Therapeutic Effects of Coccomyxagloeobotrydiformis on the Metabolic Syndrome in Rats

Background/Aims: The metabolic syndrome (MS) is a cluster of metabolic changes that carry a high risk of cardiovascular disease (CVD). A newly discovered microalga, coccomyxagloeobotrydiformis (CGD), has been reported to improve ischemic stroke and metabolism-related indicators. We observed the therapeutic effects of CGD on MS and postulated the underlying mechanism. Methods: A diet-induced MS model in rats was used to observe the therapeutic effects of CGD on MS. Blood-glucose and lipid indices were measured using enzymatic colorimetric kits. A biologic data acquisition and analysis system (BL-420F) was used to evaluate cardiac function. Expression of mitochondrial respiratory chain (MRC) enzymes was measured by immunofluorescence staining. The proteins associated with oxidative stress, apoptosis and inflammation were detected by western blotting. Results: Body weight, abdominal circumference, fasting blood glucose , blood pressure as well as serum levels of total cholesterol, triglycerides and low-density lipoprotein-cholesterol were decreased whereas serum levels of high-density lipoprotein-cholesterol was increased in CGD-treated MS rats. CGD increased left-ventricular systolic pressure, left-ventricular end-diastolic pressure, left-ventricular systolic pressure maximum rate of increase and left-ventricular diastolic pressure maximum rate of decrease in MS rats with cardiovascular complications. CGD up-regulated expression of adenosine monophosphate-activated protein kinase and peroxisome proliferator activated receptor gamma coactivator 1-alpha in the heart, adipose tissue and skeletal muscle. Expression of the MRC subunits of ATPase 6, cytochrome b and succinate dehydrogenase complex, subunit-A was increased whereas that of uncoupling protein-2 decreased in different tissues. CGD showed anti-oxidation effects by increasing expression of superoxide dismutase and decreasing that of malondialdehyde. High expression of Bcl-2 and low expression of Bax and caspase-3 supported the anti-apoptotic effect of CGD on the cardiovascular complications of MS. Conclusion: CGD has a therapeutic effect on MS and associated cardiovascular complications by eliciting mitochondrial protection and having anti-oxidation and anti-apoptosis effects. CGD could be used for MS treatment.

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Increased cardiac contractility in acute uremia: interrelationships with hypertension

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1975.229.2.501 ◽

1975 ◽

Vol 229 (2) ◽

pp. 501-505 ◽

Cited By ~ 11

Author(s):

T Nivatpumin ◽

T Yipintsoi ◽

S Penpargkul ◽

J Scheuer

Keyword(s):

Blood Pressure ◽

Systolic Hypertension ◽

Diastolic Pressure ◽

Cardiac Contractility ◽

Systolic Pressure ◽

Pressure Rise ◽

Left Ventricular ◽

Ventricular Systolic Pressure ◽

Inotropic State ◽

Left Ventricular Systolic Pressure

To study the effects of acute uremia on the inotropic state of the rat heart, we subjected rats to bilateral nephrectomy and studied their hearts in the open chest 24 h later. Uremic rats had significantly higher systolic blood pressure than sham-operated animals. Left ventricular systolic pressure and maximum dP/dt, both during ejection and isovolumic contrations, were higher for any given end-diastolic pressure in hearts of uremic rats than in sham-operated animals. This difference in performance charcteristics was not abolished by doses of propranolol that blocked the heart rate response to isoproterenol. The administration of phenoxybenzamine during the 24 h of uremia abolished the blood pressure rise in uremic rats, but the increased contractile state persisted. Treatment of sham-operated animals with methoxamine to produce the same course of blood pressure as observed in uremic rats was also associated with an increased inotropic state. These results indicate that in the rat, acute uremia is associated with an increased inotropic state that is not mediated by beta-adrenergic mechanisms. The systolic hypertension of acute uremia is not the major cause of the increased contractility, although systolic hypertension without uremia can mimic the performance characteristics found in hearts of uremic rats.

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The Effect of Gypenosides on Cardiac Function and Expression of Cytoskeletal Genes of Myocardium in Diabetic Cardiomyopathy Rats

The American Journal of Chinese Medicine ◽

10.1142/s0192415x09007491 ◽

2009 ◽

Vol 37 (06) ◽

pp. 1059-1068 ◽

Cited By ~ 4

Author(s):

Min Ge ◽

Shanfeng Ma ◽

Liang Tao ◽

Sudong Guan

Keyword(s):

