Simple method to produce acute heart failure by coronary vessel embolization in closed chest rats with muspheres

Gorodetskaya, E. A.; Dugin, S. F.; Медведев, О. С.; Allabergenova, A.E.

doi:10.1016/0160-5402(90)90048-p

Cited by 14 publications

(9 citation statements)

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“…An increase in left ventricular end‐diastolic pressure was found to be prominent in a number of studies where acute heart failure has been produced. This has been observed with acute heart failure induced by embolization of the coronary artery with mercury (Leddy et al ., 1983) or plastic microspheres (Gorodetskaya et al ., 1990). The mercury‐induced acute heart failure was associated with a significant decrease in blood pressure, cardiac output and left ventricular d P /dt, and a significant increase in left ventricular end‐diastolic pressure (Leddy et al ., 1983).…”

Section: Discussionmentioning

confidence: 99%

“…The mercury‐induced acute heart failure was associated with a significant decrease in blood pressure, cardiac output and left ventricular d P /dt, and a significant increase in left ventricular end‐diastolic pressure (Leddy et al ., 1983). The microsphere‐induced acute heart failure also caused a significant decrease in cardiac contractility, blood pressure and cardiac output, and an increase in left ventricular end‐diastolic pressure and right atrial pressure (Schölkens et al ., 1986; Gorodetskaya et al ., 1990).…”

Section: Discussionmentioning

confidence: 99%

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Effects of CGS 21680, a selective A_2A adenosine receptor agonist, on cardiac output and vascular resistance in acute heart failure in the anaesthetized rat

Nekooeian

Tabrizchi

1998

British J Pharmacology

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1 The e ects of CGS 21680, a selective A 2A adenosine receptor agonist, on cardiac output, blood pressure, mean circulatory ®lling pressure (P mcf ), arterial and venous resistances, heart rate and left ventricular end-diastolic pressure were assessed in rats with acute heart failure by means of coronary artery occlusion. 2 Animals (n=6 in each group) were divided into ®ve groups: group I, sham-operated vehicle-treated (0.9% saline; 0.018 mL min 71 ); groups II-V, subject to coronary artery occlusion and treated with vehicle (0.9% saline; 0.018 ml min 71 ) and CGS 21680 (0.1, 0.3 and 1.0 mg kg 71 min 71 ), respectively. Haemodynamic measurements were taken one hour after completion of surgery, ninety minutes after coronary artery occlusion (except in group I), and ®fteen minutes after infusion of saline or CGS 21680. 3 Baseline haemodynamic measurements before occlusion were found not to di er signi®cantly between the di erent groups of animals. However, after occlusion, cardiac output, rate of rise in left ventricular pressure (+dP/dt) and blood pressure were signi®cantly reduced when compared to corresponding values in sham-operated animals. In addition, occlusion of the coronary artery resulted in a signi®cant elevation in venous resistance, P mcf and left ventricular end-diastolic pressure as compared to corresponding values in sham-operated animals. 4 Infusion with CGS 21680 at the highest dose signi®cantly reduced blood pressure, arterial resistance and left ventricular end-diastolic pressure when compared to occluded vehicle-treated animals (group II). Administration of CGS 21680 at the highest dose also signi®cantly increased cardiac output (28%) and heart rate (10%) in comparison to occluded vehicle-treated animals. In addition, the highest dose of CGS 21680 signi®cantly reduced P mcf (9%) and venous resistance (62%) in comparison to occluded vehicle-treated animals. Administration of CGS 21680 did not signi®cantly a ect +dP/dt when compared to occluded vehicle-treated animals. 5 The results from the present investigation indicate that occlusion of the coronary artery in rats results in a state of heart failure characterized by reduced arterial pressure and cardiac output, and increased venous resistance, P mcf and left ventricular end-diastolic pressure. Administration of CGS 21680 to animals with acute heart failure resulted in increased cardiac output which was due to reduced venous resistance, as well as increased heart rate.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of CGS 21680, a selective A_2A adenosine receptor agonist, on cardiac output and vascular resistance in acute heart failure in the anaesthetized rat

