Biomedical subjects

E Chow

Publications and source records attributed to E Chow.

At least 73 records · Page 4Linked to original sources

PubMed1992

Regional contractile performance during acute ischemia in porcine right ventricle.

Studies of regional ischemia in the canine left ventricle (LV) have shown augmented systolic segmental shortening in nonischemic regions. To characterize these responses in the right ventricle (RV), acute occlusions of the right coronary artery (RCAO) were produced in anesthetized pigs. Orthogonal pairs of ultrasonic segment-length crystals were implanted in the mid-RV free wall (ischemic region) and in the outflow tract (nonischemic region). RV pressure-area work loops were generated during inferior vena caval occlusions, and both slope (M) of the preload recruitable stroke work relationship and elastance (Ees) of the end-systolic pressure-area relationship were determined by linear regression. Under control conditions, there was no significant difference in M or Ees of the two regions. After RCAO, fractional area shortening decreased by 84% in the ischemic region but increased by 21% in the nonischemic region. Although RV end-diastolic pressure and areas in both regions increased, M was significantly reduced by 78% only in the ischemic region. There was no change in contractile function in the nonischemic region as described by M and Ees despite the increase in systolic fractional area shortening. Therefore the nonischemic region of the porcine RV exhibits an apparent compensatory hyperkinesis in response to regional ischemia similar to that shown for the canine LV, consistent with the Frank-Starling mechanism.

Acute Disease↗

PubMed1992

Isolated ventricular systolic interaction during transient reductions in left ventricular pressure.

The volume and pressure of one ventricle have been demonstrated to modulate the volume and pressure in the contralateral chamber during systole and diastole. To quantitate the isolated systolic effects of left ventricular (LV) pressure on right ventricular (RV) mechanics, we rapidly withdrew blood from the LV immediately after diastole via an apex cannula during a single cardiac cycle in eight open-chest, open-pericardium anesthetized pigs (45 kg) and studied the effects on the RV. Reductions in LV pressure of up to 75 mm Hg were achieved in midsystolic without changing LV or RV diastolic volume or pressure. Resultant changes in RV flow and pressure development during these single unloaded beats may therefore be considered to result from pure systolic interaction. The instantaneous left-to-right systolic pressure gain [G(t)] was determined as the ratio of RV pressure change to LV pressure change as a function of time during systole, and the mean LV-to-RV systolic pressure gain was determined as the ratio of changes in mean systolic RV pressure to changes in mean systolic LV pressure. During LV unloading, there was an average reduction of 62.6 +/- 12.3% in the mean systolic LV pressure, which resulted in decreases of 13.6 +/- 6.4% in mean RV systolic pressure, 17.9 +/- 10.4% in RV stroke volume, and 27.0 +/- 11.3% in RV stroke work. G(t) was found to vary significantly within systole, reaching a minimum of 0.042 +/- 0.014 mm Hg/mm Hg at normalized time 0.70 of the systolic duration and a maximum of 0.079 +/- 0.029 at the end of RV ejection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Right heart function during prosthetic left ventricular assistance in a porcine model of congestive heart failure.

A left ventricular assist device was used to produce a 90% reduction in peak systolic left ventricular pressure in pigs with congestive heart failure, and the resultant effects on right ventricular function were determined. Initially, eight farm pigs underwent rapid ventricular pacing at 230 beats/min for 7 days to produce congestive heart failure. When compared with an independent series of normal pigs, cardiac output in the paced animals was 33.3% less (2.2 +/- 0.2 versus 3.3 +/- 0.5 L/min; p less than 0.05), left ventricular end-diastolic pressure was elevated (13.8 +/- 3.5 versus 6.6 +/- 1.8 mm Hg; p less than 0.05), and the slope of the right ventricular global stroke work curve was significantly depressed (0.004 +/- 0.001 versus 0.033 +/- 0.003 joules/mm Hg; p less than 0.05). Next, the left ventricular assist device was connected between left ventricular apex and ascending aorta and left ventricular pressure was reduced from 92.0 +/- 3.8 to 10.5 +/- 2.2 mm Hg, while systemic arterial pressure was maintained constant. This led to a further impairment in cardiac output (-14%), mean arterial pressure (-15%), and the slope of the right ventricular global stroke work curve (-50%). Under each condition, right ventricular preload recruitable stroke work and end-systolic pressure-dimension relationships were studied in three different regions on the right ventricle during both steady-state and transient inferior vena caval occlusion. In the right ventricular septal-free wall dimension, left ventricular pressure unloading resulted in a 47.5% +/- 5.4% (p less than 0.05) reduction in the slope and 20.1% +/- 4.8% (p less than 0.05) increase in the dimension intercept of the preload recruitable stroke work relationship. There was also a 44.6% +/- 4.8% (p less than 0.05) reduction in the slope and 15.6% +/- 2.8% (p less than 0.05) increase in the dimension intercept of the end-systolic pressure-dimension relation. These slope changes plus reductions in cardiac output and in global stroke work, which are indicative of impaired right ventricular function during left ventricular pressure unloading in the congestive heart failure pigs, are not seen in normal hearts, whereas the intercept changes associated with leftward septal shift are present in both. These results suggest that anatomic ventricular interactions have a more significant role in heart failure than in the normal heart in determining overall right ventricular function during left ventricular assist device support.

