Increase In Segment Length Research Articles

The contraction of stunned myocardium: isovolumetric bulging and wasted ejection shortening in dog heart.

The aim of the study was to assess the contraction of myocardium stunned by repetitive brief coronary occlusions by examining the response to alterations in loading and inotropy of systolic contraction on isovolumetric and ejection phase shortening. Fourteen open chest anaesthetised dogs were used for the studies. After destruction of the sinus node, the heart was atrially paced and atrial extrasystoles were introduced followed by a short (400 ms) or long (700 ms) postextrasystole. The left anterior descending coronary artery was occluded for 5 min and reperfused for 10 min a total of eight times to produce stunned myocardium, followed by a final 60 min of reflow. Regional function was assessed with segment length sonomicrometers. With successive periods of occlusion there was an increase in the end diastolic segment length and a progressive decrease in total percent systolic shortening (baseline 22.3%, 1st reflow 14.5%, 8th reflow 7.9%) with some recovery after 60 min of reflow (12.0%). This was predominantly due to the development of bulging during isovolumetric systole (4.5%, -4.9%, and -8.3%, respectively) which diminished during 60 min recovery to -3.1%. Ejection shortening was relatively constant (17.8%, 19.4%, 16.3%, and 15.1%, respectively). Postextrasystolic potentiation resulted in an increased in total percent systolic shortening, but not to the baseline value, as slight isovolumetric bulging persisted. Similar changes were seen with the short and long postextrasystoles although the latter had a greater increase in ejection shortening. The decrease in function after repetitive occlusion and reflow is predominantly due to bulging during isovolumetric systole which persists after postextrasystolic potentiation in our model of stunned myocardium.

Effects of early captopril administration on infarct expansion, left ventricular remodeling and exercise capacity after acute myocardial infarction

In a double-blind study, 99 patients (82 men, age range 40 to 75 years) with acute myocardial infarction (AMI) were randomly assigned to receive captopril or placebo. Treatment began within 24 hours of admission. Serial echocardiographic measurements of endocardial segment lengths and left ventricular (LV) volumes, and ejection fractions were obtained. The 2 groups were matched at baseline except for an excess of previous AMI in the placebo group (13 of 50 vs 2 of 49 patients, p = 0.002). The increase in anterior segment length, from baseline to 2 months, was significantly less in the captopril than in the placebo group (2.8 ± 1.6 vs 10.4 ± 2.4mm, 95% confidence interval [CI] −13.5 to −1.7, p = 0.01). The increase in posterior segment length was also less in the captopril group, but the difference was not significant (3.2 ± 1.2 vs 7.0 ± 1.8mm, 95% CI −8.0 to 0.5, p = 0.08). Fewer patients in the captopril group demonstrated increases in segment length >2 standard deviations of the measurement error (14 of 70 [20%] vs 29 of 72 [40%] patients, p = 0.009). In patients with anterior AMI, the infarct-containing anterior segment length increased by 4.5 ± 2.3 mm in the captopril versus 12.4 ± 3.1 mm in the placebo group (95% CI −15.7 to −0.2, p = 0.046), and fewer patients in the captopril group demonstrated infarct expansion (6 of 20 [30%] vs 13 of 21 [62%] patients, p = 0.04). In patients with inferoposterior AMI, the infarct-containing posterior segment length increased by 3.1 ± 1.6 mm in the captopril versus 9.8 ± 2.4 mm in the placebo group (95% CI −13.3 to −0.1, p = 0.046). No significant treatment effects were seen in LV volumes or maximal exercise performance. This study suggests that early treatment with captopril after AMI can attenuate infarct expansion and favorably influence early LV remodeling.

Permeation of CO2 through polyurethane

AbstractThe permeability of CO2 through polyurethane was investigated. It is found that the permeability increases with the decrease of hard segment content and the increase of soft segment length; however, no change of activation energy is involved. The permeability increases with the elevation of annealing temperature. The temperature dependence of permeability observes the Arrhenius equation at temperatures below 60–80°C, but it deviates at temperatures above this range. This deviation would be attributed to the increase of mixing of hard and soft segments as a result of the dissociation of short‐range order in hard segment domains.

