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Nerve degeneration studies were performed to determine the central projections of the octavus nerve in the guitarfish. Rhinobatos sp. Most first-order octavus nerve afferents are confined to the ventral longitudinal column of the medulla, which consists of four octavus nuclei: the nucleus octavus anterior (NOA), nucleus octavus magnocellularis (NOM), nucleus octavus descendens (NOD); and nucleus octavus posterior (NOP). Central projections of the octavus nerve outside of the ventral octavus nuclear column are to the vestibulolateral lobe of the cerebellum, the large multipolar cells that lie deep to the cerebellar crest of nucleus intermedius, the reticular formation, and the nucleus octavolateralis efferens. In addition, the cytoarchitectural features of the four octavus nuclei have been analyzed: the NOA consists of large spindle-shaped neurons and medium-sized multipolar neurons; the NOM is a small nucleus consisting of very large multipolar neurons; the NOD contains several types of neurons including large spindle-shaped neurons, large multipolar neurons, and polymorphic small and medium-sized neurons; and the NOP contains small spherical and small multipolar neurons evenly distributed throughout the nucleus. On the basis of the morphology of the neurons, the NOA and NOD appear to have subdivisions suggesting a more complex organization of the octavus nuclear column than previously recognized.

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Exercise electrocardiography and thallium scanning were performed a mean of 24 days after uncomplicated acute myocardial infarction in 103 patients, aged 36 to 60 years, who also underwent coronary angiography. The purpose of the study was to determine the ability of the noninvasive tests to predict multivessel coronary artery disease (CAD) and prognosis. Patients were followed up to document medical complications (incidence 12%: 3 deaths, 1 resuscitated cardiac arrest, 4 recurrent infarctions, 4 admissions with unstable angina) and combined events (medical events or bypass surgery, incidence 23%). The sensitivity, specificity and predictive accuracy for predicting multivessel CAD were 64%, 77% and 64% for a positive exercise electrocardiographic (ECG) response, 64%, 88% and 80% for a remote thallium defect, and 42%, 96% and 88% for a combination of the 2 tests. With 2 tests yielding negative findings the probability of multivessel CAD was 13%. No variable (positive exercise ECG response, remote thallium defect and presence of multivessel CAD) predicted medical events, although there were nonsignificant trends to more events in patients with any of those findings. The relative risk of combined events was 2.5 (p less than 0.05) for a positive exercise ECG response; 1.8 (NS) for a remote thallium defect; 2.6 (p less than 0.05) for multivessel CAD; and 3.1 (p less than 0.025) for both positive ECG response and remote defect. A combination of exercise electrocardiography and thallium scanning early after acute myocardial infarction helps to identify subsets of patients with high and low probabilities of multivessel CAD and combined medical or surgical events.

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The functional significance of coronary collateral flow from a nonobstructed supply artery was studied in 121 patients with severe (greater than or equal to 80%) single-vessel disease, 64 with and 57 without Q wave infarction. All patients underwent exercise thallium imaging and coronary angiography. On angiography, collateral flow was present in 85% of 74 occluded arteries compared with only 17% of 47 arteries with subtotal obstruction (p less than .001). Collateral flow was not seen in arteries with lesions of less than 90% obstruction. Collateral flow was present in 100% of 29 occluded arteries in patients without Q wave infarction compared with only 76% of 45 occluded arteries with Q wave infarction (p less than .005). Clinical variables did not correlate with collateral flow. Collateral flow did not prevent ischemia on exercise thallium imaging in patients without Q wave infarction: 30 of 33 (91%) with collateral flow had reversible thallium defects compared with 24 of 24 (100%) without collateral flow (p = NS). In patients with Q wave infarction, partially reversible exercise thallium defects (peri-infarctional ischemia) were more common with flow to the area from either subtotal obstruction (73%) or collateral flow (45%) than with no flow from total occlusion (27%; p = .05). In patients with severe single-vessel disease the presence of collateral flow is principally determined by coronary occlusion. Collateral flow may protect from Q wave infarction but does not prevent exercise ischemia on thallium imaging.