Animals↗

PubMed1991

Epidemiology of chronic paronychia in a skin hospital in Singapore.

A retrospective epidemiologic study of 110 patients with chronic paronychia (CP) showed a female-male ratio of 2.3:1, whereas the ratio of patients attending the same clinic was 1.1:1 (p less than 0.001). The peak age range of patients with CP (40-49 years) generally was greater than that of the general dermatologic patients (20-29 years). Seventy-seven percent of the patients with CP were "manual workers," of which 48% were homemakers. Chronic paronychia was more common on the right fingers than the left fingers. The most commonly affected fingers were the right thumb (62%), followed by the right middle finger (52%), left thumb (57.6%), and left middle finger (51.5%). Mechanical trauma appears to be an important predisposing factor in CP. Sixty-two percent of 68 patients who had nail fold smears had positive findings for budding yeast cells, suggestive of candidal infection. All of the six patients for whom nail fold bacterial cultures were performed had positive results for enteric flora.

Adult↗

PubMed1991

Effects of acute right ventricular ischemia on ventricular interactions during prosthetic left ventricular support.

Systolic ventricular interactions may be partially responsible for right ventricular failure that sometimes occurs during clinical use of prosthetic left ventricular assist devices. In this hypothesis, it is proposed that the left ventricular assist device reduces left ventricular pressure and its contribution to right ventricular performance, thus impairing right ventricular output. On the other hand, these effects may be small compared with other causes of right ventricular failure such as ischemia. To test the systolic interaction hypothesis in the normal and ischemic right ventricle, we used a left ventricular assist device to pressure unload the left ventricle of anesthetized pigs, and we compared its effect on right heart function before and after 2 minutes of acute right coronary artery occlusion as a model of right heart failure. Pigs were instrumented for measurements of septal to left ventricular and right ventricular free wall dimensions with ultrasonic crystals, ventricular chamber pressures, and cardiac output with a pulmonary artery blood flow probe. Without right ventricular ischemia, the left ventricular assist device produced an 80% +/- 6% reduction in left ventricular pressure-time integral while maintaining aortic pressure. This resulted in a leftward septal shift with an 11.6% +/- 1.8% decrease in left ventricular septal-to-free wall dimension and a 12.5% +/- 2.4% increase in right ventricular septal-to-free wall dimension, with no changes in right ventricular cardiac output or stroke work. In contrast, right coronary artery occlusion alone produced right heart failure, with a 50% +/- 6% reduction in right ventricular global stroke work and 26% +/- 6% and 27% +/- 3% reductions in cardiac output and right ventricular peak systolic pressure, respectively. This right heart failure persisted during left ventricular unloading with the left ventricular assist device, which resulted in further leftward septal shifting and unchanged but still depressed stroke work and flow output. These findings support the hypothesis that a preexisting pathologic condition is the dominant factor in determining right ventricular function during prosthetic left ventricular support and that direct anatomic interactions play a minor role.

Animals↗

PubMed1990

Inhibitory innervation of colonic smooth muscle cells and interstitial cells of Cajal.

