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C P Cheng

Publications and source records attributed to C P Cheng.

At least 55 records · Page 3Linked to original sources
PubMed1993

Effect of exercise on left ventricular-arterial coupling assessed in the pressure-volume plane.

The left ventricle (LV) and arterial system are nearly optimally coupled to produce stroke work (SW) at rest. However, the effect of exercise on the coupling between the LV and arterial system has not been directly determined. We evaluated 11 dogs who were instrumented to determine LV volume from three diameters. The LV end-systolic pressure (Pes)-volume (Ves) relation was determined by transient caval occlusion at rest and while the animals ran at 5-7 mph on a treadmill. During exercise, the Pes-Ves relation was shifted toward the left and the slope [end-systolic elastance (Ees)] increased from 7.7 +/- 2.8 to 12.7 +/- 4.2 (SD) mmHg/ml (P < 0.05). The arterial end-systolic elastance (Ea), calculated as Pes divided by stroke volume, increased during exercise (8.8 +/- 3.0 to 10.9 +/- 4.7 mmHg/ml, P < 0.05). The ratio of Ees to Ea increased during exercise from 0.89 +/- 0.31 to 1.27 +/- 0.12 (P < 0.05). The portion of the pressure-volume area expressed as SW increased during exercise from 0.63 +/- 0.07 to 0.69 +/- 0.10 (P < 0.05). After adrenergic blockade, the Ees-to-Ea ratio was not significantly altered during exercise (0.90 +/- 0.24 vs. 0.83 +/- 0.15, P = NS). At rest and during exercise, both with intact reflexes and after beta-adrenergic blockade, the ratio of Ees to Ea remained within the range in which SW is > 95% of maximum. We conclude that during exercise, beta-adrenergic stimulation shifts the LV Pes-Ves relation to the left with an increased slope. This more than offsets the increase in Ea.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1993

Curvilinearity of LV end-systolic pressure-volume and dP/dtmax-end-diastolic volume relations.

We investigated the effect of contractile state (CS) on the curvilinearity of the left ventricular (LV) end-systolic pressure-volume (Pes-Ves) and the dP/dtmax-end-diastolic volume (dP/dtmax-Ved) relations in eight anesthetized open-chest dogs. LV volume was determined from three orthogonal diameters measured by sonomicrometry. The Pes-Ves relation and dP/dtmax-Ved relation were assessed during transient vena caval occlusion and aortic constriction, while CS was altered with dobutamine. At all CS, both relations were linear when volumes were decreased by caval occlusion. However, at higher volumes obtained by aortic constriction, the relations became nonlinear. At enhanced CS, the nonlinearity of both the Pes-Ves relation and the dP/dtmax-Ved relation increased. The dP/dtmax-Ved relation began to deviate from linearity at larger volumes, but closer to baseline operating volume, than the Pes-Ves relation. The relation between end-systolic mean circumference stress and wall strain (sigma es-epsilon es) was linear at control CS when the Pes-Ves relation was nonlinear but became nonlinear with enhanced CS. We conclude that both the Pes-Ves relation and the dP/dtmax-Ved relation are nonlinear, saturating at higher volumes. With increased CS, the nonlinearity of both relations increases. This CS-dependent curvilinearity of the Pes-Ves relation is due to both CS-dependent nonlinearity of the sigma es-epsilon es relation (consistent with length-dependent activation) and geometric factors that alter the relation between Pes and sigma es.

Animals↗
PubMed1993

Effect of heart failure on the mechanism of exercise-induced augmentation of mitral valve flow.