Pericardial closure decreases right ventricular load tolerance in the dog

Previous studies using graded pulmonary artery (PA) occlusions were unable to determine whether the Frank-Starling relationship contributed significantly to right ventricle (RV) afterload tolerance. Hence, we wished to determine whether limitation of RV filling could decrease RV load tolerance. Anesthetized mongrel dogs were instrumented for the measurement of mean aortic pressure, pulmonary arterial flow, RV systolic (Ps) and diastolic (Pd) pressures, and myocardial segment length of the RV inflow (INF) and outflow (OUT) tracts. Filling of RV was limited by pericardial closure (PC). Before and after PC we performed graded occlusions of the PA to the point of cardiocirculatory failure (F). The magnitude of RV after load that could be tolerated without F was called the highest load tolerable (HLT). At HLT, with the pericardium open (PO), PA circumference had decreased by 33.9% ± 9.5%, and there were increases in Ps (from 28.3 ± 6.6 to 57.2 ± 17.7 torr, P < .001), Pd (from 4.4 ± 1.9 to 6.1 ± 1.5 torr, P < .01), and diastolic regional myocardial segment lengths (10.4 ± 4.2 to 11.6 ± 4.5 mm for INF, 10.4 ± 0.9 to 11.5 ± 0.5 mm for OUT; P < .05). Compared to PO, with PC, RV load tolerance decreased in that PA circumference could be decreased by only 26.2% ± 15.7% ( P < .05), and Ps increased to only 48.4 ± 22.5 torr ( P < .05). With PC, there was a significant decrease in end-diastolic fiber length for OUT, but not for INF. Further, with PC, at HLT, INF enddiastolic segment length increased (to 11.2 ± 3.3 mm) but, unlike with PO, there was no significant increase in OUT. However, for INF as well as for OUT, maximum diastolic length was significantly less with PC than with PO. By empirically fitting pressure-segment length curves to an exponential equation, we obtained an index of regional stiffness. Following PC, this was unchanged for the INF, but had increased significantly for the OUT. We conclude (1) the Frank-Starling relationship contributes to the capacity of the RV to tolerate increased afterload; and (2) the effects of pericardial closure on regional stiffness are nonhomogeneous, the outflow tract being more constrained than the inflow tract.

Reversal of dyskinesis by increased end diastolic segment length in ischaemic-reperfused myocardium.

Persistent dyskinesis is universally observed after reperfusion of a severely ischaemic segment. Although inotropic stimulation shows a latent contractile reserve, it is not known whether this reserve can be recruited by increasing end diastolic segment length (local length-tension relation). To investigate this, six anaesthetised open chest dogs were placed on right heart bypass to increase end diastolic segment length independently of mean arterial pressure. Instantaneous left ventricular pressure-segment length relations and fractional systolic shortening were determined by sonomicrometry in the centre of the region perfused by the left anterior descending coronary artery during sequential increases in end diastolic segment length. Measurements were made before occlusion of the left anterior descending coronary artery, during 1 h of occlusion, and after 2 h of reperfusion. Before ischaemia, segmental shortening increased from 11.0(SEM 1.6)% to 23.5(1.5)% (p less than 0.05) as end diastolic segment length increased. Dyskinesis developed during occlusion of the left anterior descending coronary artery [12.1(2.6)% control v -7.2(1.6)% occlusion, p less than 0.05] and was present over the entire range of end diastolic segment lengths. Following reperfusion, segmental dyskinesis [-2.5(2.4)%] persisted at the lower end of the range of end diastolic segment length, but was progressively replaced by active shortening, averaging 7.3(3.2)% (p less than 0.05) as end diastolic segment length was sequentially increased. We conclude that segmental function following reperfusion is sensitive to changes in end diastolic segment length, and that active shortening is recruited from an apparently dyskinetic segment as end diastolic segment length progressively increases.

Influence of heart rate, preload, afterload, and inotropic state on myocardial ultrasonic backscatter.

