Biomedical subjects

Chao-Yu Miao

Publications and source records attributed to Chao-Yu Miao.

At least 19 recordsLinked to original sources

PubMed2006

Blood pressure variability is more important than blood pressure level in determination of end-organ damage in rats.

OBJECTIVE: This study was designed to determine how important a novel risk factor of elevated blood pressure variability (BPV) is in the determination of end-organ damage by comparison with the classic risk factor of a high blood pressure (BP) level. METHODS AND RESULTS: The effects of haemodynamics on cardiovascular morphology were evaluated by univariate and multivariate regression analysis in two different rat models with an enlarged distribution of haemodynamics. In male sham-operated and sinoaortic-denervated Wistar-Kyoto rats and spontaneously hypertensive rats (n = 34), BPV was more important than BP in cardiac and renal damage and aortic hypertrophy. BPV and BP had independent effects, explaining 59.4% of the variation in damage to these organs. In male (n = 44) and female (n = 46) F1 hybrids of Sprague-Dawley rats and spontaneously hypertensive rats, the greater importance of BPV than BP was further demonstrated in left ventricular hypertrophy, glomerular damage and aortic hypertrophy. The phenomenon was more evident in females than males for cardiovascular hypertrophy. BPV and BP or BPV alone had independent effects, explaining 46.9% (male) or 37.5% (female) of the variation in damage to these organs. CONCLUSION: BPV is a more critical determinant than BP level for cardiac damage, renal lesions and aortic hypertrophy in rats, strongly suggesting the significance of BPV control for the protection of these organs.

Animals↗

PubMed2005

Rapid inhibitory effect of glucocorticoids on airway smooth muscle contractions in guinea pigs.

The common disease asthma is characterized by the obstruction, inflammation and increased sensitivity of the airways. Glucocorticoids (GCs) are one of the most potent anti-inflammatory agents available for treating allergic disease. In this study, we report that the GC budesonide (BUD) can rapidly inhibit the histamine-induced contractions of airway smooth muscle in a process mediated by non-genomic mechanisms. The tracheas of albino Hartley guinea pigs were used. We measured the effects of BUD on the increased isometric tension of trachea segment rings and the shrinking of single airway smooth muscle cells (ASMCs) induced by histamine. With the application of each reagent, the changes in the isometric tension of the segment rings upon maximum contraction and at four time points were recorded. We found that BUD significantly suppressed the increase in isometric tension induced by histamine in guinea pigs within 15 min. We also observed that BUD can reduce the histamine-induced shrinking of single ASMCs in an even shorter time. Mifepristone (RU486) and actidione did not depress the inhibitory effect of BUD. The results preclude action via genomic-mediated responses that usually take several hours to occur. We conclude therefore that GCs have a rapid non-genomic inhibitory effect on guinea pig airway smooth muscle contractions, and provide a new way to investigate this non-genomic mechanism. Further study can provide theoretical evidence for the clinical application of GCs in asthma and other allergic diseases.

Animals↗

PubMed2005

Chronic mild hyperhomocysteinemia induces aortic endothelial dysfunction but does not elevate arterial pressure in rats.

Mild hyperhomocysteinemia is prevalent in the general population and has been linked to endothelial dysfunction and high arterial pressure (AP) in clinical studies. The present study was designed to determine whether a rise in AP was induced by mild hyperhomocysteinemia and whether the potential rise in AP is secondary or prior to endothelial dysfunction. Experiments were performed in a rat model of mild hyperhomocysteinemia induced by oral administration of homocysteine for 1-4 months. Aortic endothelial dysfunction was observed 2 months after homocysteine treatment while endothelium-independent vasodilation was normal. In parallel, homocysteine treatment increased phenylephrine-induced contraction in aortas with endothelium, but did not modify the contraction in aortas without endothelium, suggesting a decrease of basal NO production. In conscious unrestrained rats, AP was not significantly different 1, 2, 3 and 4 months after homocysteine treatment. In correlation, endothelial function of a resistance vessel (mesenteric artery), mainly non-NO nonprostanoid factor mediated, was preserved, indicating that homocysteine treatment only affected the NO pathway. In conclusion, mild hyperhomocysteinemia alone is not sufficient to elevate arterial blood pressure, at least in the rat model. Aortic endothelial dysfunction produced by mild hyperhomocysteinemia is independent of hemodynamic factors.

Animals↗

PubMed2005

Effects of long-term treatment with candesartan on hemodynamics and organ damage in spontaneously hypertensive rats.