The exercise response of left ventricular (LV) filling dynamics may be altered by congestive heart failure (CHF). Accordingly, we studied 18 conscious dogs, instrumented to measure micromanometer LV and left atrial (LA) pressures and determine LV volume from three dimensions. CHF was produced by 4-5 weeks of right ventricular rapid pacing. Before CHF, exercise (5.5-8.5 mph for 8-15 minutes) increased the maximum rate of LV filling (dV/dtmax) (197 +/- 37 versus 297 +/- 56 ml/sec [mean +/- SD], p < 0.05) in response to an increase in the maximum early diastolic LA to LV pressure gradient (5.8 +/- 2.0 versus 9.8 +/- 1.9 mm Hg, p < 0.05) produced by a fall in minimum LV pressure (1.0 +/- 2.9 versus -3.9 +/- 3.1 mm Hg, p < 0.01), whereas mean LA pressure was unchanged (6.4 +/- 3.1 versus 6.4 +/- 4.2 mm Hg, p = NS). The time constant of LV relaxation was shortened (28.1 +/- 3.2 versus 21.0 +/- 4.2 msec, p < 0.05). After CHF, dV/dtmax (141 +/- 51 versus 200 +/- 59 ml/sec, p < 0.05) and the maximum LA to LV pressure gradient (6.0 +/- 1.1 versus 11.1 +/- 2.7 mm Hg, p < 0.05) continued to increase with exercise (3-5.0 mph for 4-8 minutes). However, the time constant of LV relaxation was prolonged (35.6 +/- 4.8 versus 38.9 +/- 5.5 msec, p < 0.05), and minimum LV pressure (15.1 +/- 5.6 versus 17.6 +/- 5.9 mm Hg, p < 0.05) and mean LA pressure increased (22.6 +/- 7.2 versus 29.1 +/- 7.3 mm Hg, p < 0.05). These altered effects of exercise on LV diastolic filling dynamics persisted when heart rate and wall stress during exercise before and after CHF were matched by varying the level of exercise. We conclude that, during normal exercise, mitral valve flow is augmented by a fall of early diastolic LV pressure without a rise in LA pressure. After CHF, early diastolic LV pressure does not fall but increases during exercise. Thus, the increase in the early diastolic LA to LV pressure gradient and the rate of mitral valve flow results from an increase in LA pressure during exercise after CHF. This study suggests that the failure of the enhancement of LV relaxation and an increase in early diastolic LV pressure with exercise after CHF may contribute to exercise intolerance in CHF.

Adrenergic beta-Antagonists↗
PubMed1992

Mechanism of augmented rate of left ventricular filling during exercise.

At rest, most of left ventricular (LV) filling occurs early in diastole. This LV filling occurs in response to the pressure gradient produced as LV pressure falls below left atrial (LA) pressure. Because mitral valve flow occurs in response to an LA to LV pressure gradient, augmented diastolic mitral valve flow during exercise may be due to an increased mitral valve pressure gradient resulting from a rise in LA pressure and/or a fall in LV early diastolic pressure. Accordingly, we studied 13 conscious dogs, instrumented to measure micromanometer LV and LA pressures, and determined LV volume from three ultrasonic dimensions during exercise. The animals ran on a treadmill for 8-15 minutes at 5-8 miles/hr. With reflexes intact, during exercise, the heart rate increased from 116 +/- 20 to 189 +/- 24 beats per minute (mean +/- SD, p less than 0.01), the maximum rate of change of LV volume (dV/dtmax) increased from 185 +/- 44 to 282 +/- 76 ml/sec (p less than 0.01), the ejection fraction and cardiac output increased, and the duration of diastole decreased from 296 +/- 83 to 162 +/- 71 msec (p less than 0.01). Mitral valve opening pressure, mean LA pressure (10.9 +/- 4.4 versus 10.2 +/- 3.9 mm Hg, p = NS), and LV end-diastolic pressure (12.8 +/- 4.8 versus 13.1 +/- 3.3 mm Hg, p = NS) were all relatively unchanged. The time constant of the fall of isovolumic LV pressure decreased from 28 +/- 3.3 to 21 +/- 4.4 msec (p less than 0.05). The early diastolic portion of the LV pressure-volume loop was shifted downward during exercise, with the minimum LV pressure decreasing from 3.3 +/- 2.8 to -2.8 +/- 3.4 mm Hg (p less than 0.05) and the maximum mitral valve pressure gradient increasing from 5.5 +/- 1.7 to 11.8 +/- 3.5 mm Hg (p less than 0.01). A similar downward shift of the early diastolic portion of the LV pressure-volume loop was produced by infusion of dobutamine (6 micrograms/kg/min i.v.) at rest, as well as by exercise when the heart rate was held constant by right ventricular pacing at 190-210 beats per minute. The downward shift during exercise was prevented by beta-blockade (metoprolol, 0.5 mg/kg i.v.). We conclude that during exercise, sympathetic stimulation and tachycardia produce a downward shift of the early diastolic portion of the LV pressure-volume loop.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗
PubMed1991