Ultrasonic backscatter is substantially modified by pathologic changes in myocardium. Influence of physiologic changes in heart rate, mean arterial pressure, preload, and inotropic state were studied in 17 anesthetized open-chest dogs. Heart rate was changed with atrial pacing/ULFS'49 (a selective bradycardiac agent). Mean arterial pressure was varied with aortic constriction/nitroprusside, preload was altered with nitroglycerin/volume infusion, and inotropic states were altered with dobutamine (10 microns/kg)/esmolol (100 microns/kg). IBR5, an optimum weighted frequency average (4 to 6.8 MHz) of the squared envelope of diffraction corrected for absolute backscatter, and the Fourier coefficient of amplitude modulation (FAM), an index of cardiac cycle-dependent variation, were measured from six sequential electrocardiographically gated intervals throughout the cardiac cycle. Heart rate, mean arterial pressure, preload, and inotropic state did not significantly affect IBR5. FAM increased from 3.5 +/- 0.3 dB (mean +/- SEM) to 7.0 +/- 0.4 dB (p less than .01) at a heart rate of 120 beats/min, and decreased to 3.9 +/- 0.4 at a heart rate of 160 beats/min. No change in FAM was noted with a rise (70 +/- 12 to 45 +/- 10 mmHg) in mean arterial pressure or preload (an increase or decrease in diastolic segment length of +/- 10% from the baseline). Dobutamine produced a significant increase in left ventricular dP/dt (2600 +/- 200 to 3475 +/- 275 mm Hg) and FAM (3.4 +/- 0.1 to 6.4; p less than .01). Esmolol significantly reduced left ventricular dP/dt (2600 +/- 200 to 2000 +/- 175 mm Hg, p less than .05) and FAM (3.4 +/- 0.01 to 6.4 +/- 0.1; p less than .01). We conclude that IBR5 is independent of heart rate, mean arterial pressure, preload, and inotropic state. Cardiac cycle-dependent amplitude modulation follows changes in cardiac contraction.

Characterization of nonischemic segment shortening during variable extent of myocardial ischemia in conscious dogs.

Studies were performed on seven conscious dogs chronically instrumented for measurement of subendocardial segment length in the central area perfused by the left circumflex coronary artery (LCCA) and left anterior descending coronary artery, LCCA flow, and left ventricular pressure. We occluded the LCCA for 2 min using an externally inflatable pneumatic occluder placed around the proximal LCCA. Two-minute LCCA occlusions were repeated hourly for 8 h, 5 days/week. The first LCCA occlusion decreased the ejection phase shortening in the ischemic area from 22.2% +/- 2.5% (SEM) to 3.1% +/- 0.7% (P less than 0.001). Concomitantly, heart rate increased from a resting rate of 76 +/- 4 to 117 +/- 6 beats/min (P less than 0.001) after 2 min of LCCA occlusion, and ejection phase shortening in the nonischemic area decreased from 25.5% +/- 1.3% to 21.6% +/- 1.1% (P less than 0.001) despite increases in end-diastolic segment length (15.31 +/- 1.46 mm to 15.69 +/- 1.52 mm, P less than 0.01). These changes in non-ischemic segment shortening and heart rate during LCCA occlusion were attenuated progressively with improvement tin the regional myocardial function at jeopardy due to the development of collateral circulation, and a significant (P less than 0.001) correlation between both the reduced nonischemic segment shortening and the increased heart rate with the degree of dysfunction in the ischemic region was obtained by linear regression analysis with Fisher's Z transformation.

Effects of myocardial ischemia on regional function and stiffness in conscious dogs.

The extent to which cardiac nerves influence responses of regional ventricular function to acute myocardial ischemia was investigated in conscious dogs with intact cardiac innervation (N) and dogs with chronic cardiac denervation (D). Following coronary artery occlusion (CAO) left ventricular (LV) end-diastolic pressure increased more (P less than 0.01) in D (18 +/- 3.2 mmHg) than in N dogs (3.4 +/- 0.7 mmHg), whereas heart rate increased more in N (32 +/- 4.8 beats/min) than in D dogs (16 +/- 3.0 beats/min). In nonischemic zones of D dogs there were greater increases, P less than 0.05, in end-diastolic segment length, systolic segment shortening, and velocity of shortening than in N dogs. In ischemic zones, significantly greater increases in end-diastolic segment length were also observed in the D group, but similar reductions in segmental shortening occurred in both N (-116 +/- 2.8%) and D (-108 +/- 5.2%) dogs. The time constant of isovolumic relaxation was not different in the two groups. However, in ischemic zones of N dogs myocardial stiffness constant (k) increased by 109 +/- 24 from 33 +/- 4.9 and end-diastolic stiffness (Eed) rose by 1527 +/- 310 from 253 +/- 34 mmHg, whereas k increased significantly less (P less than 0.05) in D dogs. Eed of ischemic zones also rose significantly less (P less than 0.05) in D dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Axonal tubulin and microtubules: morphologic evidence for stable regions on axonal microtubules.

