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Biomedical subjects

K C Chang

Publications and source records attributed to K C Chang.

At least 127 records · Page 7Linked to original sources

Immobilization of chitinase on a reversibly soluble-insoluble polymer for chitin hydrolysis.

Serratia marcescens chitinase was immobilized by covalent binding to a polymer (hydroxypropyl methylcellulose acetate succinate, AS-L) showing reversibly soluble-insoluble characteristics with pH change. The immobilized enzyme (CH-AS) was soluble above pH 5.2 and insoluble below 4.5, which offers advantages in that it can carry out hydrolysis of chitin particles in a soluble form yet be recovered after precipitation at low pH. CH-AS has much higher activity than chitinase immobilized to a water-insoluble carrier. The effects of pH and temperature on the activity and stability of CH-AS, and the adsorption of CH-AS to chitin were studied and compared with those of free chitinase. Following repeated pH cycles between 6.6 and 4.5, CH-AS lost 30% of its enzyme activity during the first cycle due to protein release and enzyme denaturation, but substantially less activity was lost in the following cycles, with minimum enzyme denaturation. Chitin hydrolysis with CH-AS could be carried out in a semi-batch mode with intermittent enzyme precipitation and product removal, this can enhance product yield up to 1.4-fold when compared with batch reaction.

Acetylglucosamine↗

The correlation of cardiac mass with arterial haemodynamics of resistive and capacitive load in rats with normotension and established hypertension.

In hypertensive animals and humans, cardiac hypertrophy may occur as a consequence of an external load on the heart. Several studies have suggested that the non-pulsatile components of arterial haemodynamics, such as arterial pressure and vascular resistance, do not adequately represent the ventricular afterload and are not well correlated with the degree of cardiac hypertrophy (CH). The present study was undertaken to analyse the correlation between the degree of CH and various haemodynamic parameters in the spontaneously hypertensive rat (SHR) with established hypertension. A total of 36 SHRs (6-8 months) with a tail-cuff pressure above 190 mm Hg were used. Control data were obtained from 32 age-matched normotensive Wistar Kyoto rats (WKY). Animals were anaesthetized with pentobarbitone sodium (40 mg/kg i.p.) and artificially ventilated with a respirator. A Millar catheter with a high-fidelity pressure sensor was used to record the aortic pressure and an electromagnetic flow transducer to monitor the aortic flow. The pressure and flow signals were subjected to Fourier transformation for the analysis of the arterial impedance spectrum. The left ventricular weight-to-body weight ratio (LVW/BW) was taken as a measure of the degree of CH. The measured haemodynamic parameters in these anaesthetized, open-chest SHRs were systolic pressure (SP) (mean +/- SE) 172 +/- 4 mm Hg, diastolic pressure (DP), 120 +/- 3 mm Hg, pulse pressure (PP) 52 +/- 2 mm Hg, peripheral resistance (Rp) 344,032 +/- 8,012 dyne.s.cm-5, characteristic impedance (Zc) 6,442 +/- 313 dyne.s.cm-5, the impedance modulus at the first harmonic (Z1) 26,611 +/- 1,061 dyne.s.cm-5, mean arterial compliance (Cm) 0.87 +/- 0.04 microliter/mm Hg and LVW/BW 3.092 +/- 0.026 mg/g.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cardiovascular effect of a naphthylmethyl substituted tetrahydroisoquinoline, YS 49, in rat and rabbit.

A novel tetrahydroisoquinoline, 1-alpha-naphthylmethyl-6,7-dihydroxy-1,2,3,4- tetrahydroisoquinoline (YS 49) 1) increased heart rate and force in isolated rat atria; 2) relaxed PE- and KCl-contracted rat aorta, and 3) decreased blood pressure and increased heart rate in anesthetized rabbit. These effects were blocked by propranolol, a nonselective beta-antagonist, but not by phentolamine, an alpha-blocker, and/or depletion of catecholamine by reserpine. These results suggest that the mechanism of action of YS 49 is due, at least in part, to beta-adrenergic receptor stimulation.

Animals↗

Photo-induced adequate nitric oxide (PIANO)-mediated relaxation in isolated rabbit corpus cavernosum.