Left ventricular ejection activation in the in situ heart.

We tested, in the in situ heart, the hypothesis that the end-systolic pressure (ESP) of small ejecting contraction (EC) is greater than that of an isovolumic contraction (IC) with a similar end-systolic volume. We produced ECs with varying amounts of ejection by partial aortic occlusion while measuring left ventricular pressure, one or two left ventricular dimensions (anteroposterior and septal-lateral), and aortic flow. In 11 dogs, we plotted ventricular pressure against the time integral of aortic flow of ECs and IC with the same end-diastolic anteroposterior dimension. The end-systolic pressure-volume line was drawn from the peak isovolumic pressure-volume point tangential to the left upper corner of the pressure-volume loop of ECs. The slope of the tangential line of the middle EC, whose stroke volume was 51 +/- 8% of that of the control EC, was decreased by 54 +/- 16% compared with that of the control EC. In eight dogs with two pairs of crystals, left ventricular volume was controlled by partial vena caval occlusion, and ICs were produced by total aortic occlusion. The end-systolic pressure of small ejections exceeded (11.3 +/- 7.7 mmHg, P less than 0.01) those of isovolumic contractions with the same end-systolic cross-sectional area, whereas the end-systolic pressure of beats with large ejections was similar (-9.4 +/- 14.4 mmHg, P = NS) to an IC with the same end-systolic cross-sectional area. We conclude that the end-systolic pressure-volume point of beats with a small ejection is located above the isovolumic end-systolic pressure-volume relation in the in situ dog left ventricle.

Animals↗
PubMed1991

Left ventricular-arterial coupling in conscious dogs.

We investigated the criteria for the coupling of the left ventricle (LV) and the arterial system to maximize LV stroke work (SW) and the transformation of LV pressure-volume area (PVA) to SW. We studied eight conscious dogs that were instrumented to measure LV pressure and determine LV volume from three ultrasonically determined dimensions. The LV end-systolic pressure (PES)-volume (VES) relation was determined by caval occlusion. Its slope (EES) was compared with the arterial elastance (EA) and determined as PES per stroke volume. At rest, with intact reflexes, EES/EA was 0.96 +/- 0.20 EES/EA was varied over a wide range (0.18-2.59) by the infusion of graded doses of phenylephrine and nitroprusside before and during administration of dobutamine. Maximum LV SW, at constant inotropic state and end-diastolic volume (VED), occurred when EES/EA equaled 0.99 +/- 0.15. At constant VED and contractile state, SW was within 20% of its maximum value when EES/EA was between 0.56 and 2.29. The conversion of LV PVA to SW increased as EES/EA increased. The shape of the observed relations of the SW to EES/EA and SW/PVA to EES/EA was similar to that predicted by the theoretical consideration of LV PES-VES and arterial PES-stroke volume relations. We conclude that the LV and arterial system produce maximum SW at constant VED when EES and EA are equal; however, the relation of SW to EES/EA has a broad plateau. Only when EA greatly exceeds EES does the SW fall substantially. However, the conversion of PVA to SW increases as EES/EA increases. These observations support the utility of analyzing LV-arterial coupling in the pressure-volume plane.