Biochemical studies indicate that axonal tubulin is composed of at least two distinct pools that differ in cold solubility and biochemical composition [Brady et al: J. Cell Biol. 99:1716-1724]. To determine the morphologic correlate of cold-insoluble tubulin, segments of rat optic nerves were exposed to a series of in vitro experimental conditions that affect microtubules (MTs), including cold, podophyllotoxin (PT), triflupromazine (TFP), and taxol, and then examined by electron microscopy. Longitudinal sections of control axons showed MTs oriented parallel to the long axis of the axons. Axons exposed to cold, PT, and TFP showed short segments of MTs in association with cytoskeletal disarray. Morphometric studies were used to distinguish between a simple malorientation of MTs (undulation or zigzags in their course) and the loss of labile segments of MTs, leaving the stable portions behind. The lengths of MT segments were measured in longitudinal sections, and the numbers of MTs were determined in the cross sections. All MT segment-length histograms showed a unimodal distribution. Cold and PT produced a simple shift of the control histogram to the shorter length MTs. In cross sections the numbers of MTs in cold- and PT-exposed axons were significantly decreased, indicating that the presence of short segments of MTs in the longitudinal plane of sections was due to a loss of portions of MTs. Taxol, an agent that promotes MT assembly, reversed the cold effect partially and resulted in increases in both MT segment length and number. These studies indicate that stable MT segments are portions of longer MTs containing both stable and labile regions. Furthermore, these findings are consistent with the hypothesis that cold-insoluble tubulin functions as a transportable MT-organizing complex in the axon.

Effects of verapamil on regional myocardial diastolic function in pacing-induced ischemia in dogs.

The upward shift in the left ventricular diastolic pressure-volume relationship during pacing-induced angina may be related to increased cytosolic calcium availability with persistent contractile element interaction in diastole. To assess the influence of calcium channel blockade on these changes in diastolic function, we studied the effects of verapamil in dogs with 90% stenoses of the left anterior descending and circumflex coronary arteries. Ultrasonic crystals were implanted in the myocardium to monitor anterior wall and lateral wall segment length. Left ventricular pressure was measured with a micromanometer catheter. The left atrium was paced at a rate 1.5 times that of the resting heart rate for 3 min. An upward shift of the left ventricular diastolic pressure-segment length relationship developed after pacing tachycardia, with a rise in the left ventricular end-diastolic pressure (LVEDP) from 4.7 +/- 1.2 to 14.3 +/- 2.2 mmHg (P less than 0.01, n = 13), and pressure was higher at any segment length throughout diastole. Increases in end-diastolic segment length were small (12.3 +/- 1.9 to 12.7 +/- 2.0 mm for the anterior wall, P less than 0.05; 15.1 +/- 1.4 to 16.4 +/- 1.5 mm for the lateral wall, P less than 0.01). Pretreatment with verapamil (0.08 mg/kg iv) did not reduce this upward shift: LVEDP rose from 6 +/- 1 to 16 +/- 1 mmHg (P less than 0.01, n = 7) and there were similar small increases in end-diastolic segment length.(ABSTRACT TRUNCATED AT 250 WORDS)

Results of a randomized prospective trial of intraaortic balloon counterpulsation and intravenous nitroglycerin in patients with acute myocardial infarction