1. We further investigated our earlier proposal that NO- and NO2-carrying molecules potentiate photorelaxation using isolated rabbit corpus cavernosum. 2. Corporal smooth muscle, in the presence or absence of endothelium, relaxed only slightly upon u.v. light (366 nm) irradiation. But, NO- and/or NO2-containing compounds such as streptozotocin and NG-nitro-L-arginine methyl ester significantly (P < 0.01) enhanced photorelaxation in this tissue. In addition, NG-nitro-D-arginine methyl ester, known to lack inhibitory action on NO synthase, showed concentration-dependent potentiation of the photorelaxation. 3. Oxygen radical generating system via xanthine+xanthine oxidase and guanylate cyclase inhibitor, methylene blue, significantly (P < 0.05) inhibited the streptozotocin-potentiated photorelaxation. 4. Nitrite was accumulated by photolysis of streptozotocin, NG-nitro-L-arginine methyl ester and NG-nitro-D-arginine methyl ester, in a concentration and exposure time-dependent manner. 5. These observations indicate that NO is a potent relaxant of rabbit corpus cavernosum and further support our hypothesis that NO is released by photolysis from NO- and NO2-carrying molecules.

Animals↗

Exponentially tapered t-tube model of systemic arterial system in dogs.

This study determines the role of an asymmetric T-tube model as a representation of arterial mechanical properties. The model consists of two non-uniform tubes connected in parallel. The non-uniform properties of each tube include geometric and elastic tapering and each tube terminates in a complex load. Pulsatile pressure and flow velocity of the ascending aorta were measured in 10 closed-chest, anaesthetized dogs. An exponentially tapered transmission line is used to describe the non-uniform properties of the vasculature. The phase constant is a function of position along the path length due to geometric and elastic tapers. This non-uniform T-tube model makes it possible to fit the measured pressure waveform in the ascending aorta. Model parameters could be estimated and used to interpret the physical properties of the arterial system. The mathematical and experimental model impedance spectra are similar. There is a close correspondence between the impedance parameters derived from the non-uniform T-tube model and values computed from measurements on dogs. The results suggest that inclusion of tube tapering improves the mathematical model so that it closely represents the experimentally derived arterial impedance in closed-chest dogs. We conclude that the non-uniform properties of wave-transmission paths may play an important role in governing the behaviour of an asymmetric T-tube for the description of the arterial system.

Animals↗

Impaired left ventricular relaxation and arterial stiffness in patients with essential hypertension.

1. This study was designed to determine how left ventricular relaxation function in patients with essential hypertension is impaired by arterial haemodynamic load that is increased in early ejection phase. These patients did not suffer from cardiac hypertrophy or disturbed coronary perfusion. We used a high-fidelity multisensor catheter to record pressure and flow signals in the ascending aorta. The timing and magnitude of wave reflection were obtained by decomposing the measured waves into their forward and backward components. Radionuclide angiography was employed to obtain the time-activity curve. The left ventricular relaxation function was assessed by analysing the time-activity curve, which was filtered using Fourier expansion with the number of harmonics for minimum error. 2. In comparison with age-matched normotensive subjects (seven subjects with mean blood pressure 97 mmHg), hypertensive subjects (seven subjects with mean blood pressure 138 mmHg) had a shorter backward wave arrival time (193 +/- 26 versus 258 +/- 35 ms) and a higher reflection factor (0.58 +/- 0.12 versus 0.42 +/- 0.07). Isovolumic relaxation period was prolonged in hypertensive subjects (118 +/- 19 versus 90 +/- 19 ms). There was an inverse correlation between isovolumic relaxation period and backward wave arrival time in all 14 subjects (r = -0.67, P < 0.05). In contrast, there were no significant differences in cardiac output and time to peak ejection rate between the two groups. 3. Our analyses revealed that early return of the enhanced wave reflection may profoundly impair left ventricular relaxation function in patients with hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteries↗

Different pharmacological characteristics of structurally similar benzylisoquinoline analogs, papaverine, higenamine, and GS 389, on isolated rat aorta and heart.