UNLABELLED: This study was designed to investigate the effects of candesartan on blood pressure (BP) and blood pressure variability (BPV) reductions, baroreflex sensitivity (BRS) amelioration, and organ protection in spontaneously hypertensive rats (SHR). METHODS: Studies were performed in two groups of SHR (n = 13 for control rats; and n = 20 for candesartan-treated rats) and one group of WKY rats (n = 13). Candesartan (3 mg /kg/d) was given in rat chow for 4 months. BP was then continuously recorded for 24 hours in conscious state. After the determination of BRS, rats were killed for organ-damage evaluation. RESULTS: Long-term treatment with candesartan significantly reduced BP and BPV expressed by both standard deviation and variation coefficient of BP, enhanced BRS and produced obvious organ protection. Compared with BP level, BPV and BRS values showed a closer or similar relationship with organ-damage parameters in SHR. Multiple regression analysis showed that the decrease in left ventricular hypertrophy was most closely associated with the increase in BRS, whereas the decrease in aortic hypertrophy was most closely associated with the decrease in 24-hour systolic BPV, and the amelioration in renal lesions, with the increase in BRS and the decrease in 24-hour systolic BPV. CONCLUSION: long-term treatment with candesartan results in organ protection in SHR. Besides BP reduction, the decrease in BPV and the restoration of BRS are significantly related to this organ protection.

Administration, Oral↗

PubMed2005

Arterial baroreflex dysfunction promotes atherosclerosis in rats.

The present study was designed to test the hypothesis that arterial baroreflex dysfunction promotes the development of atherosclerosis. Experiment 1: the baroreflex sensitivity (BRS) was measured in 30 Sprague-Dawley (SD) rats in conscious state with a computerized blood pressure monitoring system. Four weeks later, the rats were administered with Vitamin D3, and fed with the high-cholesterol diet for 8 weeks to induce atherosclerosis. The hearts and aortae were removed for pathological examination. A negative correlation was found between BRS and the scores of coronary (r=-0.464, P<0.01) or aortic atherosclerosis (r=-0.524, P<0.01) in SD rats. Experiment 2: sinoaortic denervation (SAD) was performed in SD rats. Then atherosclerosis was also induced. The atherosclerosis scores in SAD rats were significantly higher than those in sham-operated rats (aortic score: 1.50+/-0.41 versus 1.10+/-0.39, P<0.05; coronary score: 1.70+/-0.35 versus 1.25+/-0.54, P<0.05). Using immunohistochemistry and Western blotting methods, it was found that the expressions of C-reactive protein, intercellular adhesion molecule-1 and vascular-cell adhesion molecule-1 in coronary artery and aorta were increased in SAD rats compared with sham-operated rats. These results indicate that arterial baroreflex dysfunction promotes the development of atherosclerosis in rats, and that inflammation may be involved in this process.

Animals↗

PubMed2005

Reduction of blood pressure variability: a new strategy for the treatment of hypertension.

The main aims of the treatment of hypertension are to prevent end-organ damage (EOD) and to avoid consequent lethal complications associated with hypertension. Blood pressure level is a well-known determinant of EOD. However, recent studies suggest that blood pressure variability (BPV) is as important as blood pressure level in determining EOD. The reduction of BPV is an important contributory factor of the organ protection provided by some antihypertensive drugs. Thus, reduction of BPV might represent a new strategy for the treatment of hypertension.

Animals↗

PubMed2005

Synergism of atenolol and nitrendipine on hemodynamic amelioration and organ protection in hypertensive rats.