Animals↗
PubMed1991

[Effect of K+, Na+ ionic channel blocker on progesterone production by rat corpus luteal cells].

Two ionic channel blockers, TEA and TTX, were used in the present investigation to test whether blocking of Na+, K+ ion channels would affect the production of progesterone by corpus luteum (CL) cells of rat. Both TEA (10(-3) mol/L) and TTX (10(-3) mol/L) increased progesterone production significantly after treatment. This effect of the blockers could be completely inhibited by tyrosine (Tyr). In addition, Tyr was capable of reversing the combined effect of TEA, TTX and hCG on progesterone secretion. It is suggested that the concentration gradient of Na+ and K+ across the CL cell membrane in experiments mentioned above is implicated in steroidogenesis.

Animals↗
PubMed1991

[Effect of ANP on estradiol and progesterone production by rat ovarian cells].

Isolated ovarian corpus luteal cells and granulosa cells of rat were employed to investigate the effect of alpha-ANP on the secretion of progesterone and estradiol. The contents of the steroid hormones are determined by RIA. The results showed that 0.1-10 ng/ml ANP promoted progesterone production in a dose dependent manner. alpha-ANP also enhanced progesterone production by granulosa cells, but not estradiol. It seems that the effect of alpha-ANP on ovarian steroidogenesis is a direct one.

Animals↗
PubMed1991

Effect of felodipine on left ventricular performance in conscious dogs: assessment by left ventricular pressure-volume analysis.

We assessed the effect of felodipine on left ventricular (LV) performance in 10 healthy, conscious, chronically instrumented dogs, using load-independent measures derived from variably loaded pressure-volume relations. With all reflexes intact, felodipine (25 nmol/kg, intravenously) caused significant decreases in LV end-systolic pressure (132 +/- 13 vs. 109 +/- 14 mm Hg, P less than .05) and effective arterial elastance (11.1 +/- 1.6 vs. 8.7 +/- 1.1 mm Hg/ml, P less than .01), while the heart rate increased (109 +/- 15 vs. 118 +/- 16 min-1, P less than .05). There were no significant changes in LV end-systolic volume, stroke volume or the maximum time derivative of LV pressure. The plasma felodipine concentration was 16.1 +/- 1.4 nmol/l (mean +/- time S.D.). Three relations that provide load-insensitive measures of LV performance were determined from variably loaded pressure-volume loops produced by transient caval occlusions. Felodipine increased the slopes of the LV end-systolic pressure-volume relation (8.1 +/- 0.9 vs. 10.3 +/- 1.3 mm Hg/ml, mean +/- S.D., P less than .05), the maximal time-derivative of LV pressure-end-diastolic volume relation (103 +/- 28 vs. 127 +/- 34 mm Hg/sec ml, P less than .05) and the stroke work-end diastolic volume relation (82 +/- 4 vs. 93 +/- 6 mm Hg, P less than .05). All three relations were shifted toward the left after felodipine. Similar increases in slopes and leftward shifts with felodipine, indicating enhanced contractile effect, were also present after autonomic blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

[Free tyrosine and progesterone receptor contents in the rat uterine endometrial cytosol during oestrous cycle].

Free tyrosine in the rat uterine endometrial cytosol at different phases of the oestrous cycle was measured by HPLC. It was found that the content of tyrosine varied at different phases of the oestrous cycle in the normal rat, i.e. being lowest in proestrus and highest in metestrus, while the progesterone receptor content in the same cytosol sample determined by radio-receptor technique showed an opposite relationship. Experiments showed that the tyrosine content and progesterone receptor content displayed periodic but opposite changes at the two phases of the oestrous cycle. Furthermore, administration of tyrosine to the uterine lumen decreased significantly the contents of progesterone receptor in proestrus, oestrus and diestrus, but not in metestrus. It is suggested that tyrosine might exert a certain regulatory influence on the progesterone receptor content in rat uterine endometrium.

