Contraction Index Research Articles

Gallbladder volume and contractility in term and preterm neonates: normal values and clinical applications in ultrasonography

The aim of this study was to establish the normal values and evaluate associated factors of gallbladder volume and contractility in term and preterm neonates by using ultrasonography. Sonographic measurement of gallbladder volume was performed by using the ellipsoid method in 50 preterm and 46 term infants. We collected data soon after delivery and at 6‐h fasting, and at 3‐h and 6‐h fasting following regular milk feeding. Serial postprandial changes of gallbladder volume and contractility were collected at 15‐min intervals for one hour. Gallbladder contraction index (C.I.) was determined as percentage decrement of postprandial size from initial size. Fasting gallbladder volume was larger in term group (p < 0:05). Term neonates more readily showed significant contraction (C.I. > 50%;p < 0:05). In preterm infants significant contraction was clearly observed at postconceptional age > 31 weeks or body weight > 1300 g. The presence of hepatobiliary diseases might be detected by evaluating serial changes of gallbladder volume and contractility under ultrasonography in the neonatal stage.

Gallbladder volume and contractility in term and preterm neonates: normal values and clinical applications in ultrasonography.

The aim of this study was to establish the normal values and evaluate associated factors of gallbladder volume and contractility in term and preterm neonates by using ultrasonography. Sonographic measurement of gallbladder volume was performed by using the ellipsoid method in 50 preterm and 46 term infants. We collected data soon after delivery and at 6-h fasting, and at 3-h and 6-h fasting following regular milk feeding. Serial postprandial changes of gallbladder volume and contractility were collected at 15-min intervals for one hour. Gallbladder contraction index (C.I.) was determined as percentage decrement of postprandial size from initial size. Fasting gallbladder volume was larger in term group (p < 0.05). Term neonates more readily showed significant contraction (C.I. > 50%; p < 0.05). In preterm infants significant contraction was clearly observed at postconceptional age > 31 weeks or body weight > 1300 g. The presence of hepatobiliary diseases might be detected by evaluating serial changes of gallbladder volume and contractility under ultrasonography in the neonatal stage.

Comparison Between the Mean dP/dt During Isovolumetric Contraction and Other Echocardiographic Indexes of Ventricular Systolic Function.

Echocardiographic assessments of ventricular function derived from estimates of the mean dP/dt during isovolumetric contraction (mean dP/dt(ic)) were compared with those obtained from measurements of the shortening fraction and the stress-velocity index (SVI). Mean dP/dt(ic) correlated well with the shortening fraction, r = 0.74, P < 0.0001. Furthermore, 10 out of 11 patients with mean dP/dt(ic) below 800 had a shortening fraction < 0.28, whereas all patients with a mean dP/dt(ic) > 1000 mmHg/sec had a shortening fraction > 0.28. A good correlation also existed between mean dP/dt(ic) and the SVI, r = 0.73, P < 0.0001. Nine out of 11 patients with a mean dP/dt(ic) < 800 mmHg/sec had an SVI > 2 standard deviations below normal, whereas all patients with mean dP/dt(ic) > 1000 mmHg/sec had normal or increased SVI. The correlation between mean dP/dt(ic) and the SVI was strengthened when mean dP/dt(ic) was adjusted for heart rate and preload. Hence, assessments of ventricular function derived from measurements of mean dP/dt(ic) appear to agree well with those provided by the shortening fraction and SVI. Because the determination of mean dP/dt(ic) is not hampered by unusual anatomy or wall motion (conditions which compromise the validity of the shortening fraction and SVI), mean dP/dt(ic) may be a good index of ventricular function in cases where measurements of the shortening fraction and SVI would be unreliable.

