Effects of diltiazem on cardiac function and regional blood flow at rest and during exercise in a conscious rat preparation of chronic heart failure (myocardial infarction).

Drexler, Helmut; Depenbusch, J W; Truog, A. G.; Zelis, Robert; Flaim, Stephen F.

doi:10.1161/01.cir.71.6.1262

Cited by 33 publications

(11 citation statements)

References 33 publications

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“…These data are in agreement with previous studies that have demonstrated that rats with infarctions ranging from 31% to 45% of the ventricle had normal baseline hemodynamics, but had reduced peak flow indexes and reduced developed pressures with either volume loading or exercise. 16 18 19 In addition, these same studies also demonstrated that rats with infarctions greater than 45% had decompensated congestive heart failure.…”

Section: Discussionmentioning

confidence: 91%

Endurance training in rats with chronic heart failure induced by myocardial infarction.

et al. 1986

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The response to exercise was investigated in trained and sedentary rats with moderate compensated heart failure produced by myocardial infarction (MI) and in rats that underwent sham operations. Trained rats ran on a treadmill (10% grade at 20 m/min) for 60 min/day, 5 days/week for 10 to 12 weeks, whereas sedentary rats had only limited activity. Maximal oxygen consumption normalized for body weight (ml kg min`) was determined for each rat and found to be (1) greater in trained rats when compared with sedentary rats and (2) greater in sham-operated rats when compared with their counterparts that suffered infarction. In addition, skeletal muscle succinate dehydrogenase activities were greater and the blood lactic acid response to submaximal exercise was lower in trained rats compared with sedentary rats. Left ventricular infarct size for sedentary and trained rats with infarction was 36 3% and 34 + 3% of the total endocardial circumference, respectively, and resulted in (1) elevated left ventricular end-diastolic pressures at rest and during exercise, (2) lower mean arterial pressures at rest, and (3) lower maximal heart rates when compared with those in their sham-operated counterparts. However, normalization of mean arterial pressures during submaximal and maximal exercise was found along with a trend toward normalization of maximal heart rate when trained rats with infarction were compared with their sedentary counterparts. Blood flows to the kidneys, organs of the gut, and skeletal muscle during both submaximal and maximal exercise were unaffected by either myocardial infarction or training; no differences between sedentary and trained rats with infarction and sedentary and trained sham-operated rats were found. These results demonstrate that an exercise training program of moderate intensity produces beneficial hemodynamic and metabolic effects in rats with moderate compensated heart failure. Circulation 74, No. 2, [431][432][433][434][435][436][437][438][439][440][441] 1986

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Section: Discussionmentioning

confidence: 91%

Endurance training in rats with chronic heart failure induced by myocardial infarction.

et al. 1986

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“…Regarding calcium antagonists, minimal decreases in renal vascular resistance, and increases in RBF have been reported [113][114][115]. Despite the welldescribed adenosine A1 receptor-mediated renal vasoconstriction, also via the TGF system, A1 antagonism has clinically not been shown clearly to improve renal outcome.…”

Section: Pharmacologic Control Of Extracellular Fluid Volumementioning

confidence: 99%

Systemic arterial and venous determinants of renal hemodynamics in congestive heart failure

Braam

Cupples

Joles³

et al. 2011

Heart Fail Rev

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Heart and kidney interactions are fascinating, in the sense that failure of the one organ strongly affects the function of the other. In this review paper, we analyze how principal driving forces for glomerular filtration and renal blood flow are changed in heart failure. Moreover, renal autoregulation and modulation of neurohumoral factors, which can both have repercussions on renal function, are analyzed. Two paradigms seem to apply. One is that the renin-angiotensin system (RAS), the sympathetic nervous system (SNS), and extracellular volume control are the three main determinants of renal function in heart failure. The other is that the classical paradigm to analyze renal dysfunction that is widely applied in nephrology also applies to the pathophysiology of heart failure: pre-renal, intra-renal, and post-renal alterations together determine glomerular filtration. At variance with the classical paradigm is that the most important post-renal factor in heart failure seems renal venous hypertension that, by increasing renal tubular pressure, decreases GFR. When different pharmacological strategies to inhibit the RAS and SNS and to assist renal volume control are considered, there is a painful lack in knowledge about how widely applied drugs affect primary driving forces for ultrafiltration, renal autoregulation, and neurohumoral control. We call for more clinical physiological studies.

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“…Infarction was produced by left coronary arterial ligation, as described previously (13), using a modification of MacLean (34), as follows. Male Sprague Dawley rats were anesthetized with 0.3 g/kg chloralhydrate (intraperitoneally), intubated via tracheotomy, and placed on a Harvard respirator (Harvard Apparatus Model 665).…”

Section: Experimental Preparationsmentioning

confidence: 99%

Systemic and regional vascular effects of atrial natriuretic peptide in a rat model of chronic heart failure

et al. 1987

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To characterize the systemic and regional vascular effects of atrial natriuretic peptide (ANP) in chronic heart failure, central hemodynamics, regional blood flow and plasma ANP levels were determined in a rat model of myocardial infarction and failure and in sham-operated animals. Measurements were made in the conscious state before and after intravenous rANP [99-126] (8 micrograms bolus followed by continuous infusion of 1.0 microgram/kg/min). With this protocol, ANP significantly decreased cardiac output, right atrial, left ventricular end-diastolic and arterial pressures and there were increases in heart rate, systemic and intestinal vascular resistances in sham animals. Renal blood flow per gram of tissue was unchanged with ANP, but when expressed as a percentage of cardiac output, increased significantly, indicating a preferential renal vasodilatory effect of ANP. In rats with infarction and failure, this dose did not alter cardiac output or arterial pressure, but decreased right atrial and left ventricular blood flow. Although significantly reduced as compared to the control group, renal blood flow was not improved with ANP in the heart failure group. ANP plasma levels of the heart failure group were elevated at baseline (p less than 0.01), and increased 5-10 times after infusion of rANP. Thus, in rats with chronic heart failure, the renal vascular effects of ANP are blunted, which may, in part, explain the failure of ANP to restore the altered volume homeostasis in heart failure despite elevated ANP plasma levels. However, the effects on venous return were preserved which, in turn, improved cardiac performance via a reduction of preload.

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Effects of diltiazem on cardiac function and regional blood flow at rest and during exercise in a conscious rat preparation of chronic heart failure (myocardial infarction).

Cited by 33 publications

References 33 publications

Endurance training in rats with chronic heart failure induced by myocardial infarction.

Endurance training in rats with chronic heart failure induced by myocardial infarction.

Systemic arterial and venous determinants of renal hemodynamics in congestive heart failure

Systemic and regional vascular effects of atrial natriuretic peptide in a rat model of chronic heart failure

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