The resources of binocular perception.
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Depth Perception↗
Biomedical subjects
J Ross
Publications and source records attributed to J Ross.
Alterations in head shape of newborn infants after caesarean section or vaginal delivery.
Alterations of head shape in preterm, small-for-dates, and term normal infants were studied by measuring occipitofrontal circumference (OFC), biparietal diameter (BPD), and occipitofrontal diameter (OFD) at intervals after birth. In 9 preterm infants born by elective caesarean section ther was a 5-2% reduction in BPD and 2-0% reduction in OFC at the age of 7 days. In 18 term infants born by elective caesarean section these changes were 2-4% and 0% respectively in BPD and OFC. In 25 preterm infants born by vertex vaginal delivery there was a significant fall in OFC of 0-7% at the age of 7 days and of 2-4% in BPD, but no significant change in OFD. In 19 small-for-dates infants born vaginally OFC increased 1-0% and OFD 2-7% at 7 days, but BPD decreased 2-5%. After the first week all three measurements increased in both groups of vaginal deliveries. The results show that shrinkage and biparietal flattening of the skull occur during the first week of life in preterm and term infants born by caesarean section and in preterm infants born vaginally. This fact should be borne in mind when comparing the measurements of an infant's head size with published norms.
Cephalometry↗
Regional Myocardial function in the conscious dog during acute coronary occlusion and responses to morphine, propranolol, nitroglycerin, and lidocaine.
Regional myocardial function following occlusions of the circumflex coronary artery was studied in unanesthetized dogs using minature ultrasonic crystal pairs implanted subendocardially within the left ventricle for measurement of control, marginal, and ischemic lengths. As early as five beats after coronary occlusion, reduced function was apparent in ischemic zones, and an increase in heart rate occurred (78 to 115 beats/min) at an average of 25 sec. In the control zones, shortening initially increased from a constant end-diastolic length, but later end-diastolic length also increased by 7.5%. Shortening in the marginal zones was reduced by 50% at 90 sec as holosystolic expansion developed in the ischemic zones. On reperfusion, systolic function returned to normal within a few minutes while protodiastolic abnormalities persisted for up to 45 min. With coronary occlusions longer than two minutes most dogs exhibited arousal and further tachycardia; this reaction was prevented by morphine. During two minute occlusions morphine also decreased the heart rate increase by 37%, and marginal segment shortening was improved by 40%. Prior administration of propranolol also decreased heart rate during coronary occlusion and produced similar improvement in marginal segment function; however, in contrast to morphine, there was depression of contraction in the control segments. Nitroglycerin given during coronary occlusion caused decreases in end-diastolic length of all segments and increased shortening in the marginal segment by 28%. Lidocaine administered during coronary occlusion produced a mild depression of myocardial function in all regions of the heart.
Animals↗
Adaptations of the left ventricle to chronic pressure overload.
Left ventricular (LV) function during the adaptation to chronic pressure overload produced by an ascending aortic constriction was analyzed in conscious dogs, instrumented with intraventricular micromanometers and pairs of ultrasonic crystals for measurement of LV wall thickness (WTh) and internal LV chamber diameter. During inflation of the cuff to produce LV pressures averaging 220 mg Hg, calculated peak wall stress (WSt) increased by 55% above control while percent shortening decreased by 24% and mean circumferential shortening velocity (VCF) decreased by 39% from control. By 9 days (mean) after aortic constriction, the cross-sectional area (CSA) of the LV wall increased by 10% and peak WSt fell to 37% above control. End-diastolic diameter (EDD) increased to 4% above control, while percent shortening and mean VCF remained reduced at -12% and -20% of control, respectively. During the phase of concentric hypertrophy (mean 2 1/2 weeks), CSA increased further to 15% above control and WSt fell to 22% above control, while EDD and percent shortening returned to control and mean VCF increased to -7% of control (not significant). At 24 hours after release of the cuff WSt, percent shortening, mean VCF, and peak velocity of LV pressure rise (peak dP/dt) were not significantly different from control. Rapid, partial regression of hypertrophy was observed in some dogs. Thus, the left ventricle responds to chronically elevated pressure by initial dilation with increased WSt followed by gradual wall thickening and consequent reduction of WSt to near normal. After successful adaptation to the pressure overload, hypertrophy per se did not produce intrinsic depression of the myocardial inotropic state.