Animals↗
PubMed1990

Simultaneous conductance catheter and dimension assessment of left ventricle volume in the intact animal.

We compared left ventricle (LV) volume (V) simultaneously measured using the conductance catheter (VM) with volume calculated from three LV dimensions (VD) determined ultrasonically from endocardial crystals. Seven adult mongrel dogs (20-30 kg) were anesthetized and instrumented to measure micromanometer LV pressure and V. Three pairs of crystals were placed orthogonally in subendocardial positions and a conductance catheter was placed in the LV retrograde across the aortic valve. Under steady-state conditions, over the range of a single cardiac cycle, the relation between VM and VD was well described by a straight line. There was an excellent correlation of conductance and dimension volumes with r equal to 0.97 +/- 0.04 and SEE 0.8 +/- 0.5 ml. The gain (1/alpha) and parallel conductance volume (alpha VC) were constant. At lower volumes obtained during bicaval occlusion, however, the relation between VM and VD was curvilinear. 1/alpha and alpha VC both decreased as LVV fell. Thus, determination of absolute volume using the conductance catheter depended on the conditions under which the data were obtained. Under steady-state conditions, alpha VC calculated by both the saline method (mean +/- SD, 50 +/- 15 ml) and by regression of VM and VD, (45 +/- 21 ml) were similar. Consequently, absolute LV end-diastolic volumes and end-systolic volumes by the conductance and dimension methods were similar (53 +/- 14 ml and 38 +/- 14 ml vs. 56 +/- 17 ml and 44 +/- 16 ml, respectively, p = NS). When volume decreased during bicaval occlusion, there was a progressively greater decrease in VM as compared with VD. The absolute slope (EES) of the end-systolic pressure-volume relation (ESPVR) was consistently higher by the dimension method, group average, 16.3 +/- 7.6, than by the catheter, 8.5 +/- 5.9, p less than 0.05. The direction and magnitude of the change in EES at different inotropic states (autonomic blockade; dobutamine), however, was similarly measured by both the conductance catheter and dimension method. We conclude that the gain and offset of the conductance catheter are relatively constant at steady state but vary when volume is reduced by caval occlusion. Thus, the conductance catheter accurately measures absolute volumes at steady state but can underestimate the slope and position of the ESPVR when it is determined by caval occlusion. The conductance catheter does, however, accurately measure the directions and magnitude of change in contractile state.

Animals↗
PubMed1990

Effect of loading conditions, contractile state, and heart rate on early diastolic left ventricular filling in conscious dogs.

