [H+] on sino-atrial automaticity. Rabbits (2 days of age) were raised for 1, 2, 3 or 6 weeks in either a normal or hypoxic environment. At the end of 1, 2, 3 or 6 weeks, they were killed and studied using an isolated sino-atrial tissue preparation and standard microelectrode techniques. Measurements of hematocrit, ventricular weight and ventricular total protein were made. Right ventricular hypertrophy appeared at 2 and 3 weeks in the hypoxic hearts. There was no difference in left ventricular weight or total protein between normal and hypoxic groups over the time studied. Both the basal and maximal (isoproterenol stimulated) spontaneous rates decreased with age. The baseline and maximal rates from hypoxic rabbits were significantly less than those from normal rabbits at 3 and 6 weeks (p less than 0.05). The net negative chronotropic effect of elevated [H+] was more pronounced in the hypoxic than the normal preparations at 3 and 6 weeks. In summary, neonates raised in hypoxia for as short a period as 3 weeks show right ventricular hypertrophy and a decrease in sino-atrial automaticity. The net negative chronotropic effect of [H+] is enhanced with development and chronic hypoxia.
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Nicardipine is a second-generation dihydropyridine calcium antagonist with relative coronary and cerebrovascular selectivity. To study the effects of nicardipine on systolic and diastolic myocardial function, we used three experimental models. In isolated feline papillary muscle, nicardipine produced a dose-dependent calcium antagonistic effect manifested by depressed indexes of contraction and relaxation. In an autoregulating blood-perfused isolated rabbit heart preparation, nicardipine markedly increased coronary blood flow and slightly decreased systolic pressure at a given end-diastolic pressure. The systolic pressure and +dP/dt versus volume curves, however, were shifted to the left during nicardipine administration, indicating improved systolic function. This increase was accompanied by decreased volume elastance and is probably due, at least in part, to the coronary turgor effect. In humans at rest, intravenous nicardipine administration produced pronounced coronary and systemic vasodilation with improved left ventricular systolic performance and enhanced relaxation accompanied by reflex sympathetic activation. With exercise to ischemia, nicardipine preserved the salutary effects on left ventricular function seen at rest and significantly blunted the increase in left ventricular end-diastolic pressure observed in the control setting. Administration of intracoronary nicardipine to patients produced a slight and transient depression of systolic and diastolic left ventricular function that was accompanied by a pronounced coronary vasodilator response and later by improved ventricular function. This improvement was manifested by decreased end-systolic volume and increased +dP/dt without changes in heart rate, arterial pressure, end-diastolic pressure, or end-diastolic volume. Global diastolic function indexes, including the time constant for isovolumic relaxation, peak filling rate normalized for stroke volume, and volume elastance, were unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)
A 17-year-old girl collapsed during a field hockey practice on a hot August afternoon, apparently suffering from heat illness, which is responsible for about 5,000 deaths annually. A panel of experts explores this girl's case, discusses heat illness in general, and makes recommendations about diagnosis, prevention, and treatment.
The effect of hypoxia on cardiac beta-adrenergic and muscarinic receptors during the first 3 weeks of postnatal development was determined in the rabbit. After the first week of postnatal exposure to hypoxia, there was no change in the ventricular content of beta-adrenergic receptors. However, after 2 weeks of hypoxia, there was a 24% decrease in the receptor content of the left ventricle with no change in the right ventricle. At the end of 3 weeks exposure to hypoxia, the receptor content had decreased by 31% and 32% in the right and left ventricle, respectively. In control animals, there was no alteration in the beta-adrenergic receptor content of either ventricle over the 3 week period. In contrast to the beta-adrenergic receptor, there was no hypoxia-associated alteration in the muscarinic receptor content of either ventricle during the 3 weeks of postnatal study. The data suggest that hypoxia during the first 3 weeks of postnatal development in the rabbit induces alterations in the cardiac beta-adrenergic receptor with no effect on the development of the cholinergic muscarinic receptor.
The objective of this study was to test for the presence of transmural gradients of various components of the coronary microvasculature of the canine left ventricle. In order to achieve study objectives, the heart and coronary circulation were fixed in a reproducible state of myocardial and vascular tone (diastolic cardiac arrest and maximal coronary vasodilation). Morphometric methods which treat the coronary microvasculature as anisotropically arranged structures were applied for quantitative structural analysis. Eight dog hearts were fixed with a glutaraldehyde-cacodylate-buffered fixative by retrograde perfusion of the aorta with the heart in diastolic arrest and with maximal coronary vasodilation. Tissue samples were taken from areas near to the anterior and posterior papillary muscles from the subendocardium, subepicardium, and intermediate transmural locations. Morphometric results showed a homogeneously arranged array of microvascular and myocardial components with no significant differences in any of the primary morphometric measurements, down to the ultrastructural level, in myocytes relative to transmural location. The results suggest that transmural differences in coronary blood flow are not due to transmural structural differences but rather are due to physiological regulatory mechanisms of coronary blood flow. Further, the results indicate that failure to correct for anisotropy of myocardial structures can lead to erroneous conclusions concerning the structural basis of function in the heart.
Newborn rabbits were raised in either hypoxic or normoxic environments for 3 months. Data from electrophysiological studies carried out on isolated sinoatrial and ventricular preparations from the two groups show that the hypoxic group had changes in cellular transmembrane electrical activity that could be the basis for disorders of rate and conduction in vivo. This model will be useful to study the etiology and therapy of some arrhythmias seen in cyanotic congenital hypoxemic heart disease.