Animals↗
The role of cyclic adenosine 3', 5'-monophosphate and calcium in the regulation of contractility and glycogen phosphorylase activity in guinea pig papillary muscle.
We studied the relationships between the positive inotropic effects of isoproterenol, increased frequency of contraction or paired electrical stimulation, and cyclic AMP concentration and phosphorylase activity in isolated guinea pig papillary muscles. The minimum concentration of isoproterenol (10 nM) that augmented isometric force development increased cyclic AMP concentration. However 100 nM isoproterenol was required to increase the phosphorylase activity ratio (-AMP/+AMP) from 0.15 +/- 0.03 to 0.25 +/- 0.03. After addition of 1 muM isoproterenol to the bath, cyclic AMP increased within 0.5 minute from 0.58 +/- 0.03 to 1.04 +/- 0.13 mol/kg (wet weight), peak contractile force was elevated 2-fold at 1 minute, and the phosphorylase activity ratio rose to 0.40 +/- 0.02 in 4 minutes. Although an increase in contraction frequency (6/min to 36/ min) and paired stimulation produced more than a 3-fold increase in peak contractile force, there were no changes in cyclic AMP and phosphorylase activity. The cyclic AMP concentration during diastole was 0.60 +/- 0.04 and in midsystole, 0.55 +/- 0.03 mumol/kg. Anoxia increased the phosphorylase activity ratio from 0.19 +/-0.02 to 0.41 +/- 0.04 without elevation of cyclic AMP concentration. Removal of Ca2+ from the bathing medium prevented active force development and the anoxic increase in phosphorylase activity, but did not prevent the isoproterenol-induced increase in cyclic AMP and phosphorylase. These results suggest that cyclic AMP is a factor in the catecholamine-induced enhancement of inotropic state. However, it does not appear to play a role in the maintained augmentation of inotropic state produced by increased contraction frequency and paired stimulation, nor does the concentration of the cycle nucleotide appear to vary during the contraction cycle or during anoxia. Extracellular Ca2+ is required for contraction, the positive inotropic aciton of catecholamines and phosphorylase b to a conversion by anoxia.
Animals↗
The concept of afterload mismatch and its implications in the clinical assessment of cardiac contractility.
The characteristics of left ventricular ejection (velocity and extent of wall shortening) can be analysed in relation to the appropriateness of the matching between afterload and the level of inotropic state (contractility), as modified by the preload (Frank-Starling) reserve. In the normal left ventricle if the preload is not allowed to compensate for an acute increase in afterload, or if the limit of preload reserve is reached, velocity (V CF) and stroke volume will diminish; that is an afterload mismatch occurs. This acute mismatch can be corrected by administration of a positive inotropic agent. In normal conscious animals and in man the ejection phase measures in the basal state (such as ejection fraction, and VCF corrected for heart size) encompass a relatively narrow range, and when the normal heart adapts successfully to a chronic pressure or volume overload such measures remain normal per unit of muscle. These findings provide the basis for their use in detecting a depressed basal level of inotropic state, even in the presence of certain valvular lesions. When there is mild depression of the basal inotropic state, enhanced preload and dilatation can allow full compensation of VCF, but acute pressure loading can allow detection of the the reduced preload reserve by inducing a substantial fall in stroke volume and VCF. When the basal inotropic state is greatly reduced, a mismatch between afterload and contractility, expressed as reduced VCF or ejection function, will become evident in the basal state even if the afterload is normal. Any increase in aortic pressure will then cause a sharp reduction in stroke volume or VCF. Also, under these circumstances therapeutic afterload reduction with agents such as nitroprusside can increase velocity and extent of wall shortening, and the cardiac output, providing the preload is maintained. The concept of afterload mismatch with limited preload reserve provides a framework for understanding the behavior of the normal or depressed ventrile and how it can operate on a "descending limb" of function. It helps to explain why measures of the ejecting phase (which are sensitive to afterload) appear to be more reliable than isovolumic phase indices (which are relatively insensitive to afterload) for detecting depressed basal inotropic state. Finally, the concept allows for interpretation of the responses observed in the clinical setting to acute and chronic increases and decreases in loading conditions on the left ventricle.