Morphological determinants of peripheral lung mechanical changes induced by capsaicin

We studied the morphological elements associated with airway and pulmonary tissue responses to capsaicin in mechanically ventilated guinea pigs. Lungs were excised and frozen in liquid nitrogen 3 and 20 min after capsaicin infusion (1 or 100 μg/kg i.v.). Using image analysis, we obtained contraction index (CI) and peribronchial edema area (CUFF) for both central (C) and peripheral airways (P). We also assessed alveolar size (mean linear intercepts, L m) and tissue distortion (standard deviation of the number of intercepts, SDI). Multiple regression analysis showed significant associations between pulmonary tissue resistance (R ti) and CUFFP ( p<0.001); pulmonary dynamic elastance and SDI ( p=0.002); and airway resistance and CUFFC ( p<0.0001). Our results suggest that increases in R ti observed in guinea pigs after capsaicin infusion are primarily dependent on changes in the small airways, mainly peribronchiolar edema; the increase in lung elastance is related to distortion of parenchymal tissues; and large airway edema contributes significantly to airway resistance.

Low insulin and high glucose induce abnormal relaxation in cultured adult rat ventricular myocytes.

One of the most prominent myocardial defects associated with diabetes is abnormal diastole. We have recently reported that this dysfunction involves prolonged relaxation (relengthening) in isolated ventricular myocytes that occurs within days after the induction of diabetes. The present study was designed to evaluate the role of insulin and glucose int he etiology of this dysfunction with a serum-free myocyte culture system. Adult rat ventricular myocytes were cultured for 1-4 days in a "diabetic-like" medium containing five times less insulin and approximately five times more glucose than in our normal medium. Mechanical properties and Ca2+ transients (fura 2) were evaluated with a high-resolution (120-Hz) video-based edge-detection/spectro-fluormetric system. The cells were field stimulated to contract at slow and physiologically relevant rates, and indexes of contraction and relaxation were evaluated. Relengthening was markedly longer in myocytes cultured in low-insulin-high-glucose (LIHG) medium compared with those in normal medium, whereas contraction was unaffected. Intracellular Ca2+ transients showed slower rates of decay in myocytes cultured in LIHG medium. These data demonstrate that maintaining normal ventricular myocytes in an LIHG environment prolongs relaxation in a manner similar to the effects of in vivo diabetes. Furthermore, the abnormal relaxation is inducible in 1 day, suggesting rapid alterations in processes regulating relaxation, which likely include impaired Ca2+ sequestration and/or extrusion.

Neurokinin depletion attenuates pulmonary changes induced by antigen challenge in sensitized guinea pigs.

The role of neurokinins in the acute pulmonary response to antigen was studied in guinea pigs that received ovalbumin (50 mg/kg ip) on days 1 and 3 and capsaicin (50 mg/kg sc) on day 21 (OAC); ovalbumin on days 1 and 3 (OA1); capsaicin on day 1 and OA on days 8 and 10 (COA); and ovalbumin on days 8 and 10 (OA2). On day 28, guinea pigs were submitted to ovalbumin aerosol challenge. Maximal values of pulmonary dynamic elastance (Edyn) and pulmonary resistance (RL) were significantly lower in OAC and COA groups compared with OA1 and OA2 groups (P < 0.001). There was no difference between maximal Edyn and RL values obtained in OAC and COA groups. Morphometric analysis of lungs showed significantly (P < 0.05) lower values of contraction index of airways, peribronchial edema, and alveoli over inflation in guinea pigs that received capsaicin compared with intact guinea pigs. Capsaicin treatment did not influence the formation of specific IgG1 anaphylactic antibodies. We conclude that neurokinin depletion results in a decrease in the pulmonary mechanical and inflammatory responses to antigen challenge in sensitized guinea pigs. These effects are observed when capsaicin is given either before or after sensitization.

Disparate effects of early pressure overload hypertrophy on velocity-dependent and force-dependent indices of ventricular performance in the conscious baboon.