OBJECTIVE: This study was designed to investigate the possible synergism of atenolol and nitrendipine on blood pressure (BP) and blood pressure variability (BPV) reductions, baroreflex sensitivity (BRS) amelioration, and organ protection in hypertensive rats. METHOD: The dose was 20 mg/kg for atenolol, 10 mg/kg for nitrendipine and 20 + 10 mg/kg for the combination of these two drugs. In an acute study, a single dose was given via a catheter previously inserted into the stomach in spontaneously hypertensive rats (SHR). In a subacute study, SHR, deoxycorticosterone acetate (DOCA)-salt rats, and two-kidney, one-clip (2K1C) rats were used. They received the same dose by gavage daily for 10 days. BP was measured 24 h after drug administration. In chronic studies, these drugs at the aforementioned dose were mixed into rat chow. SHR were treated for 4 months. BP was then continuously recorded for 24 h. After the determination of BRS, rats were killed for organ-damage evaluation. RESULTS: In the acute study, it was found that the combination of atenolol and nitrendipine had an obviously greater and longer BP reduction than treatment with each of these two drugs separately. In the subacute study, an effective decrease in BP 24 h after administration was found only in the rats treated with the combination. In chronic studies, it was found that the combination possessed the obvious synergism on BP and BPV reduction, BRS amelioration and organ protection in SHR. Multiple-regression analysis showed that the decrease in left ventricular hypertrophy was most significantly related to the decrease in systolic BPV and BP, the decrease in aortic hypertrophy was most significantly related to the increase in BRS and the decrease in systolic BPV, and amelioration in the renal lesion was most significantly associated with the restoration of BRS. CONCLUSION: Treatment with a combination of atenolol and nitrendipine exhibited a rapid and persistent antihypertensive effect and possessed an obvious synergism on BP and BPV reduction, BRS restoration and organ protection in hypertensive rats. The decrease in BPV and the restoration of BRS may importantly contribute to organ protection in SHR with chronic treatment.

Animals↗

PubMed2005

Acute pressure-natriuresis function shows early impairment in Lyon hypertensive rats.

OBJECTIVE: This study aimed to determine whether the alteration of the pressure natriuresis seen in Lyon genetically hypertensive (LH) rats occurs early, and the possible involvement in this alteration of the most important extra-renal factors that influence natriuresis. METHODS: In LH rats and their normotensive (LL) controls, acute pressure natriuresis was studied in denervated kidneys with or without controlling extra-renal influence; that is, adrenalectomy and an intravenous infusion of vasopressin, norepinephrine, hydrocortisone and aldosterone. RESULTS: With controlling the cited extra-renal influence, LH rats already exhibited, at 5 weeks of age, a slightly higher blood pressure (+9%) and a markedly reduced renal blood flow (-33%) compared with LL rats; their pressure-diuresis and pressure-natriuresis curves were significantly blunted. Between 16 and 50 weeks of age, although BP levels did not change, renal blood flow and glomerular filtration rate declined in LH rats while their pressure-diuresis and pressure-natriuresis curves continued to shift to higher pressures. When studied without controlling extra-renal influence, the values of pressure diuresis and natriuresis were significantly higher than in controlled conditions both in LH and LL rats. However, in 16-week-old rats, the LH/LL ratios for sodium and water excretion remained close under the two experimental conditions. CONCLUSIONS: The pressure-natriuresis function in LH rat shows early impairment and aggravates with age. This alteration is observed with, as well as without, controlling the influence of the main extra-renal factors that affect natriuresis.

Acute Disease↗

PubMed2004

Restoration of baroreflex function by ketanserin is not blood pressure dependent in conscious freely moving rats.

OBJECTIVE: Since the end of the 1980s, the pathological importance of baroreflex function has attracted the attention of many investigators. In our previous studies, it was found that ketanserin lowered blood pressure (BP), decreased BP variability and enhanced baroreflex sensitivity (BRS). The present work was designed to test the hypothesis that the restoration of BRS by ketanserin is not dependent on BP level in conscious rats. DESIGN AND METHODS: Spontaneously hypertensive rats (SHR) aged 8-12 months were used. Blood pressure was recorded for 60 min and BRS was determined separately before and after intragastric administration of ketanserin, with four doses. In a second experiment, 10-week-old Sprague-Dawley rats were used for preparing a myocardial infarction (MI) model by ligating the coronary artery. MI rats were treated with ketanserin for 5 weeks, with two doses. At the end of the treatment, BP and BRS of the MI rats were studied in conscious state. In addition, the effects of ketanserin on BRS in Sprague-Dawley rats with normal BRS and the effects of prazosin and ritanserin on BRS in SHR were also observed. RESULTS: It was found that ketanserin significantly decreased BP and improved BRS in the conscious SHR. The decrease in BP was dose-dependent but the improvement of BRS was not. At the smallest dose (0.3 mg/kg), ketanserin did not lower BP but enhanced BRS. In MI rats, the treatment with ketanserin did not significantly decrease BP, but it improved BRS at both doses administered (0.6 and 10 mg/kg). Ketanserin [3 and 10 mg/kg, intragastric (i.g.)] did not affect BRS in SD rats with normal BRS. Prazosin and ritanserin did not enhance BRS in SHR when administered intravenously. Ritanserin markedly and prazosin slightly enhanced BRS in SHR following intracerebroventricular administration. CONCLUSION: The restoration of baroreflex function by ketanserin is not BP dependent and this effect is mediated by central 5-HT2A receptor.