An apparatus and method for rearing neonatal rabbits in hypoxia is described. This technique relies on the use of hypoxia chambers that need to be serviced once a day for approximately 1 h. By use of the apparatus and procedures outlined, rabbits that exhibit standard clinical signs of hypoxemia (cyanosis and elevated hematocrit) can be reliably reared and maintained for long periods of time.
Full use of nonhuman primates as a model for coronary vascular disease has been hampered by several factors, including the limited availability of detailed coronary anatomic data. This study was undertaken to identify the gross coronary arterial anatomy of the Bonnet monkey (Macaca radiata). The hearts of sixteen adult male Bonnet monkeys were subjected to postmortem coronary angiography and gross morphological examination. The main left coronary artery divided into the left anterior descending coronary artery (LAD) and the left circumflex coronary artery (LCA). The posterior descending coronary artery (PDCA) arose from the LCA in 31% of the cases and from the right coronary artery (RCA) in 56% of the hearts. Hearts from two animals (13%) had paired arteries, arising from the LCA and RCA, located in the posterior interventricular groove. The arterial supply to the sinoatrial node originated from the LCA in 69% of the animals and from the RCA in the remainder. The atrioventricular node was supplied by a branch of the RCA in 69% of the animals and from the LCA in the remainder. The coronary anatomy of the bonnet monkey resembles that of man more closely than does the dog in terms of origin of the PDCA, supply of the sinoatrial and atrioventricular nodes, and perfusion of the interventricular septum. The Bonnet monkey may therefore be a useful model for certain specific pathophysiological studies on the coronary circulation.
Evidence, obtained with in situ perfused rat liver, indicated that pyridoxine is taken up from the perfusate by a non-concentrative process, followed by metabolic trapping. These conclusions were reached on the basis of the fact that at low concentrations (0.125 microM), the 3H of [3H]pyridoxine accumulated against a concentration gradient, but high concentrations (333 microM) of pyridoxine or 4-deoxypyridoxine prevented this apparent concentrative uptake. Under no conditions did the tissue water:perfusate concentration ratio of [3H]pyridoxine exceed unity. The perfused liver rapidly converted the labeled pyridoxine to pyridoxine phosphate, pyridoxal phosphate and pyridoxamine phosphate and released a substantial amount of pyridoxal and some pyridoxal phosphate into the perfusate. Since muscle and erythrocytes failed to oxidize pyridoxine phosphate to pyridoxal phosphate, it is suggested that the liver plays a major role in oxidizing dietary pyridoxine and pyridoxamine as their phosphate esters to supply pyridoxal phosphate which then reaches to other organs chiefly as circulating pyridoxal.
Technical and interpretive limitations of equine fetal electrocardiography were evaluated in recordings obtained from 45 pregnant mares. Technical limitations were related to the small amplitude of the fetal electrocardiogram and the variability in the lead configuration providing the best recording. It was found that recording the fetal electrocardiogram at high sensitivity and high base-line fidelity in several different leads was necessary to obtain satisfactory tracings. Interpretive limitations were related in part to the small amplitude of the fetal electrocardiogram and to the marked variability in heart rate between fetuses. The great variability in normal fetal heart rate makes a diagnosis of fetal tachycardia or distress unless serial tracings are available.
The vascularly perfused small intestine and hind limb muscle of the rat were utilized to study the transport and metabolism of pyridoxine (PN), independent of other tissues, including erythrocytes. The transport of PN both into the mucosal tissue and transmurally into the perfusate was proportional to the dose over a 10,000-fold range of concentrations. The only labeled compound formed from [3H]-PN in the mucosa was PNP which accounted for 30.6% of the isotope found there. The data for the hind limb muscle suggest that transport occurs by passive diffusion followed by phosphorylative trapping. Over a 10,000-fold range of concentrations of PN in the perfusate, the percentage of 3H found in the muscle ranged from 10.4 to 15.7 for 30-minute experiments. As the dosage was increased the percentage of 3H in the muscle, present as PN increased and that in PNP decreased. In longer experiments, up to 75 minutes, with 20 nmole of [3H]-Pn, the PN in muscle decreased as phosphorylation occurred. There was no evidence of any conversion of PNP to PLP (pyridoxal phosphate) in the perfused hind limb.
The oral ammonia tolerance test was investigated in 20 clinically normal dogs and in 6 dogs with naturally occurring portosystemic shunts. The dogs with portosystemic shunting had a marked rise in venous blood ammonia following the administration of ammonium chloride, as compared with the control dogs. Fasting venous blood ammonia content was not uniformly reliable in separating the dogs with portosystemic shunting from the clinically normal dogs.
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Hemodynamics and myocardial contractility were evaluated in 6 unanesthetized ponies during hypocapnic and isocapnic hypoxia and during hypocapnic hypoxia after beta adrenergic blockade with propranolol. Hypocapnic hypoxia, with a mean arterial oxygen pressure (PaO2) of 41.9 mm of Hg, produced a decrease in stroke index and an increase in heart rate, with no change of cardiac index. A moderate increase in left ventricular contractility occurred during hypocapnic hypoxia. Beta adrenergic blockade abolished changes in nearly all indices of left ventricular contractility during hypocapnic hypoxia, suggesting that the antonomic nervous system plays a definite role in the genesis of circulatory changes during acute hypoxia. Isocapnic hypoxia produced a more well-defined increase in left ventricular contractility. Changes in right ventricular contractility were not observed in any of the hypoxia periods when the concurrent effects of a significant increase in afterload was taken into consideration. The tension-time index, measured as a guide to myocardial oxygen consumption, increased during each hypoxia period in both the right and left ventricle, and was not affected by beta adrenergic blockade.