We investigated left ventricular (LV) early diastolic filling in 10 normal conscious dogs that had been previously instrumented to measure LV and left atrial (LA) pressures and three orthogonal LV internal dimensions. LV volume was calculated as a general ellipsoid. The pressure within a passive structure increases as it is filled. If myocardial relaxation is rapid enough to substantially aid LV diastolic filling, it may overcome this effect and cause LV pressure to fall despite an increase in volume. Thus, we defined the amount of LV filling that occurred while LV pressure was falling as relaxation filling, which is a measure of the importance of LV relaxation during early diastolic filling. The time constant of relaxation (T) was derived from the exponential fall of LV pressure during isovolumic relaxation. While LV pressure was falling early in diastole (the relaxation filling period), all three LV diameters increased. Autonomic blockade with hexamethonium (5 mg/kg) and atropine (0.1 mg/kg) reduced relaxation filling from 21 +/- 6% (mean +/- SD) to 12 +/- 3% of the stroke volume (p less than 0.01). The mean LA pressure also was significantly decreased (from 12 +/- 2 to 10 +/- 5 mm Hg, p less than 0.05), while the duration of the relaxation filling period and T were unchanged. Positive inotropic stimulation with dobutamine (10 micrograms/kg/min) shortened T without changing LA pressure. The maximum LA-LV pressure gradient, dV/dtmax, and relaxation filling all increased. Augmented preload produced by dextran infusion (500 ml/10 min) caused an increase in LA pressure (from 11 +/- 3 to 21 +/- 8 mm Hg, p less than 0.05) without altering T. This also increased the maximum LA-LV pressure gradient, dV/dtmax, and relaxation filling. Augmented afterload produced by methoxamine (10 mg/3 min i.v.) significantly increased LA pressure (from 9 +/- 4 to 15 +/- 10 mm Hg, p less than 0.05) and lengthened T (from 35 +/- 4 to 50 +/- 7 msec, p less than 0.05) and the duration of relaxation filling (from 36 +/- 5 to 44 +/- 9 msec, p less than 0.01) without altering the maximum LA-LV pressure gradient, dV/dtmax, or LV relaxation filling. Incremental changes in heart rate induced by atrial pacing (from 100-180 beats/min) resulted in progressive decreases in the time constant of LV relaxation and the duration of relaxation filling. The LA pressure was also decreased. There was no corresponding increase in the amount of active LV filling until the heart rate reached 180 beats/min. During all these interventions, T correlated with the duration of LV relaxation filling (r = 0.99. p less than 0.05). The amount of relaxation filling and dV/dtmax both correlated with the maximum LA-LV pressure gradient.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Acute effects of mildly intoxicating levels of alcohol on left ventricular function in conscious dogs.

We assessed the effect of alcohol, before and after autonomic blockade, on left ventricular (LV) performance in conscious dogs. 10 animals were instrumented to determine LV volume from ultrasonic LV internal dimensions and measure LV pressure with a micromanometer. The animals were studied in the conscious state after full recovery from the operation. Blood alcohol was undetectable before and 67 +/- 14 mg/dl (mean +/- SD) at 20 min after alcohol administration. In response to alcohol, the LV systolic pressure was reduced slightly, the left ventricular end-diastolic pressure increased slightly. The maximum time derivative of LV pressure (dP/dtmax) and stroke volume were decreased. The end-systolic volume (VES), as well as effective arterial elastance, were significantly increased. There was no significant change in heart rate. Variably loaded pressure-volume loops were generated by acute caval occlusion before, immediately, and 20 min after the intravenous infusion of alcohol (0.2 g/kg). Three measures of LV performance were derived from these variably loaded pressure-volume loops: the end-systolic pressure-volume relation; the stroke work-end-diastolic volume relation; and maximum dP/dt-VED relation. The slopes of all three relations were significantly decreased in response to alcohol, and all three relations were shifted toward the right, indicating a depression of LV contractile performance. Similar, but greater depressions of LV performance with alcohol were observed following autonomic blockade. LV performance was restored by infusing dobutamine. We conclude that mildly intoxicating levels of alcohol (blood concentration less than 100 mg/dl) are capable of producing LV contractile depression in conscious animals, which is more marked after autonomic blockade. This suggests that patients with impaired LV function should avoid even small amounts of alcohol.

Animals↗
PubMed1989

Results of surgical treatment in 6,123 cases of carcinoma of the esophagus and gastric cardia.

Six thousand one hundred twenty-three cases of carcinoma of the esophagus and gastric cardia were treated surgically from 1965 to 1985. Overall resectability was 89.9%. Postoperative mortality was 3%, and incidence of postoperative complication, 10.3%. Follow-up rate was 91.3%, with 5 year survival of 36.8% (esophageal nearly twice that of gastric cardia), and 10 year survival of 17.2%. Factors affecting long-term survival were clinicopathologic staging and preoperative irradiation. Early discovery and timely treatment are the key to high resectability and improved long-term survival. More efficacious combined therapies are needed for the predominant late cases. We propose more radical resection because of the multifocal tendency of esophageal and extensive submucosal infiltration of cardia carcinoma. Continuing refinements of surgical technique helped to reduce postoperative leakage and structure.