In the present study, we compared the pharmacological properties of structurally similar benzylisoquinoline compounds, papaverine, higenamine, and GS 389, using isolated rat aorta and atrial preparations. The three benzylisoquinoline compounds, concentration dependently, relaxed phenylephrine (3 microM) induced contraction of rat aortic rings, with the rank order of potency being higenamine > papaverine > GS 389. They also relaxed high K+ (60 mM) induced contraction, with the rank order of potency being papaverine > GS 389 >> higenamine. The relaxation was not modified by the presence of endothelium. To assess whether these compounds directly interfere with Ca2+ influx, the effects of these compounds on Ca(2+)-induced contraction in Ca(2+)-free media were examined. Among the three compounds, papaverine most strongly inhibited Ca(2+)-induced contraction of both K+ stimulated and phenylephrine-stimulated aorta. Higenamine was least potent in inhibition of Ca(2+)-induced contraction in high K+ depolarized aorta. In atrial tissues, lower concentrations of papaverine increased spontaneous beats and isometric tension, whereas above 30 microM its action was reversed. GS 389 decreased heart rate without affecting the contractility. On the other hand, higenamine concentration dependently increased both heart rate and isometric tension, as well as cyclic AMP levels in atrial tissues as a result of beta-receptor activation. Cyclic AMP and cyclic GMP dependent phosphodiesterases from rat atrial and ventricular tissue homogenates were inhibited by papaverine and GS 389, but not by higenamine. These results suggest that calcium antagonistic action of these compounds is at least in part responsible for vasodilation action, but not for cardiac action.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗

Cloning of the rat alpha 1C-adrenergic receptor from cardiac myocytes. alpha 1C, alpha 1B, and alpha 1D mRNAs are present in cardiac myocytes but not in cardiac fibroblasts.

alpha 1-Adrenergic receptor (AR) activation in cardiac muscle has several different physiological effects that might be mediated through different alpha 1-AR subtypes. Two alpha 1-AR subtypes have been cloned from the rat, the alpha 1B and the alpha 1D; both are present in adult rat heart. A third subtype, the alpha 1C, cloned from the cow and human, was reported to be absent in the rat. However, we recently found alpha 1C mRNA in adult rat heart by using a partial alpha 1C cDNA. Thus, all three cloned alpha 1-AR subtypes are present in the heart, but it is unknown whether each is expressed in cardiac myocytes or in cardiac fibroblasts. In the present study, the full-length rat alpha 1C-AR was cloned from cultured neonatal cardiac myocytes. alpha 1C mRNA transcripts of 3, 9.5, and 11 kb were present in adult rat heart by Northern blot analysis. alpha 1B-, alpha 1C-, and alpha 1D-subtype mRNAs were each present in isolated adult and neonatal cardiac myocytes by RNase protection assay. In addition, cultured neonatal cardiac myocytes expressed the three alpha 1-AR subtype mRNAs. In contrast, none of the alpha 1-AR mRNAs was detected in cultured neonatal cardiac fibroblasts. In addition, alpha 1-ARs were absent in fibroblasts by [3H]prazosin binding and norepinephrine-stimulated [3H]inositol phosphate production. The absence of alpha 1-ARs in cardiac fibroblasts differs from beta-adrenergic and angiotensin II receptors, which are present in both cardiac fibroblasts and cardiac myocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

Neural dysfunction and metabolic imbalances in diabetic rats. Prevention by acetyl-L-carnitine.

The rationale for these experiments is that administration of L-carnitine and/or short-chain acylcarnitines attenuates myocardial dysfunction 1) in hearts from diabetic animals (in which L-carnitine levels are decreased); 2) induced by ischemia-reperfusion in hearts from nondiabetic animals; and 3) in nondiabetic humans with ischemic heart disease. The objective of these studies was to investigate whether imbalances in carnitine metabolism play a role in the pathogenesis of diabetic peripheral neuropathy. The major findings in rats with streptozotocin-induced diabetes of 4-6 weeks duration were that 24-h urinary carnitine excretion was increased approximately twofold and L-carnitine levels were decreased in plasma (46%) and sciatic nerve endoneurium (31%). These changes in carnitine levels/excretion were associated with decreased caudal nerve conduction velocity (10-15%) and sciatic nerve changes in Na(+)-K(+)-ATPase activity (decreased 50%), Mg(2+)-ATPase (decreased 65%), 1,2-diacyl-sn-glycerol (DAG) (decreased 40%), vascular albumin permeation (increased 60%), and blood flow (increased 65%). Treatment with acetyl-L-carnitine normalized plasma and endoneurial L-carnitine levels and prevented all of these metabolic and functional changes except the increased blood flow, which was unaffected, and the reduction in DAG, which decreased another 40%. In conclusion, these observations 1) demonstrate a link between imbalances in carnitine metabolism and several metabolic and functional abnormalities associated with diabetic polyneuropathy and 2) indicate that decreased sciatic nerve endoneurial ATPase activity (ouabain-sensitive and insensitive) in this model of diabetes is associated with decreased DAG.

Acetylcarnitine↗

Therapeutic effect of liver resection in patients with metastatic liver tumors.

