Hemodynamic alterations in chronically conscious unrestrained diabetic rats

1987 ◽  
Vol 252 (5) ◽  
pp. H900-H905 ◽  
Author(s):  
L. F. Carbonell ◽  
M. G. Salom ◽  
J. Garcia-Estan ◽  
F. J. Salazar ◽  
M. Ubeda ◽  
...  
Keyword(s):  
Weight Control ◽  
Insulin Treatment ◽  
Cardiac Contractility ◽  
Peripheral Resistance ◽  
Left Ventricular Pressure ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Diabetic State ◽  
Hemodynamic State ◽  
Male Wistar Rats

Important cardiovascular dysfunctions have been described in streptozotocin (STZ)-diabetic rats. To determine the influence of these changes on the hemodynamic state and whether insulin treatment can avoid them, different hemodynamic parameters, obtained by the thermodilution method, were studied in STZ-induced (65 mg/kg) diabetic male Wistar rats, as well as in age-control, weight-control, and insulin-treated diabetic ones. All rats were examined in the conscious, unrestrained state 12 wk after induction of diabetes or acidified saline (pH 4.5) injection. At 12 wk of diabetic state most important findings were normotension, high blood volume, bradycardia, increase in stroke volume, cardiac output, and cardiosomatic ratio, and decrease in total peripheral resistance and cardiac contractility and relaxation (dP/dtmax and dP/dtmin of left ventricular pressure curves). The insulin-treated diabetic rats did not show any hemodynamic differences when compared with the control animals. These results suggest that important hemodynamic alterations are present in the chronic diabetic state, possibly conditioning congestive heart failure. These alterations can be prevented by insulin treatment.

The antiadrenergic effect of cyclopentyladenosine on myocardial contractility is reduced in vivo in diabetic rats

1994 ◽  
Vol 72 (10) ◽  
pp. 1245-1251 ◽  
Author(s):  
Fred D. Romano ◽  
Stephen J. Kopp ◽  
June T. Daar ◽  
Cynthia A. Smith
Keyword(s):  
Insulin Treatment ◽  
Left Ventricular Pressure ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Adrenergic Agonist ◽  
Experimental Diabetes Mellitus ◽  
Ventricular Performance ◽  
And Control ◽  
Dose Dependent

The aim of this study was to test the hypothesis that the antiadrenergic action of adenosine is reduced in diabetes. This was determined by evaluating the effect of experimental diabetes mellitus on the in vivo myocardial antiadrenergic action of cyclopentyladenosine, an adenosine A1- receptor agonist. Changes in heart rate and ventricular performance in response to infusion of dobutamine, a β1-adrenergic agonist, were determined in the absence and presence of cyclopentyladenosine, in anesthetized, 10- to 12-week male diabetic (60 mg/kg streptozotocin), insulin-treated diabetic and control rats. Intravenous dobutamine (16 μg/kg) increased +dP/dtmax and −dP/dtmax in control rats from 7 706 ± 553 and 5 449 ± 403 mmHg/s (1 mmHg = 133.3 Pa) to 19 170 ± 465 and 8 855 ± 317 mmHg/s, respectively. In diabetic rats dobutamine increased +dP/dtmax and −dP/dtmax from 5 733 ± 541 and 4 016 ± 426 to 15 015 ± 1 521 and 7 039 ± 809 mmHg/s, respectively. Cyclopentyladenosine significantly attenuated dobutamine-stimulated increases in +dP/dtmax and −dP/dtmax in both control and diabetic rats in a dose-dependent (0.1–3.0 μg/kg) manner. Cyclopentyladenosine potency to attenuate dobutamine-enhanced +dP/dtmax was reduced significantly (p < 0.05) in diabetic rats compared with controls (ID50, 1.07 vs. 0.59 μg/kg, respectively) with no change in efficacy. The magnitude of cyclopentyladenosine inhibition of dobutamine-enhanced −dP/dtmax was greater in control than diabetic rats (81 vs. 54%, respectively), but ID50 values were not different. Insulin treatment of diabetic rats prevented the observed changes. These data suggest that the antiadrenergic action of adenosine is compromised in diabetes and that this may contribute to the development of diabetic cardiomyopathy.Key words: adenosine, dobutamine, ventricle, left ventricular pressure, streptozotocin.