Animals↗
Editorial: Beta adrenergic blockade for prophylaxis against recurrent myocardial infarction and sudden death.
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Adrenergic beta-Antagonists↗
Analysis of regional myocardial function, dimensions, and wall thickness in the characterization of myocardial ischemia and infarction.
Disorders of contractile function constitute one of the earliest events to follow acute coronary occlusion, and occur in the central ischemic region within approximately 10 seconds. Measurements of regional myocardial dimensions and function in the central, border, and normal zones around an area of ischemia allow assessment of such changes, and when these disorders are persistent after permanent coronary occlusion they may offer an indirect means for assessing the severity and extent of myocardial ischemia and infarction. Recent experimental studies that used pairs of miniature ultrasonic crystals implanted within the subendocardium of open-chested and chronically instrumented, unanesthetized dogs indicate that functional function may be studied simultaneously in these regions; a holosystolic bulge rapidly develops in the central zone of ischemia while hypokinesis is apparent in marginal zones bordering the central region. It has been shown that function in the marginal zone reflects the balance between oxygen supply and demand and may be favorably or unfavorably influenced by acute therapeutic interventions. This finding suggests that the extent of an ischemic region may be altered by such therapy.Our studies further indicate that regional changes in dynamic wall thickness closely parallel the characteristics of shortening of nearby subendocardial segments, indicating that measurement of wall thickness alone may be useful for characterizing regional function. Studies in chronically instrumented animals also have established that the miniature crystals are useful for measuring regional dimensions and function over prolonged periods of time; for example, reduction in end-diastolic dimensions that reflex tissue loss over a 3- to 4-week period after coronary occlusion is substantially greater in the central ischemic regions than in the marginal zones. It is proposed that persistent changes in myocardial function and progressive alterations changes in dimensions over time offer indirect measures of the extent and severity of ischemic damage and infarction. With the development of improved echocardiographic or other clinically applible methods, such measurements may be a useful tool for assessing the effects of therapy on myocardial infarct size.
Acute Disease↗
Preload, afterload, and the role of afterload mismatch in the descending limb of cardiac function.
Ventricular function can be analyzed from measures of the ejecting phase of contraction (e.g. velocity and extent of wall shortening) in terms of the appropriateness of the matching between afterload and the level of inotropic state, as modulated by the preload. In the normal heart, under controlled conditions an afterload mismatch can be readily induced if the preload is not allowed to compensate for an increased afterload, or if the limit of the Frank--Starling reserve has been reached. In the conscious animal and in man, measures such as the mean velocity of fiber shortening (VCF, corrected for heart size) are relatively constant in the basal state, and when the normal left ventricle adapts successfully over several weeks to sustained experimental volume or pressure overload, the ejection phase measures remain normal per unit of muscle. However, if the inotropic state is considerably reduced, a mismatch between afterload and contractility (reduced VCF) will be evident in the basal state even when the afterload is normal. Failure to maintain normal ejection indices under conditions of acute or chronic mechanical overload can be explained in terms of an excessive afterload relative to the degree of hypertrophy, the level of inotropic state, and the Frank--Starling rereserve. The concept of afterload mismatch is illustrated by experimental data and used as a basis for characterizing responses to afterload changes in the clinical setting.
Animals↗
Electorcardiographic ST-segment analysis in the characterization of myocardial ischemia and infarction.
The ST segments of the electrocardiogram (ECG) become elevated within 20 to 30 seconds after the onset of acute coronary occlusion and, when persistent, such changes offer a possible indirect marker of the extent and severity of myocardial ischemic injury and of eventual cell death. When ST-segment elevation on the epicardial ECG is measured 15 minutes after an acute coronary occlusion in the dog, a general correlation exists with biochemical changes, regional myocardial blood flow, and myocardial electrolyte alterations measured at 15 minutes, although when an effort is made to correlate the degree of such alterations with the magnitude of the ST-segment change there is considerable scatter. On the other hand, when the ST-segment elevation at 15 minutes is correlated with myocardial blood flow, histologic changes, and creating phosphokinase (CPK) depletion 24 hours later, the correlation is good. Possible mechanisms underlying ST-segment elevation are discussed, and data are reviewed which indicate that the epicardial ECG my be relatively insentive to subendocardial injury; in the experimental setting this problem may be partially corrected by the use of intramyocardial ECG leads. The extension of direct epicardial ECG maps to precordial ST-segment mapping poses additional problems that include reduced sensitively, problems due to reciprocal changes in the ECG at the body surface, surface contact of the electrodes, pericarditis, and individual variability in the rate of spontaneous regression of ST-segment changes. Such mapping appears reliable only for infarctions of the anterior and lacteral wall. Further research is necessary on analysis of the QRS complex, and use of vector leads. Despite these problems experimental and clinical studies indicate that precordial electrocardiographic analysis may be useful for detecting acute changes in the severity of ischemic injury over relatively short periods of time (2 to 4 hours). This indirect measure clearly will require correlation with specific markers of ischemic damage, but with further improvements it seems likely that analysis of serial ECG changes will evolve into a valuable and reliable nonivasive clinical tool for characterizing myocardial ischemia and infarction.