Animals↗

PubMed2004

Asynchronism of the recovery of baroreflex sensitivity, blood pressure, and consciousness from anesthesia in rats.

Anesthesia inhibits arterial baroreflex functions such as baroreflex sensitivity (BRS). The main objective of the present study was to determine the time course of BRS recovery from anesthesia and to determine whether BRS recovery is synchronous with the recovery of consciousness and blood pressure (BP). Experiments were performed in male Sprague-Dawley rats using different commonly used anesthetics at routine doses through intraperitoneal administration: (1) diazepam/ketamine, a mixture of diazepam (5 mg/kg) and ketamine (50 mg/kg); (2) chloral hydrate (0.3 g/kg); (3) sodium pentobarbital (30 mg/kg); and (4) urethane (1.0 g/kg). The anesthetic state, evaluated by algesthesia and cornea reflex, was maintained for 1-2.5 hours. The BRS, assessed by intravenous injection of phenylephrine, was inhibited rapidly and dramatically, with maximum depressions of 51%-80%. The BRS recovery time was approximately 5 hours for diazepam/ketamine, chloral hydrate, and pentobarbital, but more than 24 hours for urethane. Compared with BRS inhibition, BP reduction was less pronounced by 8% (not significant) for diazepam/ketamine and by 12%-30% for the others. The BP recovery time was approximately 2 hours, with the exception of chloral hydrate (>6 hours). In conclusion, after anesthesia, BRS inhibition is more obvious than BP reduction, and the recovery of BRS lags behind the recovery of consciousness or BP.

Anesthesia Recovery Period↗

PubMed2004

ATP-sensitive potassium channels are involved in adenosine-induced reduction of blood pressure variability in spontaneously hypertensive rats.

With a computerized analysis system, blood pressure was recorded continuously in conscious unrestrained spontaneously hypertensive rats. The effects of different adenosine receptor agonists and ATP-sensitive potassium channel opener and blocker on blood pressure variability in spontaneously hypertensive rats were studied. It was found that adenosine, 5'-N-cyclopropyl-carboxamidoadenosine (CPCA, a selective adenosine A2-receptor agonist) and pinacidil (a nonselective ATP-sensitive potassium channel opener) decreased blood pressure variability when one of them was used alone, whereas N -cyclopentyladenosine (CPA, a selective adenosine A1-receptor agonist) had no significant effects on blood pressure variability. When pretreated with glibenclamide (a nonselective ATP-sensitive potassium channel blocker), the inhibitory effects of adenosine and CPCA on blood pressure variability were significantly prevented. By itself, however, glibenclamide had no influence on blood pressure variability. These results suggest that the effect of adenosine on blood pressure variability in spontaneously hypertensive rats is due to activation of ATP-sensitive potassium channels mediated by adenosine A2-receptor.

Adenosine↗

PubMed2004

Increased susceptibility of ventricular arrhythmias to aconitine in anaesthetized rats is attributed to the inhibition of baroreflex.

1. Aconitine is widely used to produce ventricular arrhythmias in anaesthetized rats. The present work was designed to test the hypothesis that anaesthesia may increase the susceptibility of ventricular arrhythmia to aconitine due to the inhibition of arterial baroreflex. In addition, the susceptibility of ventricular arrhythmia to aconitine at different times during the course of a whole day was also investigated. 2. Male Sprague-Dawley rats were used. Arrhthymias were induced by aconitine infusion at six time points (01.00, 05.00, 09.00, 13.00, 17.00 and 21.00 h) with rats in both anaesthetized and conscious states. In sinoaortic-denervated (SAD) rats, ventricular arrhythmias were induced by aconitine infusion between 09.00 and 13.00 h. 3. There was a significant difference in the lethal dose of aconitine between anaesthetized and conscious rats (99.6 +/- 30.1 vs 58.2 +/- 14.7 micro g/kg; P < 0.001). Anaesthesia did increase the susceptibility of rats to ventricular arrhythmias following aconitine. 4. In SAD rats, the lethal dose of aconitine was less than that for baroreflex-intact rats when determined in the conscious state. The difference in the lethal dose of aconitine between SAD and baroreflex-intact rats disappeared when it was determined in anaesthetized rats. 5. The time of day did not affect the susceptibility of either anaesthetized or conscious rats to ventricular arrhythmias following aconitine, except for a difference in the ventricullar fibrillation threshold dose between 13.00 and 17.00 h in anaesthetized rats. 6. In conclusion, anaesthesia may increase the risk of ventricular arrhythmias following aconitine. Intact arterial baroreflex function is necessary to prevent drug-induced ventricular arrhythmias.