Weight reduction in the management of hypertension: Epidemiologic and mechanistic evidence

1986 ◽  
Vol 64 (6) ◽  
pp. 818-824 ◽  
Author(s):  
Efrain Reisin
Keyword(s):  
Blood Pressure ◽  
Weight Loss ◽  
Weight Control ◽  
Sodium Intake ◽  
Close Association ◽  
Peripheral Resistance ◽  
Volume Ratio ◽  
Epidemiological Studies ◽  
Left Ventricular ◽  
Normal Weight

A number of studies have established a close association between increased body mass and elevated blood pressure. The presence of obesity in hypertensive subjects is associated with some hemodynamic, metabolic, and endocrinic characteristics: an increased intravascular volume with a high intracellular body water/interstitial fluid volume ratio, increased cardiac output, stroke volume, and left ventricular work while peripheral resistance was reduced or normal. Weight loss of at least 10 kg can reduce blood pressure independently of changes in sodium intake in obese persons of both sexes with mild, moderate, or severe high blood pressure. The fall in arterial pressure in obese hypertensives after weight loss may reverse many of the previously mentioned altered findings and underscore previous epidemiological studies that have shown that weight control could be an important measure in the treatment of hypertension.

Muscle metabolism and cardiac function of the myopathic hamster following training

1977 ◽  
Vol 43 (6) ◽  
pp. 936-941 ◽  
Author(s):  
W. L. Sembrowich ◽  
M. B. Knudson ◽  
P. D. Gollnick
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Function ◽  
Myocardial Function ◽  
Cardiac Contractility ◽  
Muscle Metabolism ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Succinate Dehydrogenase Activity ◽  
Positive Effect

The effect of 18 wk of treadmill running on skeletal muscle metabolism and myocardial function of normal and myopathic hamsters was examined. BIO 14.6 hamsters could tolerate an exercise intensity of about 18 m/min for 40 min, 5 days/wk. Further increases in speed or number of bouts per day resulted in a falloff in performance. Normal hamsters could tolerate higher speeds and longer exercise bouts. Exercise did not change the severity of lesions of either the heart or skeletal muscle of the myopathic hamsters. A training effect was evidenced by increased succinate dehydrogenase activity in the soleus muscle. Cardiac function was evaluated as contractility measured from left ventricular pressure curves and expressed as (dP/dt)/kP. The results suggested that cardiac contractility was not as severely depressed in the trained BIO 14.6 strain of hamsters as in nontrained controls. However, (dP/dt)/kP was lower in the trained myopathic animals than in normal hamsters. ATP, CP, and glycogen levels were lower in myopathic hamsters with the lowest values occurring in the trained group. These data demonstrate that the BIO 14.6 strain of hamster can tolerate exercise training and that such training may have a positive effect on cardiac function.

scholarly journals Possible mechanism of the cardio-renal protective effects of AVE-0991, a non-peptide Mas-receptor agonist, in diabetic rats

2012 ◽  
Vol 13 (3) ◽  
pp. 334-340 ◽  
Author(s):  
Kulwinder Singh ◽  
Kuldeepak Sharma ◽  
Manjeet Singh ◽  
PL Sharma
Keyword(s):  
Blood Pressure ◽  
Receptor Agonist ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Protective Effects ◽  
Mas Receptor ◽  
Arterial Blood