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Projections of primary afferent fibers from the octavus nerve to the inferior reticular formation were determined by nerve degeneration and HRP labeling. Descending afferents from the horizontal ampullary nerve exit the ventral border of the nucleus octavus descendens via arcuate fiber tracts, and project to a group of neurons adjacent to the spinal lemniscus; to the inferior reticular formation; and to the nucleus funiculi lateralis. The possible influence of these afferent projections on directed swimming motion is discussed.

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Magnetite particles were systematically localized within the otolithic mass as a conspicuous curved band in the most ventral region of the guitarfish sacculus. The magnetite band overlaid two separated segments of neuroepithelium in the macula, a long segment oriented parallel to the longitudinal body axis, and a short segment oriented in a transverse plane. The exogenous magnetite particles differed from the endogenous otoconia both in their capacity of orienting to magnetic fields, and their difference in mass due to the higher atomic weight of iron. In addition to the normal gravistatic function of the sacculus, two additional receptor functions are hypothesized based upon the differences between the endogenous and exogenous otoconia. A geomagnetic field could induce magnetite displacements detectable by the hair cells for purposes of geomagnetic orientation. Alternatively, the greater atomic weights of magnetite, relative to that of otoconia, could result in gravitational and linear acceleration, which differed in different regions of the macula.

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We examined the relationship between coronary anatomy and anterolateral ST segment depression during inferior acute myocardial infarction (AMI) in 84 consecutive survivors of inferior AMI, who underwent prospective coronary angiography a median time of 2 weeks after AMI. Multivessel disease was defined as two or more significantly (greater than 70%) stenosed vessels. A QRS scoring system was used to estimate myocardial infarct size. Patients with ST depression had more multivessel disease compared to patients with no ST depression (53% vs 6%, p less than 0.01), more left anterior descending stenoses (36% vs 10% p less than 0.05), and higher QRS scores (5.8 +/- 3.2 vs 2.6 +/- 1.8, p less than 0.01) indicating larger infarcts. Patients with ST depression and one-vessel disease (47%) still had higher QRS scores compared to patients with no ST depression (4.8 +/- 2.9 vs 2.6 +/- 1.8, p less than 0.001) and had an increased prevalence of infarct-related vessels with a terminal branch supplying the left ventricular lateral wall or apex. We conclude that anterolateral ST depression during inferior AMI may indicate the presence of additionally stenosed vessels or that the infarct-related vessel has a large vascular territory. The absence of ST depression virtually precludes multivessel disease.

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The clinical characteristics of 84 patients with isolated circumflex disease (greater than or equal to 70% luminal stenosis) were reviewed. A total of 66 patients had angina pectoris (mean duration 17.3 months), and 60 had suffered a myocardial infarction. Risk factors averaged 2.2 per patient. In the 84 patients there were 103 discrete circumflex stenoses; 51 stenoses were central (proximal circumflex, obtuse marginal, and intermediate branches), and 52 were peripheral (distal circumflex, posterolateral, and posterior descending branches); 48 were total and 55 were subtotal. Left ventricular function was normal in 21 patients and abnormal in 63 patients, but the mean left ventricular ejection fraction of the group was normal (59 +/- 12%). Eighty-two patients had abnormal electrocardiograms: there were Q waves in 25, RV pattern in 43, ST-T wave abnormalities in 19, left bundle branch block in two, and pacemaker rhythm in one. Inferior abnormalities on the electrocardiogram correlated with peripheral stenoses (p less than .02), and lateral abnormalities on the electrocardiogram correlated with central stenoses (p less than .01). The RV pattern of true posterior infarction was seen in both central and peripheral stenoses. In the 32 patients who underwent thallium scanning, lateral defects were more common with central stenoses, but posterolateral defects occurred similarly in central and peripheral stenoses. Prognosis was good. There were two deaths during the mean follow-up time of 17 months (range 1 to 49). The cumulative survival rate was 100% at 12 months, 97.5 +/- 2.9% at 24 months, and 97.5 +/- 3.6% at 30 months.