Nekooeian

Tabrizchi

1998

British J Pharmacology

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“…[1][2][3] Those NO isoenzymes expressed constitutively in endothelial (eNOS) and neuronal cells (nNOS) are Ca 2ϩ -dependent and can be activated by elevated intracellular calcium concentration, 4,5 whereas the Ca 2ϩ -independent isoenzyme (iNOS) can be induced by cytokines in macrophages and vascular smooth muscle cells and produces an excessive amount of NO. 6,7 In the vasculature, endotheliumderived NO (EDNO) appears to play an important role in the regulation of blood pressure (BP), regional blood flow, and vascular tone, as well as receptor-mediated vasodilator responses to agonists such as acetylcholine, bradykinin, thrombin, and others. 8 -10 In addition to its vasodilator properties, NO inhibits platelet aggregation, neutrophil infiltration, and smooth muscle cell proliferation and migration.…”

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confidence: 99%

Endothelial Nitric Oxide Gene Knockout Mice

et al. 1999

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Abstract-We tested the hypothesis that nitric oxide (NO) released by endothelial NO synthase (eNOS) is not only important in blood pressure regulation but also involved in cardiac function and remodeling and in the cardioprotective effect of angiotensin-converting enzyme inhibitors (ACEi). With the use of a 2D Doppler echocardiography system equipped with a 15-MHz linear transducer, we evaluated left ventricular (LV) morphology and function in conscious eNOS knockout mice (eNOS; nϭ15) and their wild-type littermates (eNOS ϩ/ϩ ; nϭ16). We also studied whether in eNOS Ϫ/Ϫ mice (1) myocardial ischemia/reperfusion injury is more severe and (2) the cardioprotective effect of ACEi is diminished or absent. In comparison with the wild type, eNOS Ϫ/Ϫ mice had significantly increased systolic blood pressure (128Ϯ3 versus 108Ϯ5 mm Hg; PϽ0.001) and decreased heart rate (531Ϯ22 versus 629Ϯ18 bpm; PϽ0.001) associated with increased LV posterior wall thickness (0.80Ϯ0.04 versus 0.64Ϯ0.02 mm; PϽ0.001) and LV mass (18.3Ϯ0.9 versus 13.1Ϯ0.5 mg/10 g body weight; PϽ0.01). Despite hypertension and LV hypertrophy, LV chamber dimension, shortening fraction and ejection fraction (indicators of LV contractility), and cardiac output did not differ between the 2 strains, which indicates that LV function in eNOS Ϫ/Ϫ mice is well compensated. We also found that in eNOS ϩ/ϩ mice, ACEi decreased the ratio of myocardial infarct size to area at risk from 62.7Ϯ3.9% to 36.3Ϯ1.6% (PϽ0.001), whereas in eNOS Ϫ/Ϫ mice this effect of ACEi was almost abolished: the ratio of myocardial infarct size to area at risk was 67.2Ϯ2.9% in the vehicle-treated group and 62.7Ϯ3.9% in mice treated with ACEi. Moreover, infarct size in vehicle-treated eNOS Ϫ/Ϫ mice was not significantly different from eNOS ϩ/ϩ mice given the same treatment. We concluded that (1) endothelium-derived NO plays an important role in the regulation of blood pressure homeostasis; (2) NO released under basal conditions has no significant impact on cardiac function; and (3) ACEi protect the heart against ischemia/reperfusion injury in mice and that this effect is mediated in part by endothelium-derived NO. (Hypertension. 1999;34:24-30.) Key Words: nitric oxide Ⅲ myocardial ischemia Ⅲ myocardial reperfusion injury Ⅲ mice, knockout Ⅲ angiotensin-converting enzyme inhibitors Ⅲ echocardiography N itric oxide (NO) is formed from L-arginine and oxygen by 3 isoenzymes collectively called nitric oxide synthase (NOS). [1][2][3] Those NO isoenzymes expressed constitutively in endothelial (eNOS) and neuronal cells (nNOS) are Ca 2ϩ -dependent and can be activated by elevated intracellular calcium concentration, 4,5 whereas the Ca 2ϩ -independent isoenzyme (iNOS) can be induced by cytokines in macrophages and vascular smooth muscle cells and produces an excessive amount of NO. 6,7 In the vasculature, endotheliumderived NO (EDNO) appears to play an important role in the regulation of blood pressure (BP), regional blood flow, and vascular tone, as well as receptor-mediated vasodilator responses to agonists ...