The effects of early pressure overload on left ventricular (LV) chamber mechanics in the primate heart are poorly understood. To test the hypothesis that early LV pressure overload hypertrophy is associated with depression of velocity-dependent indices of LV systolic (LV dP/dt) and diastolic function (time constant of relaxation, tau) but unchanged systolic elastance (Ees), we studied six conscious baboons instrumented with LV micromanometers and LV dimension and wall thickness sonomicrometers. Loading conditions were altered by pharmacological angiotensin II generation both before and 12 weeks after producing renovascular hypertension (2 kidney, 1 clip). The LV systolic pressure (149 +/- 11 [SD] versus 114 +/- 5 mm Hg) and LV mass (125 +/- 25 versus 91 +/- 20 g) were greater 12 weeks after than before (both P < .05). Both Ees and Ees normalized for LV mass were similar before versus 12 weeks after (23.0 +/- 9.6 versus 22.3 +/- 9.8 mm Hg/mL and 26.5 +/- 14.5 versus 19.8 +/- 12.5 mm Hg/mL, respectively; both P = NS). At matched LV systolic and diastolic pressures, LV fractional shortening was similar (18.6 +/- 6.8% versus 21.6 +/- 4.9%), but the time constant of LV isovolumic relaxation was significantly longer (42.3 +/- 5.3 versus 31.4 +/- 7.0 ms, P < .05) and LV dP/dt and Vcf were significantly less (1891 +/- 352 versus 2342 +/- 284 mm Hg/s and 0.9 +/- 0.4 versus 1.1 +/- 0.3 circ/s, respectively; both P < .05) 12 weeks after than before. In conscious baboons with systemic arterial hypertension and early LV hypertrophy, there is depression of velocity-dependent indices of LV contraction and relaxation but unaltered force-dependent measures of contractility.

757-3 Chronic Angiotensin II Receptor Blockade (AT1 AT-II) Affects Myocyte Sarcolemmal Function and Electrophysiology in Dilated Cardiomyopathy

We tested the hypothesis that AT 1 , AT-II receptor activation with the progression of dilated cardiomyopathy (DCM) causes fundamental changes In myocyte (MYO) sarcolemmal processes. Six dogs were assigned to each of 3 groups: (1) DCM : tachycardia induced DCM (pace 216;4 wks). (2) DCM/AT-BLOCK; chronic pace and concomitant treatment with a specific non-peptide ATl AT-II antagonist (BMS 186295; 30 mg/kg BIDI (3) CONTROL. LV ejection fraction (LVEFO% and end-diastolic volume (LVEDV;cc) were measured by echo/cath. Simultaneous indices of MYO membrane potential (resting;RMP;mV, upstroke velocity;Vmax;V/s, time to 90% repolarization;APD9 ms) and contraction (velocity of shortening; MYOVEL;μ m/s were measured by videomicroscopy and microelectrodes. LVEF LVEDV RMP Vmax APD90 MYOVEL CONTROL 73 ± 2 69 ± 4 -78 ± 1 158 ± 9 226 ± 8 57 ± 1 OCM 35 ± 3 * 101 ± 7 * -71 ± 1 * 121 ± 5 * 257 ± 9 * 36 ± 1 * DCM/AT-BLOCK 35 ± 2 * 93 ± 6 * -76 ± 1 + 165 ± 13 + 183 ± 14 *+ 41 ± 1 * * p &lt; 0.05 vs CONTROL + p &lt; 0.05 vs DCM In the next set of experiments, Na + ,K + -ATPase binding density (Bmax), affinity (Kd), and ATPase actiVity (ACT) were computed from sarcolemmal preparations. AT1 AT-II receptor blockade normalized Na+,K + -ATPase density and Increased hydrolytic capacity. Bmax (pmol/mg) Kd (nM) ACT (μg/mg/hr) CONTROL 3.2 ± 0.3 25.3 ± 15 056 ± 0.09 OCM 1.9 ± 0.3 * 19.9 ± 1.8 * 0.37 ± 0.09 * OCM/AT-BLOCK 2.7 ± 0.2 + 22.7 ± 2.8 0.96 ± 0.23 *+ Concomitant AT, AT-II receptor blockade during the development of OCM normalized MYO membrane potentials. A fundamental mechanism for these effects were preserved sarcolemmal Na+,K+ -ATPase density and enhanced activity.

Gallbladder hypocontractility in infantile colic

We evaluated gallbladder contractility in 58 colicky infants and 57 age-matched controls. Gallbladder size was measured before and 1 h after feeding and the contraction index of the gallbladder was calculated. The results showed decreased contractility of the gallbladder in colicky infants: mean contraction index in colicky infants was 56% (95% confidence interval, 49-63%) and in controls 67% (61-73%). No difference was found in the fasting size of the gallbladder. Postprandial contraction was decreased in colicky infants examined in the evening (n = 14) compared with those examined in the morning (n = 44). Decreased contraction of the gallbladder was found in those colicky infants who presented colicky cry compared with colicky infants without symptoms at the time of examination. No structural abnormalities were found in the general abdominal survey. In conclusion, infants with colic have hypocontractility of the gallbladder. This indicates abnormal biliary tract physiology in association with infantile colic.