The effect of neural inhibition on the electrical activities of circular and longitudinal colonic smooth muscle was investigated. In addition, a comparative study was carried out between circular muscle preparations with and without the "submucosal" and "myenteric plexus" network of interstitial cells of Cajal (ICC) to study innervation of the "submucosal" ICC and to investigate whether or not the ICC network is an essential intermediary system for inhibitory innervation of smooth muscle cells. Electrical stimulation of intrinsic nerves in the presence of atropine caused inhibitory junction potentials (ijps) throughout the circular and longitudinal muscle layers. The ijp amplitude depended on the membrane potential and not on the location of the muscle cells with respect to the ICC network. Neurally mediated inhibition of the colon resulted in a reduction in amplitude and duration of slow wave type action potentials in circular and abolishment of spike-like action potentials in longitudinal smooth muscle, both resulting in a reduction of contractile activity. With respect to mediation by ICC, the study shows (i) "submucosal" ICC receive direct inhibitory innervation and (ii) circular smooth muscle cells can be directly innervated by inhibitory nerves without ICC as necessary intermediaries. The reversal potential of the ijp in colonic smooth muscle was observed to be approximately -76 mV, close to the estimated potassium equilibrium potential, suggesting that the nerve-mediated hyperpolarization is caused by increased potassium conductance.

Animals↗

PubMed1990

Rapid ventricular pacing in pigs: an experimental model of congestive heart failure.

To develop an improved animal model of congestive heart failure, 11 female farm pigs (wt, 42-46 kg) underwent rapid ventricular pacing at 230 beats/min for 7 days with a modified Medtronic unipolar pacemaker connected to an apical pacing lead. After 7 days the pacemaker was turned off, anesthesia induced, the chest opened, and cardiac hemodynamic and dimensional studies were performed. Results were subsequently compared with data from 12 control pigs that received no pacing. Two pigs died before measurements could be determined. Cardiac output in the paced animals (0.061 +/- 0.018 l.min-1.kg-1) was significantly less (P less than 0.05) than in control pigs (0.085 +/- 0.016 l.min-1.kg-1), when compared at the same resting heart rate. Left ventricular (LV) end-diastolic pressure (23.2 +/- 7.7 vs. 8.6 +/- 3.6 mmHg, P less than 0.01) and right ventricular (RV) end-diastolic pressure (9.0 +/- 3.1 vs. 4.4 +/- 1.7 mmHg, P less than 0.01) were significantly greater in the paced pigs. Significant increases in both septal-lateral LV end-diastolic dimension (60.3 +/- 3.9 vs. 52.1 +/- 7.2 mm, P less than 0.01) and RV end-diastolic dimension (47.2 +/- 5.7 vs. 40.8 +/- 4.7 mm, P less than 0.05) indicated biventricular dilation in the paced pigs. They also exhibited a significantly greater heart weight-to-total body weight ratio and clinical evidence of congestive heart failure, with hepatomegaly and ascites. These results demonstrate that 1 wk of rapid ventricular pacing at 230 beats/min produces a realistic model of congestive heart failure in the pig.

Animals↗

PubMed1989

Role of the sodium pump in pacemaker generation in dog colonic smooth muscle.

1. The role of the Na+ pump in the generation of slow wave activity in circular muscle of the dog colon was investigated using a partitioned 'Abe-Tomita' type chamber for voltage control. 2. Blockade of the Na+ pump by omission of extracellular K+, by ouabain, or the combination of 0 mM-Na+ and ouabain, depolarized the membrane up to approximately -40 mV and abolished the slow wave activity. Repolarization back to the control membrane potential by hyperpolarizing current restored the slow wave activity. 3. Slow waves continued to be present in 0 Na+, Li+ HEPES solution. 4. The depolarization induced by the procedures to block Na+ pump activity was associated with an increase in input membrane resistance. 5. Voltage-current relationships show the presence of an inward rectification. 6. Reduction of temperature depolarized the membrane, and decreased the slow wave frequency and amplitude. The slow wave amplitude was restored by repolarization of the membrane. 7. Brief depolarizing pulses evoked premature slow waves. Brief hyperpolarizing pulses terminated the slow waves. 8. We conclude that abolition of slow wave activity by Na+ pump blockade is a direct effect of membrane depolarization and that the Na+ pump is not responsible for the generation of the slow wave. 9. Our results are consistent with the hypothesis that pacemaker activity in smooth muscle is a consequence of membrane conductance changes which are metabolically dependent.