Thirty-five hepatectomies for metastatic liver malignancy were performed from January 1986 to July 1992 at the National Taiwan University Hospital. Twenty-six of them were of colorectal origin and nine were of other origins. We analyzed the risk factors for recurrence and survival rate after hepatectomy of colorectal origin under curative intention with both univariate and multivariate analysis. The calculated median disease free interval after hepatectomy was 11 months (recurrence rate 65% in one year and 85% in two years). The median survival rate was 24 months (calculated one-year survival 86%, two-year survival 41%). In univariate analysis, the number of metastatic lesions and operation procedures significantly affect the recurrence rate (p = 0.033 and p = 0.042, respectively). In survival univariate analysis, only a safety margin > 1 cm and age > 50 years had significant benefit (p = 0.0014 and p = 0.045, respectively). By multivariate analysis, only solitary metastasis was beneficial to the recurrence rate (p = 0.013), an age > 50 years had a borderline beneficial effect to the recurrence rate (p = 0.052), while earlier liver stage, older age, larger safety margin and minor operative procedures positively affected the survival rate (p = 0.039, 0.018, 0.034 and 0.017, respectively). As the sample number was small, it was hard to draw any conclusions for metastatic liver tumors of other origins. The complication rate (5/35) and mortality rate (1/35) of hepatectomy were low. We concluded that for selected cases of metastatic hepatic malignancy, especially from colorectal cancer, hepatectomy is a promising treatment of choice.

Adult↗

Pharmacological characterization of effects of verapamil and GS 283 on isolated guinea pig and rat trachealis.

The pharmacological effects of verapamil and GS 283, 1-(4'-methoxybenzyl)-6,7-dihydroxy-3,4-dihydroxyisoquinoline, were investigated using isolated rat and guinea pig trachealis. Both verapamil and GS 283 inhibited carbachol-, histamine (only guinea pig)-, and high-K(+)-induced contraction in a dose-dependent manner. GS 283 acted as a weak histamine H1 and muscarinic receptor antagonist in guinea pig and rat trachealis with respective pKB values in the range of 5.60 approximately 6.12 and 5.17 approximately 5.83. On the other hand, pyrilamine and atropine showed a typical competitive antagonism on histamine (guinea pig) and on muscarinic receptors (rat trachea) with pKB values of 9.25 +/- 0.21 and 9.37 +/- 0.32, respectively. GS 283 inhibited Ca(2+)-induced contraction on guinea pig trachealis in Ca(2+)-free media. Furthermore, very high concentrations of GS 283 and verapamil completely abolished a phasic contraction induced by carbachol in Ca(2+)-free media, suggesting that verapamil and GS 283 can enter into the cytoplasm, where they may exert secondary actions on internal sites of the muscle, such as the sarcoplasmic reticulum. It is concluded that GS 283 has a Ca2+ antagonistic action along with weak histamine and muscarinic receptor blocking activity in isolated rat and guinea pig tracheal smooth muscle and its mode of action is likely inhibition of Ca2+ influx from plasma membrane and also release from the sarcoplasmic reticulum.

Animals↗

NO- and NO2-carrying molecules potentiate photorelaxation in rat trachea and aorta.

Photorelaxation elicited by ultraviolet light (366 nm) was investigated on isolated rat thoracic aorta and trachealis. Rat tracheal smooth muscle but not aorta did not show UV-induced photorelaxation. Both streptozotocin, NO-carrying molecule and N omega-nitro-L-arginine, NO2-carrying molecule significantly enhanced photorelaxation, concentration-dependently, in rat trachealis and aorta. Methylene blue (10 microM) inhibited the potentiation action of streptozotocin and N omega-nitro-L-arginine in both tissues. Superoxide dismutase (300 U/ml) enhanced streptozotocin- and N omega-nitro-L-arginine-potentiated photorelaxation in rat trachealis, while pyrogallol (0.1 mM), a potent O2- generating agent, inhibited streptozotocin-potentiated photorelaxation in trachealis. Streptozotocin was much more effective than N omega-nitro-L-Arginine in potentiating of photorelaxation elicited by UV light in both tissues. From these findings, we conclude that streptozotocin and N omega-nitro-L-arginine produce EDRF like labile substance(s) by UV irradiation.

Animals↗

Acute adaptation and resetting of the baroreflex control of vascular resistance in the canine hindquarters and mesentery.

