Effects of a cardiac glycoside in combination with propranolol on the ischemic heart of conscious dogs.

Vatner, Stephen F.; Baig, Hank; Manders, W. T.; Murray, Patrick

doi:10.1161/01.cir.57.3.568

Cited by 20 publications

(4 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, when inotropic stimulation is coupled with tachycardia, blood flow falls and contractile function deteriorates in the ischemic myocardium. These findings are also consistent with other recent studies from our laboratory on the effects of ouabain, a positive inotropic agent, which does not elicit tachycardia but exerts a salutary effect on ischemic myocardial mechanical function and blood flow when adminsitered either alone (Vatner et al, 1978b), or in combination with propranolol (Vatner et al, 1978a).…”

Section: Discussionsupporting

confidence: 93%

See 1 more Smart Citation

Importance of heart rate in determining the effects of sympathomimetic amines on regional myocardial function and blood flow in conscious dogs with acute myocardial ischemia.

Vatner¹,

Baig²

1979

Circulation Research

Self Cite

View full text Add to dashboard Cite

We examined the effects of dopamine (DP), dobutamine (DB), and isoproterenol (ISO) in 38 conscious dogs after coronary artery occlusion on measurements of overall left ventricular (LV) function (i.e., LV pressure, dP/dt, mean arterial pressure, and heart rate), while regional myocardial function was assessed, using an ultrasonic gauge to measure segment length (SL) in normal and ischemic areas of myocardium. We measured regional myocardial blood flow, using the radioactive microsphere technique. Coronary occlusion resulted in graded reductions of blood flow and function from the normal to severely ischemic zones. DP and DB, 4.0 pg/kg per min, and ISO, 0.03 fig/kg per rain, iv, increased LV dP/dt similarly; i.e., by 20%, and increased blood flow and systolic SL shortening in the normal zone. ISO increased heart rate (29.9 ± 4.6%) and decreased SL shortening and blood flow (32.9 ± 6.1%) in the severely ischemic zone. In contrast, we observed significantly different (P < 0.01) effects with these doses of DP and DB, which caused no increases in heart rate or decreases in blood flow or contractile function in the ischemic zone. DP and DB, 10 pg/kg per min, iv, increased LV dP/dt 3-to 4-fold more than with the lower dose, but still failed to elicit reductions in contractile function or blood flow in the severely ischemic zone when heart rate did not rise. In contrast, when the same doses of DP and DB increased heart rate in another group of dogs, blood flow and contractile function fell in the ischemic zone. Thus, /J-adrenergic agents do not always elicit a "coronary steal" or deleterious effects on ischemic myocardial function, despite coronary dilation in the normal zone. However, when inotropic stimulation is coupled with tachycardia, blood flow falls and contractile function deteriorates in the ischemic myocardium. Circ Res 45: 793-803, 1979

show abstract

Section: Discussionsupporting

confidence: 93%

“…The operation of this instrument in our laboratory has been described previously (Vatner et al, 1978a;Vatner et al, 1978b;Pagani et al, 1978;Heyndrickx et al, 1975). The instrument used in this study was modified further to provide continuous measurements of the regional electrographic potential at each crystal site.…”

Section: Methodsmentioning

confidence: 99%

Importance of heart rate in determining the effects of sympathomimetic amines on regional myocardial function and blood flow in conscious dogs with acute myocardial ischemia.

Vatner¹,

Baig²

1979

Circulation Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…The time at which reperfusion of ischemic tissue occurs, however, is important in determining its ability to matintaini myocardial cell integrity ancl segmeintal myocaardial functioni (11). Pagani et al (6) (24), the combination of propranolol and oubain (25), hypothermia (26), nitroglycerin (27), and nitroprusside (27). It has also been shown that greater left ventricular wall tension can be developed during reperfusioin in dogs respiring high levels of inspired oxygen during coronary occlusion than in dogs respiring room air (28).…”

Section: Discussionmentioning

confidence: 99%

Early Recovery of Regional Performance in Salvaged Ischemic Myocardium following Coronary Artery Occlusion in the Dog