Effects of misoprostol on delayed ulcer healing induced by aspirin.

Clinical studies have suggested that treatment with the prostaglandin E1 analog, misoprostol, leads to significant healing of ulcers in patients taking regular nonsteroidal antiinflammatory therapy. This study aimed to investigate mechanisms involved in this healing using a rat model. Gastric ulcers were induced by application of acetic acid using a standard technique. Rats were treated with 200 mg/kg aspirin, 100 micrograms/kg misoprostol, a combination of both treatments, or methylcellulose vehicle for up to two weeks, starting two days after ulcer induction. Ulcers were assessed by macroscopic measurements of area and by quantitative histological measurements. Aspirin delayed ulcer healing compared with controls, while misoprostol significantly reversed this effect. Quantitative histology revealed that misoprostol cotreatment significantly increased mucosal regeneration compared with aspirin treatment alone. However, misoprostol did not reverse the effects of aspirin on an index of wound contraction. We conclude that treatment with misoprostol significantly reverses the delayed healing effect of aspirin, and this may occur via an effect on epithelial regeneration.

Asymptomatic Mitral Regurgitation: When to Operate?

The timing of surgical intervention in asymptomatic or mildly symptomatic patients with mitral regurgitation has always been a difficult clinical dilemma, especially with current options of valve replacement or valve repair. Symptomatic status should be carefully assessed and may depend upon either atrial fibrillation or progressive left ventricular dysfunction. Many patients may claim to be asymptomatic, but have profound limitations to their functional capacity and impairment of contraction indices. Because of this, every effort should be made to objectively follow the asymptomatic patient and schedule surgical intervention before irreversible left ventricular dysfunction. Left ventricular ejection fraction continues to be an inappropriate parameter, for the regurgitant fraction increases the preload to the left ventricle, and the regurgitant orifice reduces left ventricular afterload with increase to the left ventricle, and the regurgitant orifice reduces left ventricular afterload with increase in ejection fraction. End-diastolic dimension of volume is dependent upon such preload, and hence not accurate. End-systolic diameter is a better prognostic index; an end-systolic dimension of 4.5 cm (2.6 cm/m2) and a calculated end-systolic volume of 50 mL/m2 seem to be reasonable discriminators of outcome following surgery. More recent investigations suggest that left ventricular dP/dt, measured from a Doppler profile of mitral regurgitation, is perhaps a better predictor. In the asymptomatic patient, it is difficult to justify a role for intense medical therapy. The patient who develops atrial fibrillation does require a long-term anticoagulation therapy, and valve repair might be considered in this patient. Sinus rhythm may be restored with early surgical intervention, thereby reducing complications of thromboembolism or anticoagulant therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive evaluation of chronic cumulative and acute cardiotoxicity induced by anthracycline in children with acute leukemia. Assessment of mainly left ventricular contractile state by M mode echocardiography

The cardiotoxic effects of Daunomycin (DM) ad Adriamycin (ADR), Anthracyclines (ATC), were studied mainly by echocardiography to evaluate their chronic cumulative cardiotoxicity and acute cardiotoxicity during consolidation therapy. Electrocardiographic findings were less sensitive and therefore less reliable for evaluation of the chronic cumulative cardiotoxicity and acute cardiotoxicity induced by ATCs during consolidation therapy. With echocardiography ESS/ESVI, the index of the left ventricular contraction, had the highest sensitivity among indices for cardiotoxicity. SF was useful for easy measurement and calculation of cardiotoxicity. Evaluation of the chronic cumulative cardiotoxicity of ATC drugs indicated that cumulative doses of 300 mg/m2 or more resulted in abnormally low ESS/ESVI levels suggesting cardiotoxicity in many cases, and doses of 500 mg/m2 or more caused abnormally low levels in all cases. Evaluation of acute cardiotoxicity showed that post-consolidation therapy ESS/ESVI levels were significantly lower than pre-consolidation therapy levels in the group treated with doses of 500 mg/m2 or more, but the condition was reversible except in those patients with heart failure. As for the relation between cumulative doses and cardiotoxicity, the indices studied showed no differences between DM and ADR. These results indicate that careful follow-up mainly by echocardiography is required after doses reaching 300 mg/m2 or more of ATC drugs.