Adenosine Triphosphate↗
Series elasticity in the intact heart. Evidence for the application of the Hill model for muscle to the intact left ventricle.
Several recent studies have shown that the contractile state of the intact heart may be described by the instantaneous relationships between contractile element velocity, length and stress. However, there is little direct evidence that the intact heart can be described by a model containing at least a contractile element and a series elastic component (SEC). In isolated muscle the series elastic component can be analyzed by determining the length changes following quick releases to known loads during contraction. The characteristics of the effective SEC of the intact left ventricle (LV) were determined by a quick release method in 8 dogs in which the left ventricle contracted isovolumically against a balloon inserted via the mitral annulus. During active contraction, sequential withdrawals of 0.5 to 7.0 ml of fluid were performed rapidly (5-18 msec) by an electrically-timed, springloaded syringe. From these releases the calculated maximum extension of the SEC averaged 4.03 +/- 0.27% of LV circumference at LV pressures averaging 79/6 mmHg (systolic/end-diastolic; range 66-107/0-15 mmHg.) The reductions of the left ventricular midwall circumference were plotted against the corresponding changes in mean wall stress. The load extension curve determined in this manner was unchanged by varying the time of release and by norepinephrine infusion. These data support a model for the intact LV that contains an undamped SEC, the characteristics of which resemble those of isolated cardiac muscle.
Animals↗
Effects of changes in preload, afterload and inotropic state on ejection and isovolumic phase measures of contractility in the conscious dog.
Despite much investigation, the usefulness of various indexes employed clinically for detecting alterations in ventricular contractility in the intact circulation remains controversial. The effects of acute preload, afterload and contractility changes on both ejection and isovolumic phase measures of left ventricular function were analyzed in normal, trained conscious dogs instrumented with micromanometers and endocardial ultrasonic diameter gauges. Rapid volume overload increased the excursion of the left ventricular diameter (delta LVD) by 7 percent above the control level, but mean velocity of circumferential shortening (VCF) did not change significantly; peak rate of left ventricular pressure rise (dP/dt) increased by 11 percent and (dP/dt)/DP40 (DP = developed pressure) was augmented by 10 percent, but maximal [(dP/dt)/LVP], or "Vpm," decreased by 20 percent. Pressure overload by phenylephrine infusion decreased delta LVD by 15 percent and mean VCF fell by 26 percent; peak dP/dt and (dP/dt)/DP40 remained unaltered, but VPM was reduced by 37 percent. Isoproterenol augmented peak dP/dt by 55 percent, and (dP/dt)/DP40, Vpm and mean VCF were increased comparably. Propranolol decreased these measures equally by about 16 percent. Therefore, in the conscious animal in the steady state, isovolumic phase indexes were mildly influenced by acute volume loading, wheras ejection phase indexes were not. Acute increases in aortic pressure markedly reduced ejection phase measures, whereas the isovolumic indexes were unaffected. All of the indexes studied were comparably sensitive to acute alterations in contractility, but we conclude that no single measure can always be used for defining an acute contractility change in the intact circulation.
Animals↗
Primary aldosteronism. A study in contrasts.
Two patient with primary aldosteronism, one with a solitary adrenal adenoma and the other with bilateral nodular hyperplasia, are described. Both patients showed the classic features of primary aldosteronism in electrolyte and hormone patterns, but there were important differences in the biochemistry of their excised adrenal tissue. In addition, the injection of plasma from the patient with bilateral adrenal hyperplasia into the sheep's transplanted adrenal gland elicited a definite aldosterone secretory response, but there was no aldosterone response to the injection of plasma from the patient with a solitary adrenal adenoma. The findings support the hypothesis that an extra-adrenal stimulus may contribute to the pathogenesis of bilateral adrenal hyperplasia.