Animals↗

PubMed1989

Binding and aggregation of the 25-kilodalton toxin of Bacillus thuringiensis subsp. israelensis to cell membranes and alteration by monoclonal antibodies and amino acid modifiers.

The 25-kilodalton toxin of Bacillus thuringiensis subsp. israelensis binds irreversibly to Aedes albopictus cells, Choristoneura fumiferana cells, and erythrocytes. The binding to cells increased with both toxin concentration and time and when the cells were first preincubated with unlabeled toxin. Binding data indicated a two- to threefold increase in the rate of binding after the amount of the membrane-bound toxin reached approximately 3.5 fmol/3 x 10(5) A. albopictus cells or 3.3. fmol/2 x 10(5) C. fumiferana cells. When this level of bound toxin was reached, the toxins also began forming aggregates at the cell membrane. The toxin aggregates were extracted with 10% Triton X-100 and separated from the monomers with a 5 to 20% sucrose density gradient. The toxin aggregates isolated from A. albopictus and C. fumiferana cell membranes were ca. 400 kilodaltons, while those isolated from human erythrocytes were significantly smaller. The proportion of the toxin found in aggregate form increased rapidly with the amount of toxin bound; however, the molecular size of the aggregates remained constant. Eleven monoclonal antibodies raised against the native form of the toxin blocked 80 to 97% of the toxin binding to cells. The epitope of one of these monoclonal antibodies was mapped to a domain which included the cysteine, suggesting the importance of the domain around this amino acid to binding. Toxin binding and cell lysis were also inhibited by treating the toxin with HgCl2, further indicating the importance of the C-terminal hydrophobic cysteine-containing domain in cytolytic activity of the 25-kilodalton protein.

Animals↗

PubMed1989

Effects of left ventricular pressure reductions on right ventricular systolic performance.

Reductions in left ventricular pressure (LVP) have been shown to produce a leftward shift of the interventricular septum and to reduce left ventricular contribution to right ventricular performance. To evaluate the magnitude of this contribution in the intact heart, five anesthetized pigs were implanted with a left prosthetic ventricle to gradually decrease LVP while maintaining arterial systemic pressure. Three descriptors of RV global and regional systolic function were studied in the septum to free wall (RVSFW) and anterior to posterior (RVAP) dimensions and in an outflow tract segment length (RVSL), during both steady state and transient inferior vena cava occlusion. LVP gradual reduction from 102 +/- 4 to 11 +/- 3 mmHg (90% decrease in peak systolic pressure) produced no changes in the RV global stroke work curve or in the RVAP and RVSL pressure-dimension relationships. However, the reduction in LVP resulted in parallel shifts in the RVSFW dimension, with 16.6 +/- 6.7% increase in the intercept D(o) of the end-systolic relationship and 16.5 +/- 2.5% increase in D(o) of the dimensional stroke work relationship, with no significant changes in their respective slopes as calculated by linear regression. Therefore, in the normal intact heart, large reductions in left ventricular pressure affect the geometry of the right ventricle because of septal shifting, but there is a negligible net effect of this anatomic ventricular interaction on overall right ventricular performance.

Animals↗

PubMed1989

Successful biventricular circulatory support as a bridge to cardiac transplantation during prolonged ventricular fibrillation and asystole.

The indications for biventricular versus left ventricular mechanical circulatory support as a bridge to cardiac transplantation are not well established. In this study, 27 potential heart transplant candidates who were in imminent risk of dying before donor heart procurement were implanted with Thoratec prosthetic ventricles (21 biventricular and six left ventricular) at three medical centers. A total of 21 patients (16 biventricular and five left ventricular) underwent successful cardiac transplantation after 1-65 days of circulatory support, and 19 were discharged from the hospital. Seven of the patients (all biventricular; diagnoses: four cardiomyopathy, two acute myocardial infarction, one end-stage coronary artery disease plus acute myocardial infarction) had prolonged arrhythmias that normally would have been lethal (six cases of ventricular fibrillation from 2 to 22 days, one asystole for 3 hours), but complete support of the systemic and pulmonary circulations was maintained in all seven patients with biventricular devices. Mean systemic blood flow during this period (4.6 +/- 0.6 l/min) was unchanged compared with that during sinus rhythm. Six of these patients survived to receive heart transplants. The use of right plus left prosthetic ventricles does not prevent the occurrence of arrhythmias but removes the threat and simplifies patient management. We conclude that biventricular support is indicated in bridge-to-transplant patients with potentially lethal arrhythmias.