EFFECTS OF CARDIAC WORK ON THE THRESHOLD FOR VENTRICULAR FIBRILLATION

Ventricular fibrillation threshold (VFT) was measured in anesthetized dogs, while cardiac work was altered by changing arterial pressure (pressure work) or by opening an aorta to left atrial shunt (flow work). When VFT during pressure work was compared with that during flow work, at a constant heart rate, it was found that there was a negative correlation (a lower threshold for fibrillation) between VFT and flow work but not pressure work. VFT also had negative correlations with the rate of contraction and relaxation indexes; maximal +/- dp/dt and negative dp/dt were the most significant variables. On the other hand, coronary flow, oxygen consumption, end diastolic pressure, and tension time index were not correlated with VFTs. Thus, VFT depended on mechanical factors not necessarily correlated to alterations in myocardial perfusion.

Lung volume changes during relatively fluent speech in stutterers.

We investigated breathing patterns in stutterers during relatively fluent speech and compared these with normal subjects for similar speech tasks. Rib cage and abdominal displacements and esophageal, gastric, and transdiaphragmatic pressures provided indexes of diaphragmatic, rib cage, and abdominal muscle contraction. We found that stutterers spoke either at substantially higher or lower lung volumes than normal subjects, confining their speech to the inspiratory capacity or expiratory reserve volume. During spontaneous speech, stutterers did not cross functional residual capacity (FRC) for most breaths. In addition, stutterers used several different motion pathways from breath to breath. At high lung volumes stutterers used the diaphragm to provide inspiratory braking. At lung volumes below FRC stutterers recruited their abdominals. This contrasted with normal subjects who spoke in the middle part of the vital capacity and who recruited inspiratory and expiratory rib cage muscles above and below FRC, respectively. Breath sizes were log-normally distributed in stutterers compared with a gaussian distribution in normal subjects (P < 0.001). During reading, stutterers tended to cross FRC (P < 0.01), used very similar initiation lung volumes from breath to breath (P < 0.001), and used similar motion pathways to achieve deflation. We conclude that stutterers sustain fluency by speaking at abnormally high or low lung volumes and that this may account for the different muscle patterns observed in stutterers compared with normal subjects.

Time-course of left atrial performance during coronary artery occlusion followed by reperfusion in anesthetized dogs by densitometric analysis of digital atrioventriculographic images.

The left atrial (LA) function during coronary artery occlusion followed by reperfusion using densitometric analysis of digital atrioventriculographic images was evaluated. Eight anesthetized dogs underwent atrioventriculography at baseline, 10 and 60 min after left circumflex coronary artery (LCX) occlusion and 5, 30, 60, and 120 min of reperfusion. Time-density curves were obtained for LA and left ventricle (LV). The ratios of passive atrial video-densitometric change (VC) to total VC (Passive Ratio), and active VC to total VC (Active Ratio) were calculated. Left ventricular ejection fraction (LVEF), peak ejection rate (PER), and peak filling rate (PFR) were derived. Active Ratio, an index of atrial contraction, increased to 144%, and Passive Ratio decreased to 75% of baseline at 60 min of LCX occlusion. Two hours after reperfusion, both Active and Passive Ratios returned to control level. While LVEF reduced to 70%, PER to 67%, LV peak positive dP/dt to 88% of baseline at 60 min after occlusion, and remained depressed at 2 h after reperfusion. However, PFR, LV peak negative dP/dt and LV isovolumic pressure decay rate showed recovery at 2 h after reperfusion. There were significant correlations between PFR and Passive Ratio (r = 0.41), and between Active and Passive Ratios (r = 0.55). Thus, time-course of recovery of LV post-ischemic systolic and diastolic function was different. Return of LA function to control level during 2 h after reperfusion may be depend on recovery of LV diastolic function.