Darsee¹,

Kloner²,

Braunwald³

1981

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T Although numerous agents have been shown experimentally to protect ischemic myocardium, a critical unanswered question is whether function is preserved in the salvaged tissue. Accordingly, 38 openchest dogs had measurements of percent segment length shortening (%SS) and velocity of segment length shortening either in midmyocardial or subepicardial and subendocardial ischemic segments before and after 60 min of left anterior descending coronary artery occlusion during 5 h of reperfusion; 10 additional dogs were subjected to 3 h of coronary occlusion followed by 72 h ofreperfusion. 15 min after coronary artery occlusion, radiolabeled microspheres were injected into the left atrium for measurement of regional myocardial blood flow, and dogs were treated with 1 mg/kg i.v. (n = 23) of an anti-inflammatory drug, flurbiprofen or an equal volume of saline (n = 25). The ischemic myocardiumat-risk for necrosis was determined by injecting methylene blue dye into the left atrium with the coronary artery reoccluded at the end of the reperfusion period, slicing the left ventricle into thin transverse sections, and measuring the areas of each slice that were not perfused (pink unstained tissue) by methylene blue. The quantity of necrotic tissue in each transverse section was measured by planimetry after incubation ofthe slices in triphenyltetrazolium chloride, and by direct histological examination in dogs with 72 h of reperfusion.Regional myocardial blood flow of the ischemic segments between the ultrasonic dimension crystals was similar in treated (0.34+0.03 ml/min per g) and control dogs (0.35+0.03 ml/min per g). In saline-treated control dogs subjected to a 1-h coronary occlusion, 17.9+1.8% of the myocardium-at-risk became necrotic. but in flurbiprofen-treated dogs none of the tissue became necrotic. In saline-treated dogs passive lengthening of the previously ischemic segments persisted through 5 h of reperfusion in all three regions of myocardium after a 1-h coronary occlusion. In flurbiprofen-treated dogs regional function returned to normal within 5 min of reperfusion in both the subendocardium (%SS preocclusion = 17.2±2.0%; 5 min reperfusion = 17.8+3.1%; P = NS) and in the midmyocardium (%SS preocclusion = 17.8±+2.2%; 5 min reperfusion = 17.9+2.3%; P = NS) and was not significantly different after 5 h of reperfusion from what it was before coronary occlusion. In the subepicardium oftreated dogs regional function began to improve within 15 min of drug administration even during coronary occlusion. Regional function was not different from preocclusion values after either 5 min or 5 h of reperfusion (%SS preocclusion = 21.0±2.4%; 5 min reperfusion = 20.6 ±+3.8%; P = NS). In dogs subjected to 3 h of coronary occlusion and 72 h of reperfusion, the administration of flurbiprofen was also associated with significantly smaller infarcts and a significantly more rapid rate of functional recovery than in control dogs.Thus, it appears that flurbiprofen not only decreased the quantity of necrosis in tissue made isc...

show abstract

“…The most important factor is the reduction in heart rate [2], Over all there is a reduction in coronary blood flow secondary to the reduction in myocardial oxy gen consumption [3]. However, some animal experiments suggest that beta blockade may improve coronary blood flow distribution, diverting blood from the relatively well per fused myocardium into poorly perfused isch aemic parts of the heart [4],…”

mentioning

confidence: 99%

Carvedilol in Ischaemic Heart Disease

Prichard

1993

Cardiology

View full text Add to dashboard Cite

β-adrenoceptor-blocking drugs, first introduced for the treatment of symptomatic angina pectoris, have been found effective across the whole spectrum of ischaemic disease. Labetalol was the first combined-action beta-blocking drug to be described and was shown to be capable of increasing exercise tolerance in patients with angina pectoris. Carvedilol also possesses a peripheral vasodilating action mainly due to an α₁- adrenoceptor blockade. Haemodynamic studies with carvedilol in patients with ischaemic heart disease have shown a reduction in peripheral vascular resistance in contrast to propranolol which increases systemic resistance and reduces cardiac output. Additionally, in ischaemic heart failure there is evidence of improved myocardial function, as shown by an increase in ejection fraction, after the administration of carvedilol. Carvedilol has been shown to improve exercise tolerance in patients with angina pectoris and reduce the occurrence of episodes of silent myocardial ischaemia. Carvedilol, unlike many beta-blocking drugs, does not adversely affect the plasma lipid profile qualitatively or quantitatively. In contrast to many non-selective beta-blocking drugs, carvedilol has a more favourable haemodynamic profile, and its lack of adverse influence on the plasma lipid profile may be important in its long-term use.

show abstract

Effects of a cardiac glycoside in combination with propranolol on the ischemic heart of conscious dogs.

Cited by 20 publications

References 18 publications

Importance of heart rate in determining the effects of sympathomimetic amines on regional myocardial function and blood flow in conscious dogs with acute myocardial ischemia.

Importance of heart rate in determining the effects of sympathomimetic amines on regional myocardial function and blood flow in conscious dogs with acute myocardial ischemia.

Early Recovery of Regional Performance in Salvaged Ischemic Myocardium following Coronary Artery Occlusion in the Dog

Carvedilol in Ischaemic Heart Disease

Contact Info

Product

Resources

About