Adult↗

PubMed1988

Toxicity of an acute dose of agent VX and other organophosphorus esters in the chicken.

The neurotoxicities of single doses of a chemical warfare agent VX [phosphonothioic acid, methyl-S-(2-[bis(1-methylethyl)amino/ethyl) O-ethyl ester], a metabolite of the agricultural chemical parathion, paraoxon, PO (phosphonothioic acid, diethyl paranitrophenyl ester), and the known neuropathic agents DFP] phosphorofluoridic acid, bis(1-methylethyl) ester] and TOCP (phosphoric acid, tri-o-tolyl ester) were compared in the chicken. Single injections (subcutaneous, sc) of VX as high as 150 micrograms/kg (5 times the LD50, intramuscular, im) were tolerated by laying tens if atropine and 2-pralidoxime were used as antidotes before and immediately after injection. The 150 of VX for inhibition of chicken brain acetylcholinesterase was approximately 5 X 10(-10). Plasma acetylcholinesterase, but not butyrylcholinesterase, was depressed 2 h after injections of 2-20 micrograms VX/kg im without antidotes. Levels of plasma enzymes such as creatine kinase, indicative of tissue damage, were increased after exposure to both VX and PO. Injections of up to 150 micrograms/kg of VX with antidotes did not cause locomotor or histological signs of organophosphorus-induced delayed neuropathy, but single injections of 400 mg TOCP/kg did.

Acetylcholinesterase↗

PubMed1988

Relationship between transmural potential difference and smooth muscle slow waves and contractility in the rabbit small intestine in vitro.

The relationship between transmural potential difference (PD) and smooth muscle electrical and mechanical activity was investigated in the rabbit ileum in vitro. Transmural PD was monitored using agar salt bridge electrodes connected via calomel half cells to an electrometer. Force displacement transducers recorded predominantly longitudinal smooth muscle activity. Concurrently, predominantly circular muscle activity was recorded at three sites using intraluminal pressure probes. At the same sites, suction electrodes monitored electrical activity of the smooth muscle. In all experiments, fluctuations in transmural PD were temporally linked to smooth muscle mechanical and electrical activity. The frequency of PD oscillations, electrical slow waves, and cyclic pressure changes were identical within each segment. Adrenaline abolished smooth muscle electrical spiking, all mechanical activity, and transmural fluctuations in PD. However, the slow waves were not abolished, though their frequency was increased. Phentolamine but not propranolol reversed the effects of adrenaline, thus slow wave frequency is influenced by alpha-adrenergic stimulation in the rabbit ileum. In conclusion, oscillations in transmural PD are unrelated to the ionic processes associated with the slow wave. However, they are in some way linked to smooth muscle contractile activity, possibly via an intrinsic neural mechanism as observed in the guinea pig.

Animals↗

PubMed1988

Electrical coupling and pacemaker activity in colonic smooth muscle.

The effect of heptanol on electrical coupling between submucosal circular muscle cells of the dog colon and consequences for slow-wave activity were investigated. Electrotonic potentials showed exponential decay giving a length constant of 2.6 +/- 0.5 mm and a time constant of 157 +/- 48 ms. Heptanol reversibly abolished electrotonic current spread, and subsequently no slow-wave activity was recorded. The length constant decreased to less than 0.2 mm. The input resistance increased from 3 to 36 M omega, suggesting a change from tissue syncytium to electrically isolated cells. D600 (5 X 10(-6) M) also abolished slow wave activity but had opposite effects on electrotonic current spread. The data are consistent with the hypothesis that heptanol reversibly inhibits intercellular coupling, resulting in loss of spread of extracellularly applied current, uncoupling of cells, and loss of pacemaker activity. Regulation of intercellular communication may be important in the control of intestinal motility.

Alcohols↗

PubMed1988

Electrotonic current spread in colonic smooth muscle.