Markers of left ventricular dysfunction induced by exercise, dipyridamole or combined stress on ECG-gated myocardial perfusion scans.

An index of left ventricular contraction can be extracted from the cavitary time-activity curve of electrocardiographic (ECG)-gated myocardial perfusion scans. To assess the induction of stress-induced myocardial depression, we compared contraction indexes derived from immediate poststress and delayed 201Tl images with indexes of ventricular dilation and lung uptake in the prediction of severe coronary artery disease (defined as two or more 90% stenoses). Stress procedures were performed in 93 patients with symptom-limited supine bicycle exercise alone, and in 227 with intravenous dipyridamole, combined where possible with exercise. The immediate and delayed contraction indexes reflected left ventricular dysfunction on ventriculography (P < 0.0001), but additionally the immediate index was reduced (P < 0.0001) in severe coronary disease. Stress-induced hypokinesis was seen frequently after each of the test modes. The relationship with angiographic findings was better defined for indexes of contraction than for lung uptake or ventricular dilation (P < 0.01). The prediction of severe coronary disease was optimized by combining the poststress contraction index and lung uptake. These data support the use of ECG-gated myocardial scans in evaluating the functional consequences of stress/imaging procedures.

Cocaine significantly impairs myocardial relaxation

To determine the immediate effects of intravenous "recreational" doses of cocaine on myocardial ventricular relaxation and contraction and on coronary blood flow. To determine the cardiac effects of cocaine after the administration of propranolol, as propranolol has been used to limit the cardiovascular effects of cocaine. Prospective study. Twenty mongrel dogs. We continuously recorded central aortic pressure, left atrial and ventricular pressures, coronary artery blood flow, and electrocardiograms in each dog. We determined from the left ventricular pressure waveforms the maximum rate of pressure increase [(dP/dt)max] and the time constant of isovolumic ventricular relaxation as our indices of ventricular contraction and relaxation. In our initial series of experiments, we obtained pressure, coronary artery blood flow, and electrocardiographic recordings in ten anesthetized dogs before and for 40 mins after the intravenous administration of cocaine, in doses of 2.5 and then 5 mg/kg. In our second series of experiments in ten additional dogs, we injected 0.5 mg/kg of propranolol intravenously 30 mins before the injection of cocaine (2.5 mg/kg), and obtained hemodynamic and electrocardiographic recordings before and for 40 mins after the injection of propranolol and cocaine. Cocaine, 2.5 mg/kg, abruptly increased the time constant of isovolumic ventricular relaxation from 22.9 +/- 1.2 to 29 +/- 2.2 msecs at 1 min (p < .05) and to 35.3 +/- 2 msec at 40 mins (p < .01) but did not significantly change the mean arterial pressure, left atrial pressure, heart rate, coronary blood flow, or the maximum rate of left ventricular pressure increase [(dP/dt)max]. Cocaine also progressively displaced the electrocardiographic ST segments by 3.2 +/- 0.6 mm (p < .01) over 40 mins. Cocaine, 5 mg/kg, rapidly increased the time constant of isovolumic ventricular relaxation from 28.5 +/- 2.5 to 41 +/- 3 msecs in 1 min (p < .05) and to 48.7 +/- 4 msecs at 40 mins (p < .01) and reduced (dP/dt)max from 2905 +/- 370 to 1422 +/- 121 mm Hg/sec at 1 min (p < .01); (dP/dt)max returned to 2351 +/- 415 mm Hg/sec during the next 39 mins. Cocaine did not significantly change either the mean arterial or left atrial pressures. However, this dose of cocaine did decrease, over 40 mins, the heart rate from 184 +/- 11 to 139 +/- 11 beats/min (p < .01) and reduced coronary blood flow by 20% (p < .01). Cocaine also displaced the electrocardiographic ST segments by 3.3 mm over 40 mins (p < .05). Cocaine and propranolol abruptly increased the time constant of isovolumic ventricular relaxation from 26.4 +/- 1.3 to 43.2 +/- 2.1 msecs (p < .01) at 1 min and to 46.8 +/- 1.5 msecs at 3 mins (p < .01). The time constant of isovolumic ventricular relaxation remained abnormally increased at 43.0 +/- 1.4 msecs at 40 mins. Cocaine and propranolol reduced (dP/dt)max from 2760 +/- 458 mm Hg/sec to a minimum value of 1400 +/- 119 mm Hg/sec at 2 mins (p < .01). However, (dP/dt)max then returned to 2201 +/- 359 mm Hg/sec during the next 38 mins. Cocaine and propranolol did not significantly change the mean arterial and left atrial pressures, or heart rate, but did reduce coronary blood flow, over 40 mins, by 25% (p < .001). Cocaine also maximally displaced the electrocardiographic ST segments by 1 +/- 0.2 mm (p < .01). Cocaine substantially impairs myocardial ventricular relaxation for periods of at least 40 mins. Propranolol significantly intensifies cocaine's depressant effect on ventricular relaxation.