To determine whether acute adaptation and resetting occur in the baroreflex control of regional vascular resistance, experiments were conducted in anesthetized and vagotomized dogs. The carotid sinuses were vascularly isolated to regulate the carotid sinus pressure (CSP) in an open-loop fashion. The hindquarters (n = 12) and mesenteric (n = 10) beds were perfused with constant flow and arterial perfusion pressures (HPP and MPP) were used to reflect changes in hindquarters and mesenteric resistance respectively. We first observed alterations in HPP and MPP during the course of CSP holding (conditioning pressure) at various levels for 15 min. Thereafter, the CSP was lowered to 50 mm Hg and increased stepwise to obtain the CSP-HPP and CSP-MPP baroreflex function curves. In experiments in the hindquarters bed, HPP stabilized at an average of 104.7 mm Hg during the initial conditioning pressure at 100 mm Hg. When conditioning pressure decreased to 50 mm Hg, the HPP increased to 125.5 mm Hg and then gradually declined to a steady level (115.6 mm Hg) in 5 min. An increase in conditioning pressure from 100 to 150 mm Hg caused HPP to decrease to 54.8 mm Hg followed by an upward adaptation to a steady level (80.2 mm Hg) in 5 min. The CSP/HPP curves constructed from the CSP step protocol were also affected by conditioning pressure. There were significant increases in the threshold and saturation pressures as conditioning pressure was elevated. However, the resetting was characterized by a parallel shift of the CSP/HPP curves without significant changes in baroreflex gain or sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

Endothelial potentiation of relaxation response to ascorbic acid in rat and guinea pig thoracic aorta.

The role of the endothelium was evaluated in the relaxation of rat and guinea pig aortic rings induced by ascorbic acid. Ascorbic acid relaxed rat and guinea pig aortic rings that were previously contracted with submaximal dose of phenylephrine (PE), in a concentration dependent manner. Removal of the endothelium significantly reduced the sensitivity but not the magnitude of the response to ascorbic acid. Methylene blue, but not propranolol, blocked the endothelial augmentation of vascular relaxation to ascorbic acid. Vessels precontracted with potassium chloride (high K+) were also relaxed by ascorbic acid. Methylene blue also inhibited the response to ascorbic acid in the intact vessels precontracted with high K+. A23187 and acetylcholine, but not ADP, variably caused endothelium dependent component relaxation in guinea pigs, whereas all of these three probes constantly caused it. In Ca(2+)-free medium, Ca(2+)-induced contraction of high K(+)-depolarized rat aorta was inhibited by the presence of ascorbate, which was more pronounced in endothelium intact rings than in endothelium denuded ones. PE-induced contraction in the presence of different concentrations of ascorbate reduced both the sensitivity and the maximal contractile force in rat aorta. Ascorbic acid (0.125-32 mM) did not change the pH in the medium. From these findings, it is speculated that 1) receptor- and potential-operated Ca2+ channels may be modulated by ascorbate, 2) endothelium has a significant role in promoting relaxation induced by ascorbic acid.

Animals↗

Angiotensin II is mitogenic in neonatal rat cardiac fibroblasts.

Angiotensin II has been reported to be a hormonal stimulus of cardiac growth, a response that may involve myocyte hypertrophy as well as growth of nonmyocytes. This study was designed to determine whether neonatal rat cardiac fibroblasts have an angiotensin II receptor that is coupled with hypertrophic and/or proliferative growth. Competitive radioligand binding studies showed that cardiac fibroblasts have a single class of high-affinity (IC50, 1.0 nM) angiotensin II binding sites (Bmax, 778 fmol/mg protein) that are sensitive to the competitive nonpeptide AT1 receptor antagonist losartan (IC50, 13 nM). Other angiotensin peptides competed for [125I]angiotensin II binding in the following rank order: angiotensin II > angiotensin III > angiotensin I > > [des-Asp1-des-Arg2]angiotensin II. A nonhydrolyzable analogue of guanosine triphosphate increased the dissociation rate of bound [125I]angiotensin II and decreased hormone binding to the receptor at equilibrium. The angiotensin II receptor was coupled with increases in intracellular calcium. Incorporation of precursors into protein, DNA, and RNA in response to angiotensin II was determined. In serum-deprived cultures, a 24-hour exposure to 1 microM [Sar1]angiotensin II increased rates of phenylalanine, thymidine, and uridine incorporation by 58%, 103%, and 118%, respectively. These increases were blocked by the noncompetitive AT1 receptor antagonist EXP3174. After 48 hours, [Sar1]angiotensin II increased total protein and DNA of cardiac fibroblasts by 23% and 15%, respectively, with no change in the protein/DNA ratio. [Sar1]Angiotensin II increased cell number by 138% after a 24-hour exposure, without affecting cell area. In summary, cardiac fibroblasts have G protein-linked AT1 receptors that are coupled with proliferative growth. These results suggest that angiotensin II-induced cardiac hypertrophy is, in part, secondary to stimulated increases in nonmyocyte cellular growth.