Aconitine↗

PubMed2004

Greater hypertrophy in right than left ventricles is associated with pulmonary vasculopathy in sinoaortic-denervated Wistar-Kyoto rats.

1. Biventricular hypertrophy has been described in a high blood pressure variability (BPV) model of sinoaortic-denervated (SAD) rats without systemic hypertension. To explore the possible involvement of the lung in SAD-induced right ventricular hypertrophy (RVH), we examined lung morphology, in addition to systemic haemodynamics and ventricle morphology, in Wistar-Kyoto rats 32 weeks after SAD. 2. In Wistar-Kyoto rats 32 weeks after SAD, there existed a substantial elevation in BPV, with no change in the average level of arterial pressure. Biventricular hypertrophy following SAD was characterized by a greater hypertrophy in right than left ventricles; both absolute and normalized right ventricular weights were significantly increased by 22 and 27%, respectively, and only normalized left ventricular weight was significantly increased by 12%. No infarcts were found in any ventricles examined. 3. In the lung, the most prominent change following SAD was pulmonary vasculopathy, including wall thickening, perivascular fibrosis and cell infiltration. In pulmonary arteries with an internal diameter of 70-130 microm, the external diameter, wall thickness and wall thickness to internal diameter ratio were increased in SAD compared with control rats. 4. There was no correlation between right and left ventricular weights. In contrast with BPV-correlated left ventricular weight, right ventricular weight was correlated with the wall thickness of the pulmonary artery, but not with BPV. 5. These findings suggest that greater RVH following SAD is associated with pulmonary vasculopathy, but is not secondary to the left ventricular problems or high BPV.

Animals↗

PubMed2004

Conditions affecting hydrodynamics-based gene delivery into mouse liver in vivo.

1. It has been demonstrated that the hydrodynamics-based procedure has high efficiency to deliver foreign genes into the liver. The widespread use of this procedure in gene function studies and as a treatment option for liver and other organ diseases puts considerable importance on the investigation of various conditions that affect hydrodynamics-based gene delivery into mouse liver in vivo. 2. Various conditions, including the volume, speed and solution of the injection and the state, gender and strain of the animal were manipulated to evaluate their effect on the expression levels in mice of human factor IX (hFIX) 8 h after tail vein injection of the plasmid pCMV-hFIX. 3. It was found that an injection volume of 2-2.5 mL and an injection speed of 5-7 s were very effective in delivering DNA into the mouse liver. Using Ringer's solution as an injection fluid increased the efficiency of hFIX expression. 4. Anaesthetized mice expressed higher hFIX than conscious mice. Males expressed higher hFIX than females. The ICR mouse strain demonstrated higher expression of the foreign gene than did the C57 strain. 5. The effects of these specific factors on hFIX expression may be caused by variations in hydrostatic pressure, the degree of liver damage and liver size. 6. It can be concluded that there are optimal conditions for hFIX expression in the liver. This information may be helpful for the application of hydrodynamics-based procedures in the investigation of gene expression and gene therapy.

Animals↗

PubMed2004

Synergism of atenolol and amlodipine on lowering and stabilizing blood pressure in spontaneously hypertensive rats.

This study was designed to investigate the possible synergism of atenolol and amlodipine on lowering and stabilizing blood pressure (BP) in spontaneously hypertensive rats. Sixty-four spontaneously hypertensive rats were randomly divided into eight groups. They were given 0.8% carboxymethylcellulose sodium (control), atenolol (10 mg/kg), amlodipine (0.5, 1 and 2 mg/kg) and the combinations of atenolol and amlodipine (10 + 0.5, 10 + 1 and 10 + 2 mg/kg), respectively. The drugs were given via a catheter of gastric fistula. BP was recorded for 25 h from 1 h before drug administration to 24 h after administration, in conscious, freely moving rats. It was found that combination of atenolol and amlodipine significantly decreased BP and systolic BP variability. From probability sum analysis it was found that the combination of atenolol and amlodipine, in a proportion as 10 : 1, was the best one (q = 1.54). In conclusion, the present work clearly demonstrated that there is a synergistic effect between atenolol and amlodipine in lowering and stabilizing the BP. The synergistic effect is highest when the dose proportion of the two drugs is 10 : 1.