Current-induced changes in the membrane potential (electrotonic potentials) were measured intracellularly. The electrotonic potentials were seen to decay exponentially over many cells, suggesting electrotonic current spread. The characteristics of the electrotonic current spread were used to determine passive membrane properties of both circular and longitudinal muscle cells of human and dog colon. Electrotonic current spread was first determined along the long axes of the cells. The space constant of the circular muscle of human colon was 2.14 mm and that of the longitudinal muscle was 1.63 mm. The space constants for the dog colon were similar. The value for the time constant of dog colon circular muscle was 160 ms, whereas much higher time constants, averaging between 500 and 800 ms, were recorded from dog longitudinal muscle and both human colon muscle layers. These data suggest good electrotonic coupling in all tissues studied, along the long axes of the cells. They further suggest a relatively high membrane resistance and junctional resistance in the longitudinal muscle. Electrotonic coupling along the short axes of circular muscle cells, along the long axis of the colon, was studied in the dog. The space constant was 0.43 mm, suggesting a relatively high resistance to current flow along the short axes of the cells. In addition, along the short axes of the cells from the submucosa to the myenteric plexus side (i.e., in radial direction) a gradient was observed in resting membrane potential, slow-wave amplitude, and rate of rise of the slow-wave upstroke.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Automated temperature control system for vagal cooling.

An automated cooling system for vagal cold blockade was developed. A simple electronic circuit is described that enabled regulation of the steady-state nerve or circulant temperature to within +/- 0.1 degree C by alternating the cold circulant between low and high flows (10 and 350 ml/min, respectively). The 90% rise time ranged from 15 to 40 s depending on the desired steady state and the surrounding temperatures. The present apparatus can be conveniently and safely used, especially for differential vagal cold blockade.

Animals↗

PubMed1988

Ventilatory responses to increased blood flow and decreased lung volume in awake dogs.

The effect of decreased lung volume on ventilatory responses to arteriovenous fistula-induced increased cardiac output was studied in four chronic awake dogs. Lung volume decreases were imposed by application of continuous negative-pressure breathing of -10 cmH2O to the trachea. The animals were surgically prepared with chronic tracheostomy, indwelling carotid artery catheter, and bilateral arteriovenous femoral shunts. Control arteriovenous blood flow was 0.5 l/min, and test flow level was 2.0 l/min. Arterial blood CO2 tension (PaCO2) was continuously monitored using an indwelling Teflon membrane mass spectrometer catheter, and inhaled CO2 was given to maintain isocapnia throughout. Increased fistula flow alone led to a mean 52% increase in cardiac output (CO), whereas mean systemic arterial blood pressure (Psa) fell 4% (P less than 0.01). Negative-pressure breathing alone raised Psa by 3% (P less than 0.005) without a significant change in CO. Expired minute ventilation (VE) increased by 27% (P less than 0.005) from control in both of these conditions separately. Combined increased flow and negative pressure led to a 50% increase in CO and 56% increase in VE (P less than 0.0025) without any significant change in Psa. Effects of decreased lung volume and increased CO appeared to be additive with respect to ventilation and to occur under conditions of constant PaCO2 and Psa. Because both decreased lung volume and increased CO occur during normal exercise, these results suggest that mechanisms other than chemical regulation may play an important role in the control of breathing and contribute new insights into the isocapnic exercise hyperpnea phenomenon.

Animals↗

PubMed1988

Lung hyperinflation in isolated dog lungs during high-frequency oscillation.

To study the phenomenon of lung hyperinflation (LHI), i.e., an increase in lung volume without a concomitant rise in airway pressure, we measured lung volume changes in isolated dog lungs during high-frequency oscillation (HFO) with air, He, and SF6 and with mean tracheal pressure controlled at 2.5, 5.0, and 7.5 cmH2O. The tidal volume and frequency used were 1.5 ml/kg body wt and 20 Hz, respectively. LHI was observed during HFO in all cases except for a few trials with He. The degree of LHI was inversely related to mean tracheal pressure and varied directly with gas density. Maximum expiratory flow rate (Vmax) was measured during forced expiration induced by a vacuum source (-150 cmH2O) at the trachea. Vmax was consistently higher than the peak oscillatory flow rate (Vosc) during HFO, demonstrating that overall expiratory flow limitation did not cause LHI in isolated dog lungs. Asymmetry of inspiratory and expiratory impedances seems to be one cause of LHI, although other factors are involved.

Airway Resistance↗