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Patterns of growth and regeneration in 2-, 4-, 8-, and 17-week-old murine dystrophic (129 ReJ dy/dy) extensor digitorum longus muscles have been determined. Necrosis and myofiber loss, hypertrophy, and regeneration result in a reduced population of myofibers whose diameter distribution is more extensive than that found in the extensor digitorum longus muscles of age-matched normal mice. At the onset of dystrophic symptoms (2 weeks postnatal), the ratio of myosatellite cell nuclei to the total sublaminal nuclear population (myonuclei + myosatellite cells) is similar to that found in 2-week-old control muscles. The frequency of finding myosatellite cells decreases with age in both control and dystrophic muscles. Myosatellite cells account for 11%, 6%, 5%, and 3% of the total sublaminal nuclear population in control muscle and 12%, 8%, 6%, and 5% of the total sublaminal nuclear population in dystrophic muscle at 2, 4, 8, and 17 weeks, respectively. No preferential association of myosatellite cells with myofibers of a particular diameter is found in control muscle or in the two youngest dystrophic groups. At 8 and 17 weeks, myosatellite cells are less frequently encountered on small-diameter, regenerating myofibers of dystrophic muscle, and they are preferentially associated with large diameter, hypertrophied myofibers. The labeling index of myosatellite cells decreases with age in both normal and dystrophic muscle. At all ages the myosatellite cell labeling index is higher in dystrophic muscle (23%, 7%, 5%, and 2% at 2, 4, 8, and 17 weeks, respectively) than in normal muscle (5%, less than 1% at 2 and 4 weeks, respectively), with no labeled myosatellite cells being found in 8- and 17-week-old normal muscles. It is suggested that the magnitude of the regenerative response of dystrophic murine muscle decreases with age and that this factor may be responsible for the inability of the regenerative response of dystrophic muscle to keep pace with the rapid muscle deterioration.

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To compare serial functional and perfusion scintigraphic changes after myocardial infarction, we performed left ventricular (LV) cineangiograms and thallium (TI)-201 myocardial perfusion scintigrams before and 1 hour, 2 days, 9 days, and 1 month after closed chest coronary occlusion in 14 dogs as survival permitted. Survivors were studied with technetium-99m (stannous) pyrophosphate (TcPYP) scintigrams at 48 hours, and at postmortem examination infarction was documented and measured after nitroblue tetrazolium (NBT) staining. The TcPYP image was abnormal in 10 dogs, each of which had infarcts on NBT staining measuring 3 to 23 gm. In all 14 dogs, perfusion scintigrams became abnormal and LV ejection fraction (EF) fell when measured within 48 hours of occlusion. In the nine late survivors studied over 1 week after the event, perfusion scintigrams and EF improved in those which developed infarcts and normalized in those without infarction. The decrement in LVEF after coronary occlusion generally showed serial improvement and correlated with the size of the defect in the accompanying TI-201 scintigram (r = 0.74). TI-201 defect size seen in late studies correlated well with NBT infarct size (r = 0.89) and TcPYP image infarct size (r = 0.82), as it did with the decrement in LVEF noted in late studies (r = 0.86). The results suggest that early perfusion scintigrams together with TcPYP images may be useful for estimating the amount of reversible dysfunction after coronary occlusion.