Hypothesis: This study was designed to investigate the cardio-renal protective effect of AVE-0991, a non-peptide Mas-receptor agonist, and A-779, a Mas-receptor antagonist, in diabetic rats. Materials and methods: Wistar rats treated with streptozotocin (50 mg/kg, i.p., once), developed diabetes mellitus after 1 week. After 8 weeks, myocardial functions were assessed by measuring left ventricular developed pressure (LVDP), rate of left ventricular pressure development (d p/d tmax), rate of left ventricular pressure decay (d p/d tmin) and left ventricular end diastolic pressure (LVEDP) on an isolated Langendorff’s heart preparation. Further, mean arterial blood pressure (MABP) was measured by using the tail-cuff method. Assessment of renal functions and lipid profile was carried out using a spectrophotometer. Results: The administration of streptozotocin to rats produced persistent hyperglycaemia, dyslipidaemia and hypertension which consequently produced cardiac and renal dysfunction in 8 weeks. AVE0991 treatment produced cardio-renal protective effects, as evidenced by a significant increase in LVDP, d p/d tmax, d p/d tmin and a significant decrease in LVEDP, BUN, and protein urea. Further, AVE-0991 treatment for the first time has been shown to reduce dyslipidaemia and produced antihyperglycaemic activity in streptozotocin-treated rats. However, MABP and creatinine clearance remained unaffected with AVE-0991 treatment. Conclusions: AVE-0991 produced cardio-renal protection possibly by improving glucose and lipid metabolism in diabetic rats, independent of its blood pressure lowering action.

Role of reflexes following myocardial necrobiosis

1965 ◽  
Vol 209 (6) ◽  
pp. 1081-1088 ◽  
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.

Chronic alcohol-induced changes in cardiac contractility are not due to changes in the cytosolic Ca2+ transient

1998 ◽  
Vol 275 (1) ◽  
pp. H122-H130 ◽  
Author(s):  
Vincent M. Figueredo ◽  
Kevin C. Chang ◽  
Anthony J. Baker ◽  
S. Albert Camacho
Keyword(s):  
Cardiac Contractility ◽  
Left Ventricular Pressure ◽  
Alcohol Exposure ◽  
Left Ventricular ◽  
Polyacrylamide Gel ◽  
Chronic Alcohol ◽  
Protein Levels ◽  
Chronic Alcohol Exposure ◽  
Induced Changes ◽  
And Control

Long-standing heavy alcohol consumption acts as a chronic stress on the heart. It is thought that alcohol-induced changes of contractility are due to altered Ca2+ handling, but no measurements of cytosolic Ca2+([Ca2+]c) after chronic alcohol exposure have been made. Therefore experiments were performed to determine whether alcohol-induced changes in contractility are due to altered Ca2+ handling by measuring [Ca2+]c(indo 1) in hearts from rats drinking 36% ethanol for 7 mo and age-matched controls. Peak left ventricular pressure was depressed (−16%), whereas rates of contraction (12%) and relaxation (14–20%) were faster in alcohol-exposed hearts. Systolic [Ca2+]c(808 ± 45 vs. 813 ± 45 nM), diastolic [Ca2+]c(195 ± 11 vs. 193 ± 10 nM), and rates of [Ca2+]crise and decline were the same in alcohol-exposed and control hearts. Protein levels of Ca2+-handling proteins, sarcoplasmic reticulum Ca2+-ATPase and phospholamban, were the same in myocytes isolated from alcohol-exposed and control hearts (SDS-polyacrylamide gel). These data suggest that chronic alcohol-induced contractile changes are not due to altered Ca2+ handling but may be due to changes at the level of the myofilament. As a first step in elucidating the mechanism(s) of alcohol-induced changes at the myofilament, we assessed myosin heavy chain (MHC) isoform content (SDS-polyacrylamide gel). α-MHC was decreased relative to β-MHC ( a/ a+ b = 0.55 ± 0.03 vs. 0.66 ± 0.02; P < 0.02) in alcohol-exposed hearts, which cannot account for the observed alcohol-induced contractile changes. In conclusion, changes of myocardial contractility due to chronic alcohol exposure do not result from altered Ca2+ handling but from changes at the level of the myofilament that do not involve MHC isoform shifts.