A randomized prospective clinical trial compared combined treatment with intraaortic balloon pumping and intravenous nitroglycerin for 4 to 5 days with routine clinical management in 20 patients with extensive myocardium at risk for infarction as evidenced by a thallium defect score of 7.0 units or greater. No significant differences in mortality or clinical outcome were observed between the 10 patients receiving the combined treatment and the 10 receiving routine management. In 14 patients two-dimensional echocardiograms obtained 6 to 24 hours after the onset of symptoms and at follow-up 6 to 16 days later (after completion of combined intraaortic balloon pumping plus nitroglycerin therapy) were analyzed to determine whether infarct segment or noninfarct segment lengths were affected by therapy. Among these 14 patients, 5 (3 receiving the combined therapy and 2 receiving routine management) demonstrated an increase in infarct segment length of greater than 1.0 cm. Mean infarct segment length increased 0.30 +/- 0.44 cm in patients receiving the combined therapy and 0.29 +/- 0.36 cm in patients on routine management (p = NS). In contrast, noninfarct segment length increased greater than 1.0 cm (mean increase 1.20 +/- 0.39) in five of seven patients on routine management but in none of 7 patients receiving intraaortic balloon pumping plus nitroglycerin therapy (mean decrease 0.22 +/- 0.20 cm) (p less than 0.05). No significant differences were noted in left ventricular ejection fraction, as measured by gated blood pool scintigraphy, or thallium perfusion defect score in a comparison of day 1 (pretreatment) with day 4 thallium or day 7 to 14 gated blood pool scintigrams. Thus, in patients with extensive myocardium at risk, it is unlikely that a reduction in mortality or a significant improvement in myocardial perfusion or ventricular function can be obtained by early intervention with intraaortic balloon pumping in combination with nitroglycerin. Although this combined therapy failed to prevent infarct segment lengthening (infarct expansion), the combined afterload-lowering effects of intraaortic balloon pumping and nitroglycerin did appear to prevent dilation or remodeling of noninfarcted segments during the first 2 weeks after acute myocardial infarction.

Different effects of two types of ischemia on myocardial systolic and diastolic function.

Acute increases in left ventricular (LV) diastolic pressure relative to volume occur during angina in humans and after pacing tachycardia in dogs with coronary stenoses. In this study we assessed myocardial function following pacing tachycardia in dogs with coronary stenoses and compared it with function of the same myocardial segment during coronary occlusion. Also we calculated regional wall stiffness following pacing tachycardia in dogs with coronary stenoses. In anesthetized dogs with two-vessel critical (90%) coronary stenoses, ultrasonic crystals were implanted subendocardially to measure either anterior wall (AW) and lateral wall (LW) segment lengths (SL; n = 14) or LV wall thickness (h; n = 7). LV pressure was measured using a high-fidelity micromanometer catheter. After pacing tachycardia in dogs with two-vessel coronary stenoses, there was a substantial rise in LV end-diastolic pressure (from 6 +/- 1 to 15 +/- 1 mmHg; P less than 0.001), a slight increase in end-diastolic segment length (AWEDSL from 15.6 +/- 1.0 to 16.4 +/- 1.0 mm; p less than 0.01; and LWEDSL from 13.8 +/- 1.4 to 14.3 +/- 1.4 mm; P greater than 0.01) and a reduction of percent systolic shortening of the ischemic segments. An upward shift of the diastolic pressure-SL relation was observed in the postpacing period. During coronary occlusion the diastolic pressure-SL relation of the same segment shifted rightward, or rightward and downward, and systolic shortening became holosystolic bulging. Ischemia due to coronary stenoses plus increased O2 demand had substantially different effects on regional wall motion and segmental diastolic mechanics than did ischemia due to coronary occlusion. Over the same range of residual transmural LV diastolic pressure, the radial stiffness modulus was higher after pacing tachycardia in the presence of coronary stenoses.

Effects of the acylcarnitine-transferase blocking agent sodium 2[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate (POCA) on metabolism and regional function in the underperfused canine myocardium.

We investigated the effects of sodium 2[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate (POCA) on regional myocardial function and metabolism in anesthetized, thoracotomized dogs subjected to a 53.5% reduction in flow through the circumflex branch of the left coronary artery (LCX). Regional function in the area supplied by the LCX and the left anterior descending coronary artery (LAD) was assessed by means of two pairs of subendocardially inserted ultrasonic transducers. Hemoglobin content, oxygen saturation, pH, PCO2, PO2, lactate, glucose, and free fatty acids were determined in arterial and local venous blood obtained from the area supplied by the LCX. POCA (20 mg/kg/20 min i.v.) induced a transient decrease in left ventricular power and cardiac output. Arterial free fatty acid (FFA) levels increased continuously throughout the experiment, whilst arterial glucose levels showed a continuous decrease. FFA uptake, lactate release, and oxygen uptake were reduced in the underperfused area by POCA. At the same time, POCA induced a transient increase in end-diastolic segment length and a sustained decrease in systolic shortening during the ejection phase in the underperfused area. No changes in regional function were observed in the area perfused by the nonconstricted LAD.