Adult↗
PubMed1989

Comparison of measures of left ventricular contractile performance derived from pressure-volume loops in conscious dogs.

Three measures of left ventricular (LV) performance derived from pressure (P)-volume (V) loops have been proposed: the end-systolic P-V (PES-VES) relation, the stroke work-end-diastolic V (SW-VED) relation, and maximum dP/dt-VED (dP/dtmax-VED) relation. We evaluated the variability of repeated determinations, and inotropic and load sensitivity of these relations in conscious dogs. LVV was determined from three orthogonal LV diameters measured by sonomicrometry. Three to six sets of variably loaded P-V loops were generated by transient caval occlusions before and again after increasing inotropic state by infusing dobutamine (6 +/- 1 microgram/kg/min, mean +/- SD) and after increasing PES by 49 +/- 17 mm Hg with phenylephrine following autonomic blockade. The slope (MSW) of the SW-VED relation was the least variable at constant inotropic state (coefficient of variation, 4 +/- 3%) compared with the slope (EES) of the PES-VES relation (8 +/- 3%) or the slope (dE/dtmax) of the dP/dtmax-VED relation (11 +/- 6%, p less than 0.05). The extrapolated volume-axis intercept of the SW-VED relation was much less variable than the intercepts of the PES-VES or dP/dtmax-VED relations. MSW, EES, and dE/dtmax all increased (p less than 0.05) in response to dobutamine. The extrapolated volume-axis intercepts of the PES-VES and dP/dtmax-VED relations increased with dobutamine, whereas the volume intercept of the SW-VED relation was unchanged. MSW had the smallest increase in response to dobutamine (124 +/- 22% of control) compared to EES (178 +/- 67% of control) and dE/dtmax (211 +/- 68% of control, p less than 0.05). The position of the PES-VES relation, quantified as the VES at PES = 100 (V100), showed less variability (2 +/- 1%) than the slope of the PES-VES relation (8 +/- 3%, p less than 0.05). V100 decreased from 30.8 +/- 17.4 to 26.7 +/- 13.7 ml during dobutamine (p less than 0.05). After phenylephrine, EES, MSW, and dE/dtmax decreased by less than 10% (p = NS). The PES-VES relation shifted to the left with this increased afterload and V100 decreased by 3.2 +/- 1.5 ml (p less than 0.05), whereas the position of the SW-VED and dp/dtmax-VED relations were relatively unchanged.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

[The content of tyrosine in rat luteal cell and the changes caused by hCG, cAMP and progesterone].

The ovaries taken from the immature female rats primed with PMSG-hCG were digested with collagenase-DNAase solution to obtain the luteal cell suspensions. Luteal cells were then incubated with different doses of hCG, cAMP or progesterone for 1.5 hours. The contents of tyrosine in luteal cell suspensions were determined by thin layer chromatogram using dual-wavelength chromatogram scanner. It was found that the content of tyrosine in rat luteal cell suspensions was 1.41 + 0.24 nmol/L/10(6) cells after one hour incubation. hCG, cAMP and progesterone all could significantly increase the content of tyrosine in the suspensions, suggesting the release of "endogenous tyrosine". The increase of tyrosine was not due to increased transformation of phenylalanine, the precursor of tyrosine, and increased protein synthesis, because both phenylalanine and cycloheximide failed to influence such increase.

Animals↗
PubMed1988

Effect of combined treatment of anti-inflammatory drug and mannoheptulose on the production of tumour necrosis factor and endotoxin shock in mice.

The endotoxin shock induced in mice by injection of viable Listeria monocytogenes and challenged with endotoxin can be alleviated by combined administration of mannoheptulose with acetylsalicylate or sulindac. The ability of animals to secrete tumour necrosis factor into the blood was, however, not affected. The significance of these observations are discussed.

Animals↗