Cardiac Function ◽

Diabetic Cardiomyopathy ◽

Diastolic Pressure ◽

Pure Water ◽

Systolic Pressure ◽

Left Ventricular ◽

Control Group ◽

Sprague Dawley ◽

Gene Expressions ◽

Ventricular Systolic Pressure

The relationship between changes of cardiac function and the gene expressions of two major myocardial skeleton proteins, titin and nebulin, and the effect of gypenosides on these gene expressions in diabetic cardiomyopathy rat were explored in the present study. Forty Sprague-Dawley rats were randomly divided into three groups: control group, diabetic cardiomyopathy group and gypenosides-treated diabetic cardiomyopathy group. The diabetic cardiomyopathy was induced in rats by injecting streptozotocin (STZ, 55 mg/kg) intraperitoneally. Seven weeks after the rats suffered from diabetes, the rats were treated with gypenosides 100 mg/kg per day orally for six weeks in gypenosides-treated group. In the meanwhile, the pure water was given to diabetic cardiomyopathy and the control groups. Subsequently, the cardiac functions, including left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), ± dP/dtmax and t–dP/dmaxt, as well as the mRNA content and proteins of titin and nebulin in myocardium were determined. The results indicated that (1) the diabetic cardiomyopathy rats had decreased LVSP and ± dP/dtmax, increased LVEDP, and prolonged t–dP/dtmax than normal rats; (2) LVSP and ± dP/dtmax in diabetic cardiomyopathy rats treated with gypenosides were significantly higher and LVEDP and t–dP/dtmax were significantly lower than those without giving gypenosides; (3) the mRNA contents and proteins of titin and nebulin in diabetic cardiomyopathy rats were remarkably lower than those in the control rats and gypenosides had no effect on mRNA and protein expression levels of titin and nebulin in diabetic cardiomyopathy rats. We conclude that (1) the cardiac function as well as the mRNA expressions of titin and nebulin decreased in diabetic cardiomyopathy rats; (2) gypenosides secure cardiac muscles and their function from diabetic impairment and these beneficial effects of gypenosides are not by changing the expressions of titin and nebulin.

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Effect of human urotensin-II infusion on hemodynamics and cardiac function

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y03-004 ◽

2003 ◽

Vol 81 (2) ◽

pp. 125-128 ◽

Cited By ~ 33

Author(s):

Ghada S Hassan ◽

Fazila Chouiali ◽

Takayuki Saito ◽

Fu Hu ◽

Stephen A Douglas ◽

...

Keyword(s):

Cardiac Function ◽

Diastolic Pressure ◽

Cardiac Contractility ◽

Systolic Pressure ◽

Left Ventricular ◽

Urotensin Ii ◽

Ventricular Systolic Pressure ◽

Wide Range ◽

Dose Dependent Decrease

Recent studies have shown that the vasoactive peptide urotensin-II (U-II) exerts a wide range of action on the cardiovascular system of various species. In the present study, we determined the in vivo effects of U-II on basal hemodynamics and cardiac function in the anesthetized intact rat. Intravenous bolus injection of human U-II resulted in a dose-dependent decrease in mean arterial pressure and left ventricular systolic pressure. Cardiac contractility represented by ±dP/dt was decreased after injection of U-II. However, there was no significant change in heart rate or diastolic pressure. The present study suggests that upregulation of myocardial U-II may contribute to impaired myocardial function in disease conditions such as congestive heart failure.Key words: urotensin-II, rat, infusion, heart.

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Role of reflexes following myocardial necrobiosis

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1965.209.6.1081 ◽

1965 ◽

Vol 209 (6) ◽

pp. 1081-1088 ◽

Cited By ~ 19

Author(s):

G. Ascanio ◽

F. Barrera ◽

E. V. Lautsch ◽

M. J. Oppenheimer

Keyword(s):

Peripheral Resistance ◽

Systolic Pressure ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Hemodynamic Changes ◽

Ventricular Systolic Pressure ◽

Arterial Blood ◽

Bilateral Vagotomy ◽

Left Ventricular Systolic Pressure

Intracoronary administration of hexachlorotetrafluorobutane (Hexa) into non-thoracotomized dogs produced a statistically significant decrease in left ventricular systolic pressure (LVSP), mean femoral arterial blood pressure (MFAP), first derivative of left ventricular pressure pulse (dP/d t), total peripheral resistance (TPR), and cardiac output (C.O.) lasting up to 1 hr after injection. Femoral vascular resistance decreased during the first 3 min after production of necrobiosis. Fifty percent of the dogs died of ventricular fibrillation (VF) after Hexa infarction. Prereserpinized dogs did not show significant changes in the parameters which were significantly changed in normal dogs after Hexa necrobiosis except in the case of VF which was almost absent in this group. Bilateral vagotomy prior to Hexa administration prevented most hemodynamic changes after necrobiosis whereas atropine did not. Bilateral vagotomy and atropine 1 hr after necrobiosis increased MFAP, dP/d t, LVSP, C.O., and TPR. Apparently excitatory efferent sympathetic activity on heart and femoral arterial vessels is reflexly inhibited by the effects of intracoronary injection of Hexa. The afferent pathway is via the vagus nerve.