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To determine whether cardiomyopathy could be distinguished from coronary artery disease, we used thallium scanning to study 25 patients with severe left ventricular dysfunction and chronic heart failure. Ten patients had normal coronary arteries and idiopathic cardiomyopathy (ejection fraction 20 +/- 5%), and 15 patients had multivessel coronary disease and left ventricular dysfunction (ejection fraction 25 +/- 6%). The exercise time and maximal heart rate were similar in the two groups. Two patients with cardiomyopathy and 11 with coronary artery disease had a positive exercise ECG (p less than 0.05). Thallium scans showed perfusion defects in all 25 patients. The perfusion defects were complete in nine coronary artery disease patients (60%) and in one patient (10%) with cardiomyopathy (p less than 0.05). Extensive defects involving more than 40% of the left ventricular circumference, the number of segments involved, redistribution on the 4-hour scan, lung uptake and ventricular size were similar in the two groups. Perfusion defects on thallium scanning can occur in patients with idiopathic dilated cardiomyopathy and chronic heart failure. Thallium scanning cannot be reliably used in patients with chronic heart failure to distinguish coronary artery disease from cardiomyopathy unless complete defects are present.

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Thallium -201 myocardial perfusion scanning can assess regional myocardial perfusion noninvasively. As it is both time-consuming and expensive its use should be restricted to specific diagnostic problems. The clinical indications in known or suspected coronary artery disease are reviewed. In suspected coronary artery disease thallium scanning is most useful in patients with chest pain when the exercise ECG is uninterpretable, in men with probable angina but a negative exercise ECG, or conversely a positive exercise ECG without typical angina, and in women with probable angina and either a positive or a negative exercise ECG. In known coronary artery disease, thallium scanning may help determine the functional significance of a coronary obstruction found at angiography and may determine the site of myocardial ischaemia when multiple obstructions are present.

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The potential of nitroglycerin for improving global and regional ventricular function after acute myocardial infarction and predicting serial change in ventricular function at the time of hospital discharge was investigated. Equilibrium multiple gated blood pool scintigrams were performed at rest before and after sublingual administration of nitroglycerin in 18 patients an average of 36 hours after infarction and again at discharge. Global right and left ventricular function and regional left ventricular function of infarct and noninfarct zones were determined scintigraphically. In the early study nitroglycerin increased both mean (+/- standard deviation) left ventricular ejection fraction (0.51 +/- 0.15 to 0.55 +/- 0.15 ; p less than 0.02) and mean right ventricular ejection fraction (0.42 +/- 0.14 to 0.47 +/- 0.13; p less than 0.05). Left ventricular ejection fraction significantly increased in 5 of the 18 patients. It increased late in five of the six patient who exhibited an increase early after nitroglycerin but in only 2 of the 12 patients who did not exhibit an early increase (p less than 0.06). Regional ejection fraction in the infarct zone increased late in 7 of the 12 patients who exhibited an early increase after nitroglycerin and in none of the 6 who did not exhibit an early increase (p less than 0.05). Both right and left ventricular global ejection fraction and regional ejection fraction showed little late responsiveness to nitroglycerin. Early after infarction, sublingual nitroglycerin improved left, right and regional ejection fraction at the infarct site in some patients. These nitroglycerin-induced changes predicted those patients whose global ventricular function and regional left ventricular function at the infarct site improved late.

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In 61 patients with single vessel coronary artery disease (70 percent or greater obstruction of luminal diameter in only one vessel) and no previous myocardial infarction, the sites of ischemic changes on 12 lead exercise electrocardiography and on thallium-201 myocardial perfusion scanning were related to the obstructed coronary artery. The site of exercise-induced S-T segment depression did not identify which coronary artery was obstructed. In the 37 patients with left anterior descending coronary artery disease S-T depression was most often seen in the inferior leads and leads V4 to V6, and in the 18 patients with right coronary artery disease and in the 6 patients with left circumflex artery disease S-T depression was most often seen in leads V5 and V6. Although S-T segment elevation was uncommon in most leads, it occurred in lead V1 or a VL, or both, in 51 percent of the patients with left anterior descending coronary artery disease. A reversible anterior defect on exercise thallium scanning correlated with left anterior descending coronary artery disease (probability [p] less than 0.0001) and a reversible inferior thallium defect correlated with right coronary or left circumflex artery disease (p less than 0.0001). In patients with single vessel disease, the site of S-T segment depression does not identify the obstructed coronary artery; S-T segment elevation in lead V1 or aVL, or both, identifies left anterior descending coronary artery disease; and the site of reversible perfusion defect on thallium scanning identifies the site of myocardial ischemia and the obstructed coronary artery.