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“…Experiments were carried out on male Wistar rats weighing 330-370 g. Coronary embolisln was induced by injecting plastic 15-g microspheres (NEN) into the left ventricle with occluded ascendant aorta [6]. Controls were sham-operated rats injected with the same volume of physiological saline via the same route.…”

Section: Methodsmentioning

confidence: 99%

Pulmonary elimination of angiotensin-I after experimental damage to the myocardium

et al. 1998

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In a rat model of heart failure induced by microembolization of coronary vessels puhnonary elimination of angiotensin-I directly depends on the degree of myocardial damage, the clearance of angiotensin-I being mediated through angiotensin-conveiling enzymeindependent factors. Insufficient release of angiotensin-II from the lungs into circulation in embolized animals can be partially responsible for activation of peripheral reninangiotensin systems and aggravation of heart failure.Key Words: angiotensin-converting enzyme; lung clearance; cardiac sclerosis; heart ./ailure Activation of the renin-angiotensin system (RAS) depends on the degree of myocardial damage and the severity of heart failure [8]. Increased plasma renin activity at the late [5] and, under physical strain, early stages of heart failure [9] probably results from accelerated elimination of angiotensin-I (AT-I) in the circulation. Plasma concentrations of AT-I can remain unchanged because its production and utilization are compensated. The aim of the present study was to evaluate the relationship between the degree of myocardial damage induced by embolization of the coronary vessels and the rate of AT-I clearance. MATERIALS AND METHODSExperiments were carried out on male Wistar rats weighing 330-370 g. Coronary embolisln was induced by injecting plastic 15-g microspheres (NEN) into the left ventricle with occluded ascendant aorta [6]. Controls were sham-operated rats injected with the same volume of physiological saline via the same route. The intensity of AT-I elimination into pulmonary circulation was assessed 21 days postoperaRussian Cardiology Research-and-Production Complex, Russian Ministry of Health; M. V. Lomonosov Moscow State University tion. To this end, arterial and venous catheters werc implanted, and on the next day uSI-AT-I (14xl0 s cpm 2, 50 ng/min) was injected intravenously until attaining the equilibrium concentration. Arterial blood was sampled into the mediuna for pcptidc extraction [3]. The vortexed mixture was centrifuged, the supernatant was diluted with distilled water to 5 ml, and peptides were extracted on a Sep-pak C18 microcolumn (Waters Ass.) [211. The peptide fraction was eluted with 2 ml ethanol and dried under a nitrogen stream. Quantitative analysis of 12SI-AT-I and 12SI-AT-II was performed using high-performance liquid chromatography followed by radiometry of the corresponding nfinute eluate fractions. Puhnonary clearance was calculated as the ratio of infusion rate to blood concentration of 12SI-AT-I.For morphological analysis, the hears we re fixed in 10% neutral fornlaldehyde and elnbedded in paraffin. Microtome longitudinal sections (5-7 ~t) through the atria and ventricles were stained with hematoxylin and eosin and picrofuchsin by the van Oieson method. The following pathological phenomena were assessed: the nulnber of scars per section, focal cardiosclerosis, and cardiomyocyte hypertrophy and dystrophy. Each phenomenon was scored using a 5-point scale. The data were processed

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Simple method to produce acute heart failure by coronary vessel embolization in closed chest rats with muspheres

Cited by 14 publications

References 10 publications

Effects of CGS 21680, a selective A_2A adenosine receptor agonist, on cardiac output and vascular resistance in acute heart failure in the anaesthetized rat

Effects of CGS 21680, a selective A_2A adenosine receptor agonist, on cardiac output and vascular resistance in acute heart failure in the anaesthetized rat

Endothelial Nitric Oxide Gene Knockout Mice

Pulmonary elimination of angiotensin-I after experimental damage to the myocardium

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Simple method to produce acute heart failure by coronary vessel embolization in closed chest rats with muspheres

Cited by 14 publications

References 10 publications

Effects of CGS 21680, a selective A2A adenosine receptor agonist, on cardiac output and vascular resistance in acute heart failure in the anaesthetized rat

Effects of CGS 21680, a selective A2A adenosine receptor agonist, on cardiac output and vascular resistance in acute heart failure in the anaesthetized rat

Endothelial Nitric Oxide Gene Knockout Mice

Pulmonary elimination of angiotensin-I after experimental damage to the myocardium

Contact Info

Product

Resources

About

Effects of CGS 21680, a selective A_2A adenosine receptor agonist, on cardiac output and vascular resistance in acute heart failure in the anaesthetized rat

Effects of CGS 21680, a selective A_2A adenosine receptor agonist, on cardiac output and vascular resistance in acute heart failure in the anaesthetized rat