Angiotensin II↗

In vivo expression and molecular characterization of the porcine slow-myosin heavy chain.

We report on the molecular characterization of the porcine slow-myosin heavy chain (HC) beta gene and the isolation of its 5' end cDNA. In vivo expression study, by in situ hybridization and histochemistry, revealed a highly regular rosette pattern of fiber arrangement, with a slow fiber occupying the central core, in all the skeletal muscles examined. This feature can be advantageous in the distinction of primary and secondary fibers in myogenic lineage studies. In the neonatal heart, beta isoform expression is diffuse, with higher expression occurring in the ventricle than in the atrium. Transient transfection assays showed the porcine promoter functions in a muscle- and differentiation stage-specific manner. In the 5' regulatory region are several putative positive and negative regulatory elements, including a positive and a negative element in close proximity to each other in intron 1.

Amino Acid Sequence↗

Evaluation of left ventricular functional status using thermodynamic indices.

Conventional methods to assess cardiac contractility have been focused on the mechanical properties of the myocardium. Many of these have suffered from theoretical and practical drawbacks. In this study, we have attempted to evaluate the left ventricular contractile status using the thermodynamic principle and compared these indices with the conventional index (dP/dt). A total of 8 mongrel dogs were anesthetized and artificially ventilated. A Millar catheter with high-fidelity multiple sensors was inserted into the aorta to record the simultaneous changes in aortic flow and pressure waves. Cardiac inotropy was increased by graded doses (2-32 micrograms/kg/min) of dobutamine. Angiotensin injection (100-300 micrograms) to achieve a blood pressure elevation of 30 mmHg was employed for afterload augmentation. Preload was increased by rapid infusion of 6% dextran solution (20 ml/kg). Several thermodynamic parameters were calculated at steady state during the control period and after drug interventions. These included power-averaged rate of power density generation (ARPD), peak ejection rate of change of power (PREP), energy-averaged power density (APD) and frequency-normalized ARPD (FARPD). PREP and APD were unchanged by afterload increment while FARPD, ARPD and dP/dt decreased significantly with an increase in afterload, ARPD was highly sensitive to an increased preload (p < 0.001), and PREP was also changed significantly by an increase in preload. dP/dt was boarderlinely affected by Dextran infusion (p = 0.05), and APD was independent of preload (P > 0.05). Inotropic stimulation increased ARPD, PREP, APD, FARPD and dP/dt by 139.0 +/- 48.0%, 98.0 +/- 51.4%, 74.0 +/- 49.7%, 60.0 +/- 30.4% and 44.6 +/- 10.4%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

Effect of mitral regurgitation and aortic regurgitation on Doppler-derived mitral orifice area in patients with mitral stenosis.

Traditional Doppler pressure half-time (T1/2) method (mitral valve area = 220/T1/2) is widely used for evaluating the mitral orifice area in patients with mitral stenosis (MS). However, the effect of mitral regurgitation (MR) and aortic regurgitation (AR) on the calculation of the mitral valve area by this method is still controversial. Therefore, we examined 493 consecutive patients with MS to evaluate the effect of MR and AR on Doppler-derived mitral orifice area. The mitral orifice area planimetered from two-dimensional echocardiogram was used as the standard reference. Excluding 16 patients with either unsatisfactory Doppler or echocardiographic tracings, 477 patients were enrolled in the study. There were 162 males and 315 females with a mean age of 49 years. They were divided into 4 groups: group A, 327 patients with MS but no MR and AR; group B, 68 patients with MS + MR but no AR; group C, 64 patients with MS + AR but no MR; group D, 18 patients with MS + MR + AR. The differences between echo and Doppler area were 0.02 +/- 0.02 cm2 (mean +/- SE), p = 0.220, in group A; 0.13 +/- 0.04 cm2, p = 0.004, in group B; 0.11 +/- 0.05 cm2, p = 0.026 in group C; and 0.31 +/- 0.08 cm2, p = 0.001, in group D. Thus, in patients with MS, the associated MR or AR may invalidate the pressure half-time method for the derivation of mitral valve area.

Adult↗