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Exercise thallium myocardial scintigrams were analyzed in 76 consecutive patients with documented normal coronary arteries to identify the factors associated with abnormal or "false positive" studies. The thallium scintigrams had been judged normal in 60 patients (79 percent) and abnormal in 16 (21 percent). Analysis of the location of thallium defects in the 16 patients with abnormal scintigrams revealed a pattern that was consistent with coronary artery disease in 5, including 4 with an abnormal left ventricle, and a pattern that was inconsistent in the other 11. In 9 of these 11 patients the pattern of defects suggested soft tissue attenuation, by the diaphragm in 2 and breast or adipose tissue in 7, whereas in the other 2 patients isolated apical defects were seen. Among exercise myocardial scintigrams performed in 68 randomly selected patients with abnormal coronary arteries, 6 (9 percent) were reported to be normal. In four patients with abnormal scintigrams, the diagnosis of coronary artery disease was based on an inconsistent pattern. In three of these the pattern was related to isolated apical defects and in one it was related to apparent soft tissue attenuation. "Consistent" scintigraphic defects, seen frequently in patients with normal coronary arteries, in whom they are usually associated with an abnormal left ventricle. In patients with normal coronary arteries, "inconsistent" thallium defects are probably related to soft tissue attenuation or to normal apical thinning. Although defects caused by isolated apical abnormalities and soft tissue attenuation are also seen in patients with coronary diseases and add somewhat to scintigraphic sensitivity, they are a rare cause of diagnostic scintigraphic abnormalities in patients with coronary disease. The incidence of false positive thallium scintigrams could be reduced and overall accuracy improved by careful attention to the pattern of thallium defects.

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Six patients who had documented coronary spasm and no coronary artery with organic obstruction greater than 50% developed angina and ST-segment elevation on exercise testing. Oral verapamil, 160-480 mg/day, prevented exercise-induced ischemia in all patients and increased maximal work capacity from 611+/- 250 kpm to 808 +/- 160 kpm (p less than 0.02). In two patients, a relationship between the prevention of exercise-provoked ischemia and the plasma concentration of verapamil was demonstrated, and in one of these, the relationship had a diurnal pattern. Patients with variant angina may develop coronary spasm on effort and often respond to verapamil.

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Exercise-induced ST-segment elevation in leads V1 and/or aVL in the absence of anterior Q waves occurred in 46 of 190 patients (24%) who underwent 12-lead exercise electrocardiography with thallium-201 myocardial perfusion imaging and coronary arteriography. Significant left anterior descending coronary artery (LAD) disease was present in 38 of 46 patients (83%) with V1/aVL ST evaluation and in 72 of 144 patients (50%) without V1/aVL ST elevation (p less than 0.0005). Anterior myocardial ischemia, indicated by reversible anterior perfusion defects on thallium scanning, was present in 40 of 46 patients (87%) with V1/aVL ST elevation and in 25 of 144 patients (17%) without V1/aVL ST elevation (p less than 0.0005). Exercise ST elevation in V1/aVL was detected in 38 of 110 of the patients (35%) with LAD disease, for a specificity of 90%, and in 40 of 65 of the patients (62%) with anterior myocardial ischemia, for a specificity of 95%. We conclude that during 12-lead exercise electrocardiography, ST-segment elevation in V1 and/or a VL in the absence of anterior Q waves predicts anterior myocardial ischemia and LAD disease.

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Black magnetic particles are intermixed with white crystalline otoconia in the inner ear gravity receptors of a saltwater ray. Their size and composition suggest that they are multidomains of magnetite-ilmenite.

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