Segmental orientation studies of polyether polyurethane block copolymers with different hard segment lengths and distributions

The orientation behavior of two series of segmented polyether polyurethanes containing different hard segment length distributions has been studied as a function of the average hard segment length which was varied from one to five methylene bis (p-phenyl isocyanate) (MDI) units. The orientation behavior of the soft segments, isolated hard segments, and of hard segments aggregated in hard domains was determined from the dichroic behavior of representative infrared bands. As the hard segment length increases, a transition in orientation behavior is observed which corresponds to a change in sample morphology.

Left ventricular diastolic pressure-segment length relations and end-diastolic distensibility in dogs with coronary stenoses. An angina physiology model.

Isovolumic relaxation abnormalities have been noted in the ischemic left ventricle, but altered end-diastolic distensibility, as well as the role of right ventricular distention, is debated. Accordingly, left ventricular end-diastolic pressure and myocardial segment length were studied in the open-chest dogs with critical (90% diameter reduction) stenoses on both left anterior descending and circumflex coronary arteries. Regional segment length was measured with ultrasonic crystals placed subendocardially, and ischemia was induced by pacing tachycardia for 3 minutes. Transient vena caval occlusion was done to unload the right ventricle and to produce a series of left ventricular end-diastolic pressure and left ventricular end-diastolic segment length points before and after pacing tachycardia. After pacing tachycardia, left ventricular end-diastolic pressure (9.3 +/- 0.9 to 16.9 +/- 1.5 mm Hg, P less than 0.001) and time constant T of left ventricular isovolumic pressure decline (46 +/- 3 to 60 +/- 5 msec, P less than 0.01) increased, with an increase in left ventricular end-systolic segment length (9.8 +/- 0.3 to 10.5 +/- 0.3 mm, P less than 0.001), and a decrease in fractional shortening (17.6 +/- 1.7 to 14.5 +/- 1.3%, P less than 0.01) in the ischemic region, although right ventricular end-diastolic pressure was unchanged. With vena caval occlusion, right ventricular diastolic pressure fell promptly to near zero, followed by decrease in left ventricular pressure and segment length. In each dog, the left ventricular end-diastolic pressure-end-diastolic segment length relation shifted upward after pacing tachycardia. Pacing tachycardia was performed again in six dogs without stenoses. In this group, fractional shortening was preserved after pacing tachycardia (15.7 +/- 2.3 to 15.3 +/- 2.3%, NS), and left ventricular end-diastolic pressure (9.4 +/- 1.8 to 9.8 +/- 1.8 mm Hg, NS) was unchanged. The left ventricular end-diastolic pressure-segment length relation did not shift upward after pacing tachycardia. These data indicate that extrinsic compression of left ventricle by right ventricle is unlikely to be responsible for the upward shift in this model, and the upward shift in end-diastolic left ventricular pressure-segment length relations, as well as dynamic left ventricular diastolic pressure-segment length, supports the concept that persistent myosin-actin interaction throughout diastole plays an important role in the diastolic abnormalities in this angina physiology model.

Synthesis and characterization of MDI‐butanediol urethane model compounds

AbstractHard‐segment model compounds containing one to five 4,4′‐methylene bis(p‐phenylisocyanate) (MDI) units extended with 1,4‐butanediol (BD) were synthesized. The ends of the model compounds were reacted with ethanol. The melting point (Tm) of the model compounds increased with the number of MDI units to an extrapolated value of 299°C for the homopolymer using Flory's equation accounting for chain end defects. The ΔH of fusion was 5.3 kcal/mol. Intrinsic viscosity measurements in DMA solutions revealed a Mark Houwink exponent of 1.43 suggesting that the hard‐segment model compounds are rodlike in solution. Wide‐angle X‐ray diffraction showed that the percentage of hard‐segment crystallinity decreased as the oligomer length increased. Infrared spectroscopy studies showed that the distribution of hydrogen bond distances between CO and NH groups became broader with increasing segment length.

