Initial myocardial adjustments to brief periods of ischemia and reperfusion in the conscious dog.

Pagani, Massimo; Vatner, Stephen F.; Baig, Hank; Braunwald, Eugene

doi:10.1161/01.res.43.1.83

Cited by 118 publications

(22 citation statements)

References 36 publications

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“…This overshoot in function was prevented by inhibiting the reactive hyperemia by gradually releasing the coronary occlusion (11). Moreover, a postexercise augmentation ofleft ventricular function associated with coronary hyperemia was observed in a prior study conducted in this laboratory, in which the normal increase in left main coronary inflow was restricted during exercise (12).…”

Section: Influence Of Perfusion Pressure On Coronary Vascular Responsmentioning

confidence: 82%

“…NS of myocardial ischemia induced by coronary artery occlusion, the resultant reactive hyperemia is associated with a transient overshoot in myocardial function above preischemic levels in the region rendered ischemic (11). This overshoot in function was prevented by inhibiting the reactive hyperemia by gradually releasing the coronary occlusion (11).…”

Section: Influence Of Perfusion Pressure On Coronary Vascular Responsmentioning

confidence: 99%

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Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Murray¹,

Vatner²

1981

J. Clin. Invest.

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A B S T R A C T Measurements of right coronary artery blood flow, aortic and right ventricular (RV) pressures and heart rate were radiotelemetered during strenuous, spontaneous exercise in normal dogs and dogs with severe RV hypertrophy induced by chronic (5-6 mo) pulmonary artery stenosis. With fixed pulmonic stenosis, dogs with RV hypertrophy exhibited a decrease (P < 0.01) in arterial pressure during exercise. Under these conditions, exercise increased right coronary artery blood flow and decreased right coronary vascular resistance less (P < 0.05) in dogs with RV hypertrophy compared with normal. This attenuated response of right coronary artery blood flow of dogs with RV hypertrophy was not observed when arterial pressures remained at preexercise values during exercise. However, regardless of changes in arterial pressures during exercise, all dogs with RV hypertrophy demonstrated a striking postexercise coronary hyperemia (P < 0.01), suggesting a perfusion deficit of the hypertrophied right ventricle during exercise. These results imply a fundamental defect in the ability of the coronary circulation of the severely hypertrophied right ventricle to provide sufficient nutrient supply in the face of elevated metabolic demands of exercise.

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Section: Influence Of Perfusion Pressure On Coronary Vascular Responsmentioning

confidence: 82%

Section: Influence Of Perfusion Pressure On Coronary Vascular Responsmentioning

confidence: 99%

Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Murray¹,

Vatner²

1981

J. Clin. Invest.

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“…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.

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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...

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“…In each of these cases, hemodynamic and electrocardiographic alterations can precede pain or occur in the absence of it. These circulatory changes suggest a various participation of pressor, depressor, and baroreceptive reflex mechanisms (Peterson and Bishop, 1974) associated with the direct striking depressing effects of ischemia on ventricular function (Pagani et al, 1978).…”

Section: Pathophysiological Implicationsmentioning

confidence: 99%

Analysis of the pressor sympathetic reflex produced by intracoronary injections of bradykinin in conscious dogs.

Pagani¹,

Pizzinelli²,

Furlan³

et al. 1985

Circulation Research

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SUMMARY. The reflex hemodynamic effects of intracoronary bradykinin were tested in 20 conscious instrumented dogs. When the experiments were performed after full recovery from surgery and anesthesia, graded doses (10-300 ng/kg) of bradykinin always produced graded pressor responses, in the absence of any pain reaction. At the maximum pressor response obtained with 100 ng/kg, mean arterial pressure rose 28 ± 3% from 89 ± 4 mm Hg, left ventricular pressure 20 ± 3% from 121 ± 2 mm Hg, heart rate 30 ± 4% from 88 ± 5 beats/min, rate of change of left ventricular pressure 18 ± 3% from 2812 ± 65 mm Hg/sec (P < 0.01). Higher doses of bradykinin did not produce greater responses. The magnitude of the response was similar when the injection was performed in either the left anterior descending (change in mean arterial pressure 29 ± 3%) or circumflex (change in mean arterial pressure 27 ± 2%) coronary artery. The reflex nature of the response was proved by its disappearance after appropriate pharmacological blockades; moreover, after vagotomy, the pressor rise was maintained, the heart rate response was reduced (change in heart rate 10 ± 2%), and the inotropic response was enhanced (rate of change of left ventricular pressure 24 ± 3%). This suggested that the afferent pathway of the pressor reflex was in the sympathetic nerves and that a subordinate vagal depressor reflex was also operative. No pain reaction was obtained even when injecting very large amounts (1000-2000 ngAg) of bradykinin, which, instead, induced arterial hypotension. Pain reactions (as inferred by agitation and vocalization) were observed in three out of nine dogs studied during the first week after surgery. This reaction was no longer present when the same animals were tested later on, at the time of complete recovery. In five of the nine dogs studied during the first week after surgery, the intracoronary injection of bradykinin produced a depressor (change in mean arterial pressure -31 ± 6%) response, which, however, reverted to a pTessor effect (change in mean arterial pressure 22 ± 4%) later, when recovery was complete. In five additional dogs, the pressor response observed after full recovery from surgery was no longer present when the injection of bradykinin was repeated under anesthesia. The present experiments in conscious dogs show that the chemical stimulation of the fully innervated heart with intracoronary bradykinin can initiate pressor reflexes independent of pain and in the presence of intact buffering mechanisms. (Circ Res 56:175-183, 1985)

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Initial myocardial adjustments to brief periods of ischemia and reperfusion in the conscious dog.

Cited by 118 publications

References 36 publications

Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

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

Analysis of the pressor sympathetic reflex produced by intracoronary injections of bradykinin in conscious dogs.

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