Effects of arterial input impedance on mean ventricular pressure-flow relation

1984 ◽  
Vol 247 (6) ◽  
pp. H978-H983 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Characteristic Impedance ◽  
Peripheral Resistance ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Pressure Flow ◽  
Inotropic State ◽  
End Diastolic Volume ◽  
State Compliance ◽  
Slope Change

The mean left ventricular pressure-flow relationship (Pv-Fv), determined under a constant preload and variable peripheral resistance, has been proposed as a quantitative representation of ventricular pump function (9). We determined the Pv-Fv relation in seven isolated cross-perfused canine hearts by varying resistance of a simulated arterial load in five steps from 6.0 to 0.375 mmHg X s X ml-1 while keeping end-diastolic volume, inotropic state, compliance, and characteristic impedance at various constant values. All of the 27 Pv-Fv relations thus determined were moderately nonlinear. Varying end-diastolic volume at three levels shifted the relation curve in an approximately parallel fashion (P less than 0.0001). At three levels of inotropic state (mean LVP of isovolumic contractions 34.3 +/- 8.2, 48.0 +/- 6.3, and 59.2 +/- 9.6 mmHg), the Pv-Fv relation shifted with predominantly a slope change (P less than 0.0001). Changing compliance at three levels (0.2, 0.4, and 0.8 ml/mmHg) caused a statistically significant but quantitatively small crossover of the Pv-Fv curves (P less than 0.0001). Changing characteristic impedance to 0.1, 0.2, and 0.4 mmHg X s X ml-1 caused a highly significant (P less than 0.0001) divergence of Pv-Fv relation over the high Fv range. We conclude that this sensitivity of the Pv-Fv relation to characteristic impedance limits its use as a contractility index.

Epicardial Coronary Blood Flow Including the Presence of Stenoses and Aorto-Coronary Bypasses—I: Model and Numerical Method

1985 ◽  
Vol 107 (4) ◽  
pp. 361-367 ◽  
Author(s):  
E. Rooz ◽  
T. F. Wiesner ◽  
R. M. Nerem
Keyword(s):  
Blood Flow ◽  
Numerical Method ◽  
Coronary Blood Flow ◽  
Wave Speed ◽  
Peripheral Resistance ◽  
Left Ventricular Pressure ◽  
Systematic Investigation ◽  
Left Ventricular ◽  
Resistive Component ◽  
The One

A computer model and numerical method for calculating left epicardial coronary blood flow has been developed. This model employs a finite-branching geometry of the coronary vasculature and the one-dimensional, unsteady equations for flow with friction. The epicardial coronary geometry includes the left main and its bifurcation, the left anterior descending and left circumflex coronary arteries, and a selected number of small branches. Each of the latter terminate in an impedance, whose resistive component is related to intramyocardial compression through a linear dependence on left ventricular pressure. The elastic properties of the epicardial arteries are taken to be non-linear and are prescribed by specifying the local small-disturbance wave speed. The model allows for the incorporation of multiple stenoses as well as aorto-coronary bypasses. Calculations using this model predict pressure and flow waveform development and allow for the systematic investigation of the dependence of coronary flow on various parameters, e.g., peripheral resistance, wall properties, and branching pattern, as well as the presence of stenoses and bypass grafts. Reasonable comparison between calculations and earlier experiments in horses has been obtained.

Altered sensitivity of chronic diabetic rat heart to calcium

1983 ◽  
Vol 245 (6) ◽  
pp. E560-E567 ◽  
Author(s):  
D. R. Bielefeld ◽  
C. S. Pace ◽  
B. R. Boshell
Keyword(s):  
Rat Heart ◽  
Calcium Metabolism ◽  
Left Ventricular Pressure ◽  
Calcium Sensitivity ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Diabetic Rat ◽  
Isolated Hearts ◽  
Pressure Development

An alteration in calcium metabolism in cardiac muscle was observed in diabetic rats 3 mo after streptozotocin treatment. Depression of cardiac output and left ventricular pressure development were more sensitive to decreased extra-cellular calcium in hearts from diabetic than from control animals and occurred within the normal physiological range of freely ionized serum calcium. This decrease in calcium sensitivity was not present after 2 wk of diabetes. In vivo treatment with insulin for 1 mo completely reversed the effect. Addition of octanoate (0.3 mM) to the perfusate of isolated hearts completely reversed the defect, whereas epinephrine (25 nM) only partially reversed it. When the glucose concentration of the perfusate was decreased, the function of diabetic hearts declined and was further diminished at decreasing calcium levels. Hearts from normal rats were unaffected. These results suggest that there is a defect in calcium metabolism or flux in the chronic diabetic rat heart.

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