Adrenergic beta-Antagonists↗

PubMed2003

Comparative study of sinoaortic denervated rats and spontaneously hypertensive rats.

BACKGROUND: Both hypertension and high blood pressure variability (BPV) are involved in cardiovascular damage. This comparative study was designed to explore the possible effects of both of these phenomena on the cardiovascular system. METHODS: The high BPV model of 16-week sinoaortic denervated (SAD) rats and the hypertension model of spontaneously hypertensive rats (SHR) were used for comparison at the same age of 26 weeks. The comparison was focus on hemodynamics, cardiovascular hypertrophy, and hemodynamic responses to ketanserin. Linear regression analysis was performed to study the role of hemodynamics in cardiovascular hypertrophy. RESULTS: In SHR, hypertension was accompanied by a moderately high BPV, whereas in SAD rats, substantially high BPV existed alone, without hypertension. Left ventricular hypertrophy was severe in SHR but was mild in SAD rats. Aortic hypertrophy was present in SAD rats but was absent in SHR. In SAD rats, the hypertrophy was correlated with BPV but not with blood pressure (BP) level. However, in SHR, hypertrophy was correlated with both BP and BPV level. The BP-lowering effect of ketanserin was comparable in both models, whereas its BPV-lowering effect was greater in SAD rats than in SHR. This hypersensitivity was associated with basal BPV level in SAD rats. CONCLUSIONS: These results indicate that hypertension may be more important than high BPV in causing left ventricular hypertrophy, and that the aorta may be more sensitive to substantially high BPV.

Animals↗

PubMed2003

Ketanserin stabilizes blood pressure in conscious spontaneously hypertensive rats.

1. It has been demonstrated that blood pressure variability (BPV) is increased in hypertension and related to organ damage. It will be important to lower BPV in the treatment of hypertension. The present study was designed to investigate the effect of ketanserin, a 5-HT2A receptor antagonist with a weak alpha1-adrenoceptor blocking effect, on BPV in conscious spontaneously hypertensive rats (SHR). 2. It was found that ketanserin decreased blood pressure (BP) and BPV in SHR when administered intravenously (3 mg/kg, i.v.). Ketanserin decreased BPV, but not the BP level, when administered intracerebroventricularly (50 microg/rat, i.c.v.). 3. Prazosin, an alpha1-adrenoceptor antagonist, lowered BP but did not affect BPV when given either i.v. (0.5 mg/kg) or i.c.v. (30 microg/rat). Ritanserin (0.625 mg/kg, i.v.; 40 microg/rat, i.c.v.), a 5-HT2A receptor antagonist, decreased BPV only when administered i.c.v. and did not modify the BP level. 4. Ketanserin enhanced arterial baroreflex function in SHR when given either i.v. or i.c.v. 5. The stabilizing effect of ketanserin on BP was persistent when administered intragastrically. This administration route is similar to oral administration clinically. 6. It is concluded that ketanserin is an antihypertensive agent with an effect of reducing BPV. This effect is mainly mediated by central 5-HT2A receptors and is probably attributable to the restoration of arterial baroreflex function.

Animals↗

PubMed2003

Effects of glucose-insulin-potassium on baroreflex sensitivity, left ventricular function and ventricular arrhythmia in the subacute phase of myocardial infarction in rats.

Glucose-insulin-potassium (GIK) is clinically used for reducing mortality in acute myocardial infarction (MI). It is known that ventricular arrhythmia, left ventricular dysfunction and impaired baroreflex sensitivity (BRS) are the three major determinants for predicting the mortality after acute MI. The present work was designed to study the effects of GIK on BRS, ventricular arrhythmia, and left ventricular function in rats with coronary artery ligature. Sprague-Dawley rats were used and the myocardial infarction was produced by ligature of the left anterior descending artery. Five weeks after coronary artery ligation, BRS was measured in conscious state with a computerized blood pressure monitoring system and left ventricular function and electrocardiogram were determined in the anaesthetized state in the subacute phase of myocardial infarction. It was found that GIK did not affect the blood pressure and heart period in both conscious and anaesthetized rats. GIK did not enhance BRS, but reduced ventricular arrhythmia and improved left ventricular function by reducing left ventricular end diastolic pressure in anaesthetized rats with MI. It is proposed that reducing ventricular arrhythmia and improving left ventricular function contribute to the effect of GIK on reducing the mortality after MI.

Animals↗