Gall bladder contractility in preterm infants.

Postnatal response of the gall bladder to feeding was studied in 28 preterm infants (gestational age 24-37 weeks) by ultrasonography immediately before feeding and one hour after feeding. Nineteen of the infants were studied once during the first week of life, and nine infants were studied weekly from a postconceptional age of 27-31 until a postprandial gall bladder contraction was seen. A contraction index was calculated as a percentage decrement of the surface area of the gall bladder from its initial value. All preterm infants of more than 33 weeks' gestation showed a gall bladder response to feeding with a contraction index of at least 50%. Very preterm infants (gestational age 27-32 weeks) showed no postprandial gall bladder contraction or the contraction index was under 50%. In a follow up study of nine very preterm infants, the contraction index exceeded 50% at a postconceptional age of 29 to 32 weeks. One infant with prolonged feeding problems had no postprandial gall bladder response before the postconceptional age of 38 weeks. The contraction index increase was dependent on gestational age at birth and on the bolus volume of feeds.

The changes in contractile status of single vascular smooth muscle cells and ventricular cells induced by bPTH-(1–34)

Single smooth muscle cells from rat tail artery and ventricular myocytes from neonatal rat were isolated by repeated enzyme digestion. The change in cell area as determined photographically was used as an index of cell contraction. The photographic areas of single smooth muscle cells bathed in normal Tyrode solution were 403±22 (n=13) square micra. Exposure of smooth muscle cells to a modified Tyrode solution containing 60 mM KCl induced cell contraction. This contraction was inhibited by bPTH-(1–34) at a concentration of 1 μM. The inhibitory effect of bPTH-(1–34) was time-dependent with maximum inhibition at 5 min after administration. The photographic areas of ventricular myocytes bathed in the culture medium without fetal calf serum were 516±47 (n=29) square micra. At a concentration o of 1 μM, bPTH-(1–34) produced a time-dependent contraction in ventricular myocytes as shown by the decrease in the photographic cell area (88±2% of the control value at 15 min, n=9, p<0.01). Furthermore, 1 μM nifedipine inhibited the effect of bPTH-(1–34) on the contraction of ventricular myocytes, indicating that bPTH-(1–34) might exert its action via a calcium channel related mechanism. In addition, bPTH-(1–34) increased the contraction frequency of single ventricular cells, which could also be inhibited by nifedipine. The present study suggests that bPTH-(1–34) directly relaxes pre-contracted single vascular smooth muscle cells and contracts single ventricular myocytes.

Bounds on the trellis size of linear block codes

The size of minimal trellis representation of linear block codes is addressed. Two general upper bounds on the trellis size, based on the zero-concurring codewords and the contraction index of the subcodes, are presented. The related permutations for attaining the bounds are exhibited. These bounds evidently improve the previously published general bound. Additional bounds based on certain code constructions are derived. The focus is on the squaring construction, and specific constructive bounds for Reed-Muller and repeated-root cyclic codes are obtained. In particular, the recursive squaring construction of Reed-Muller codes is explored and the exact minimal trellis size of this design is obtained. Efficient permutations, in the sense of the trellis size, are also demonstrated by using shortening and puncturing methods. The corresponding bounds are specified. >