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Cardiac response to submaximal exercise in dogs susceptible to sudden cardiac death

Journal of Applied Physiology ◽

10.1152/jappl.1985.59.3.890 ◽

1985 ◽

Vol 59 (3) ◽

pp. 890-897 ◽

Cited By ~ 28

Author(s):

G. E. Billman ◽

P. J. Schwartz ◽

J. P. Gagnol ◽

H. L. Stone

Keyword(s):

Ventricular Fibrillation ◽

Diastolic Pressure ◽

Stress Test ◽

Systolic Pressure ◽

Left Ventricular ◽

Submaximal Exercise ◽

Rate Of Change ◽

Cardiac Response ◽

Exercise Stress ◽

Ventricular Systolic Pressure

The hemodynamic response to submaximal exercise was investigated in 38 mongrel dogs with healed anterior wall myocardial infarctions. The dogs were chronically instrumented to measure heart rate (HR), left ventricular pressure (LVP), LVP rate of change, and coronary blood flow. A 2 min coronary occlusion was initiated during the last minute of an exercise stress test and continued for 1 min after cessation of exercise. Nineteen dogs had ventricular fibrillation (susceptible) while 19 animals did not (resistant) during this test. The cardiac response to submaximal exercise was markedly different between the two groups. The susceptible dogs exhibited a significantly higher HR and left ventricular end-diastolic pressure (LVEDP) but a significantly lower left ventricular systolic pressure (LVSP) in response to exercise than did the resistant animals. (For example, response to 6.4 kph at 8% grade; HR, susceptible 201.4 +/- 5.1 beats/min vs. resistant 176.2 +/- 5.6 beats/min; LVEDP, susceptible 19.4 +/- 1.1 mmHg vs. resistant 12.3 +/- 1.7 mmHg; LVSP, susceptible 136.9 +/- 7.9 mmHg vs. resistant 154.6 +/- 9.8 mmHg.) beta-Adrenergic receptor blockade with propranolol reduced the difference noted in the HR response but exacerbated the LVP differences (response to 6.4 kph at 8% grade; HR, susceptible 163.4 +/- 4.7 mmHg vs. resistant 150.3 +/- 6.4 mmHg; LVEDP susceptible 28.4 +/- 2.1 mmHg vs. resistant 19.6 +/- 3.0 mmHg; LVSP, susceptible 122.2 +/- 8.1 mmHg vs. resistant 142.8 +/- 10.7 mmHg). These data indicate that the animals particularly vulnerable to ventricular fibrillation also exhibit a greater degree of left ventricular dysfunction and an increased sympathetic efferent activity.

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Effect of acute regional ischemia on pressure in the subepicardium and subendocardium

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1982.242.2.h240 ◽

1982 ◽

Vol 242 (2) ◽

pp. H240-H244 ◽

Cited By ~ 4

Author(s):

H. N. Sabbah ◽

P. D. Stein

Keyword(s):

Diastolic Pressure ◽

Control Period ◽

Systolic Pressure ◽

Left Ventricular ◽

Acute Ischemia ◽

Ventricular Systolic Pressure ◽

Intramyocardial Pressure ◽

Ischemic Region ◽

Catheter Tip ◽

Extravascular Resistance

The effects of acute ischemia on regional intramyocardial pressure were studied in eight open-chest dogs. Aortic, left ventricular, subepicardial, and subendocardial pressures were measured with catheter-tip micromanometers. During the control period subendocardial pressure during systole (180 +/- 13 mmHg; mean +/- SE) was higher than left ventricular intracavitary pressure (137 +/- 9 mmHg; P less than 0.001). Subepicardial pressure during systole was lower (95 +/- 6 mmHg; P less than 0.001). Acute ischemia caused a reduction of subendocardial pressure during systole to levels below left ventricular systolic pressure (92 +/- 7 mmHg vs. 116 +/- 6 mmHg; P less than 0.01). Ischemia also caused a reduction of systolic subepicardial pressure to 67 +/- 2 mmHg (P less than 0.001). After reperfusion all pressures returned nearly to control values. During diastole subendocardial pressure during the control period (13 +/- 1 mmHg) was high than left ventricular end-diastolic pressure (6 +/- 1 mmHg; P less than 0.001). Subepicardial pressure during diastole (29 +/- 2 mmHg) was higher than subendocardial pressure and left ventricular end-diastolic pressure (P less than 0.001). Acute ischemia had little or no effect on subendocardial pressure during diastole, whereas it caused a reduction of subepicardial diastolic pressure to 16 +/- 1 mmHg (P less than 0.001). Reperfusion of the ischemic region caused a return of all diastolic pressures nearly to control values. These observations indicate that coronary extravascular resistance is affected by ischemia and that the most prominent effects are in the subendocardium during systole and in the subepicardium during diastole.