Late effects of acute infarct dilation on heart size: a two dimensional echocardiographic study

Dilation of the infarct zone (infarct expansion) has been shown to be a cause of regional left ventricular dilation within days of transmural anterior myocardial infarction. Whether this process stabilizes, continues or regresses thereafter, and whether uninfarcted myocardium is affected is unknown. To explore this, two to six (mean four) serial two dimensional echocardiographic studies were obtained over a 3 to 30 month period (mean 13) in 13 patients beginning 10 to 21 days after anterior transmural myocardial infarction. With use of the papillary muscles as internal left ventricular landmarks, anterior and posterior segmental dilation in each patient was assessed from the slope of the regression line of segment length versus time. Study patients were classified into those with (seven patients) and those without (six patients) infarct expansion. Infarct expansion was defined as an anterior segment length 10 to 21 days after infarction that exceeded the upper limit of normal determined from 13 age-and sex-matched normal control subjects. Ten to 21 days after infarction, the average anterior segment length in the seven patients with expansion was 65 percent greater than that in normal control subjects. The seven patients with infarct expansion showed significant and continuing dilation during long-term observation of both the infarcted anterior (p < 0.01) and the uninfarcted posterior (p < 0.05) segments. The average increase in anterior segment length was 1.1 cm (8 percent) and in posterior segment length 0.9 cm (19 percent). This represents an average increase in overall left ventricular circumference of 11 percent during the observation period. The six patients without infarct expansion showed no significant change in anterior or posterior segment length (mean ± standard error of the mean [SEM] −0.7 ± 0.3 and 0.2 ± 0.3 mm/mo, respectively). Six of the seven patients with infarct expansion were functionally limited by dyspnea or angina, or both; no patient without infarct expansion had functional cardiac limitation. Thus, infarct expansion occurring within 3 weeks of transmural myocardial infarction appears to be the main contributor to left ventricular dilation, and is associated with impaired functional status. Moreover, a significant increase in ventricular size due to infarct expansion appears to predict chronic progressive ventricular enlargement due to lengthening of both the infarcted zone and the uninfarcted segment.

Rhodopsin content and rod outer segment length in albino rat eyes: Modification by dark adaptation

Whole eye rhodopsin content and rod outer segment length have been determined in albino rat eyes after different periods of dark adaptation, dark-rearing or cyclic light maintenance. The rhodopsin content in the eyes of dark-reared albino rats is approximately 50% higher than that in the eyes of littermates reared in cyclic light (in-cage illumination less than 15 ft-cd). The same increase in rhodopsin can be obtained in albino rats after only a 10-day dark adaptation period. Furthermore, the increased level of rhodopsin is the same as that in the eyes of pigmented rats reared in cyclic light. The increase in rhodopsin content in the albino rat eyes is due at least in part to an increase in rod outer segment length. The increase in length with dark adaptation and dark-rearing was somewhat variable, with an average increase of approximately 25%. No apparent increase was found in rod outer segment diameter, rod outer segment disc packing density or eye size. Rod outer segment lengths were consistently longer in the superior hemisphere of the eye than in the inferior hemisphere in both dark-adapted albino rats and pigmented rats maintained in cyclic light, but not in albino rats maintained in cyclic light.

Quantitative effects of methylazoxymethanol acetate on purkinje cell dendritic growth

A quantitative analysis was made of alterations in the dendritic organisation of Purkinje cells in the cerebellum of the rat following the administration of the degranulating agent, methylazoxymethanol acetate (MAM). This drug depleted the granule cell population of the cerebellar cortex and disturbed Purkinje cell alignment such that a number of Purkinje cells became inverted and grew in the white matter. The quantitative changes that occurred in the dendritic trees of these cells (increase in segment length, decrease in segment numbers, trichotomy and branching probability) were similar to those seen following other degranulation procedures. The size of the Purkinje cell dendritic tree was found to be related to the number of parallel fibres present in the molecular layer. These results were discussed in relation to current theories of neuronal development and were shown to lend further support to the filopodial attachment hypothesis of dendritic growth.

Rod outer segments elongate in constant light: Darkness is required for normal shedding

Shedding of large rod outer segment fragments is greatly reduced when Rana pipiens are maintained under moderate levels of continuous light. This inhibition of shedding results in an increase in outer segment length, since disc addition continues even as shedding stops. Some shedding will occur when constant-light frogs are subjected to a brief period of darkness, suggesting that darkness alone may stimulate shedding. Massive shedding, resulting in a reduction to normal outer segment length, occurs when constant-light animals are maintained for as little as 30 min in darkness and are then returned to constant light. This shedding response will occur even after both optic nerves are severed, and after pinealectomy or hypophysectomy.