Adenoma↗
Cylindrical organelles associated with microtubules during sperm elongation in a mealybug.
Spermiogenesis in the mealybug Pseudococcus obscurus involves the elongation of a cytoplasmic papilla from the surface of a spermatid. Longitudinally oriented fibers and microtubules, with diameters of 250 A and a non-9+2 arrangement, are associated with this process. Fibers alone are found in early stages of papilla emergence and in the basal region of the elongated papilla. They appear to be continuous with the microtubules in the more distal region of an elongated papilla. Disk-shaped, circular, and rectangular profiles are associated with the basal ends of the fibers. Probably the fibers are microtubular "anlagen" and the associated structures may be microtubular "organizing centers".
Animals↗
Letter: The Pulfrich effect and short-term memory in stereopsis.
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Depth Perception↗
The ultrastructure of mouse neuroblastoma cells in tissue culture.
Neuroblastoma cells grown in suspension culture are round and have no distinctive structural characteristics. However, cells transferred to substrates flatten, develop long neurites, and assume the morphology of normal neurons. The resemblance of monolayered neuroblastoma cells to normal neurons is amplified by treatment with hypertonic medium; under these conditions, cell division is inhibited and the neurites become long and differentiated. The treated cells contain clusters of clear vesicles, 400-600 A in diameter, which are morphologically indistinguishable from the synaptic vesicles of normal neurons. Specialized cell contacts are observed between the treated cells as well as between confluent cells grown in normal medium.
Animals↗
Lack of detectable change in cyclic AMP during the cardiac inotropic response to isoproterenol immobilized on glass beads.
Changes in contractility and the levels of adenosine 3':5'-cyclic monophosphoric acid (cAMP) were assessed in isolated cat cardiac muscle in response to soluble isoproterenol and isoproterenol immobilized on glass beads. Drug-induced positive inotropic responses were compared to the maximum isometric force achieved with paired electrical stimulation, a potent physiological inotropic stimulus. Isoproterenol (1 muM) in solution increased the force of contraction 0.832 plus or minus 0.165 g at 60 sec in eight muscles tested, which at 60 and 120 sec averaged 65.5 plus or minus 6.5% and 82.9 plus or minus 8.8%, respectively, of the force with paired electrical stimulation. Isoproterenol immobilized on glass beads gave positive inotropic responses similar to those for the soluble form of the drug. Placement of only three isoproterenol-glass beads on the muscles increased the force of contraction 0.742 plus or minus 0.166 g at 60 sec (n equals 11), which at 60 and 120 sec averaged 45.1 plus or minus 7.0% and 58.6 plus or minus 6.4%, respectively, of the force with paired electrical stimulation. The magnitude of this response indicates that the increased force was developed by at least 60% of the cells in each muscle. Control levels of cAMP were 0.527 plus or minus 0.049 pmol/mg of tissue wet weight, n equals 11. cAMP levels 60 sec after 1 muM soluble isoproterenol was added were 1.212 plus or minus 0.085 pmol/mg; in contrast, the levels of cAMP in response to isoproterenol immobilized on glass beads at 60 sec were 0.490 plus or minus 0.060 pmol/mg, not significantly different from control levels. These data indicate that cAMP may not be involved in the propagation of the inotropic response that must have occurred in these cardiac muscles and raise questions as to the physiological significance of the large cAMP increases that occur in response to soluble drugs and hormones.
Animals↗
Systolic pressure--diameter relations in the normal conscious dog.
Pressure--diameter loops were generated in normal, conscious dogs during left ventricular contraction by means of endocardial ultrasonic gauges and micromanometers. Studies were made in the control state, during volume and pressure loading, and during enhancement of contractility. The diameter at the end of ejection was linearly related to systolic pressure, and the pressure--diameter relation at end-ejection was not affected by changes in preload. However, this relation was substantially displaced by changes in inotropic state, suggesting that the instantaneous pressure--length plane produced by pressure loading is unique to a given level of contractility.
Animals↗