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Role of autoregulation in spatial and temporal perfusion heterogeneity of canine myocardium

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1978.235.1.h64 ◽

1978 ◽

Vol 235 (1) ◽

pp. H64-H71 ◽

Cited By ~ 4

Author(s):

F. J. Sestier ◽

R. R. Mildenberger ◽

G. A. Klassen

Keyword(s):

Spatial Heterogeneity ◽

Perfusion Pressure ◽

Diastolic Pressure ◽

Systolic Pressure ◽

Ventricular Myocardium ◽

Small Region ◽

Left Ventricular ◽

Left Ventricular Myocardium ◽

Temporal Heterogeneity ◽

Ventricular Systolic Pressure

Spatial heterogeneity, the region-to-region variation in flow at an instant, and temporal heterogeneity, the time variation of flow in a small region of myocardium, were investigated with radioactive labeled microspheres in 111 regions of left ventricular myocardium. The error of the method was measured by simultaneously injecting four differently labeled microspheres (15 +/- 5 (SD) micron). The coefficient of variation (CV) was 6.5 +/- 1.0%. Spatial variation with autoregulation intact was 21.7 +/- 1.4% (CV); with autoregulation abolished and low perfusion pressure, it was 34.3 +/- 3.7%; and with normal perfusion pressure, 30.8 +/- 6.4% (differences not significantly). This degree of variation was similar in the entire left ventricle and its layers. Forces which tended to cause vessel closure (low perfusion pressure, ventricular systolic pressure, and ventricular diastolic pressure) tended to increase CV. Temporal heterogeneity as measured by 20-s intervals between microsphere injections was 11.1 +/- 1.0% (CV) with autoregulation, 9.8 +/- 1.3% (P less than 0.05) with autoregulation abolished, and 8.4 +/- 0.8% (P less than 0.05) when perfusion pressure was restored. A periodicity of flow cycles of 30-90 s was suggested by the data. These results suggest that spatial heterogeneity is less influenced by autoregulation than by hydraulic considerations, whereas temporal heterogeneity is a component of autoregulation.

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Effects of sympathetic stimulation during cooling on hypothermic as well as posthypothermic hemodynamic function

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y06-051 ◽

2006 ◽

Vol 84 (10) ◽

pp. 985-991 ◽

Cited By ~ 9

Author(s):

T.V. Kondratiev ◽

T. Tveita

Keyword(s):

Mean Arterial Pressure ◽

Arterial Pressure ◽

Saline Solution ◽

Systolic Pressure ◽

Pressure Rise ◽

Left Ventricular ◽

Mechanical Function ◽

Ventricular Systolic Pressure ◽

Hemodynamic Variables ◽

Left Ventricular Systolic Pressure

This experimental study was performed to explore hemodynamic effects of a moderate dose epinephrine (Epi) during hypothermia and to test the hypothesis whether sympathetic stimulation during cooling affects myocardial function following rewarming. Two groups of male Wistar rats (each, n = 7) were cooled to 15 °C, maintained at this temperature for 1 h, and then rewarmed. Group 1 received 1 μg/min Epi, i.v., for 1 h during cooling to 28 °C, a dose known to elevate cardiac output (CO) by approximately 25% at 37 °C. Group 2 served a saline solution control. At 37 °C, Epi infusion elevated CO, left ventricular systolic pressure, maximum rate of left ventricle pressure rise, and mean arterial pressure. During cooling to 28 °C, these variables, with the exception of mean arterial pressure, decreased in parallel to those in the saline solution group. In contrast, in the Epi group, mean arterial pressure remained increased and total peripheral resistance was significantly elevated at 28 °C. Compared with corresponding prehypothermic values, most hemodynamic variables were lowered after 1 h at 15 °C in both groups (except for stroke volume). After rewarming, alterations in hemodynamic variables in the Epi-treated group were more prominent than in saline solution controls. Thus, before cooling, continuous Epi infusion predominantly stimulates myocardial mechanical function, materialized as elevation of CO, left ventricular systolic pressure, and maximum rate of left ventricle pressure rise. Cooling, on the other hand, apparently eradicates central hemodynamic effects of Epi and during stable hypothermia, elevation of peripheral vascular vasopressor effects seem to take over. In contrast to temperature-matched, non-Epi stimulated control rats, a significant depression of myocardial mechanical function occurs during rewarming following a moderate sympathetic stimulus during initial cooling.

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