Effects of Nitroglycerin and Propranolol on the Distribution of Transmural Myocardial Blood Flow during Ischemia in the Absence of Hemodynamic Changes in the Unanesthetized Dog

Swain, Judith L.; Parker, John P.; McHale, Philip A.; Greenfield, Joseph C.

doi:10.1172/jci109395

Cited by 37 publications

(7 citation statements)

References 24 publications

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“…These dogs were considered to have collateral development stimulated by the partial stenosis of the left circumflex coronary artery. All myocardial blood flow changes are greater than the error associated with the microsphere method for this laboratory (Swain et al, 1979). Mean flow to the collateral-dependent region increased from 0.10 ± 0.07 ml/min per g on day 7 to 0.25 ± 0.18 ml/min per g on day 14 (P = 0.01).…”

Section: Resultsmentioning

confidence: 70%

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Increase in collateral blood flow following repeated coronary artery occlusion and nitroglycerin administration.

Brazzamano¹,

Mays²,

Rembert³

et al. 1984

Circulation Research

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SUMMARY. The effects of occlusion, reperfusion, reocclusion (n = 13), and nitroglycerin (n = 10) on regional transmural myocardial collateral blood flow was tested in conscious dogs in which collateral development was stimulated by partial stenosis of the left circumflex coronary artery. Hemodynamics and collateral blood flow were measured during the awake state using 9-/im radioactive microspheres. Regional transmural flow was measured during transient occlusion of the circumflex artery at 7 and at 14 days postoperatively. On the 14th postoperative day, two sets of circumflex occlusions and blood flow measurements were carried out. The first set consisted of two occlusions separated by 15 minutes. The second set performed 2 hours later included two occlusions, separated by 15 minutes, and nitroglycerin administration. Mean collateral blood flow increased significantly (P = 0.002) from 0.10 ± 0.07 ml/min per g on day 7 to 0.25 ± 0.18 ml/ min per g on day 14. A significant increase in mean collateral blood flow from occlusion one to two was observed (0.28 ± 0.17 to 0.37 ± 0.22 ml/min per g, P = 0.005). Mean collateral flow increased significantly (P = 0.01) between pre-to post-nitroglycerin occlusions, 0.28 ± 0.20 to 0.46 ± 0.32 ml/min per g. Although this increase appeared to be greater than during the first set of occlusions, it did not reach statistical significance (P = 0.08). These data indicate that when immature collaterals are present, occlusions, reperfusion, and reocclusions of a major coronary artery produce augmentation in collateral flow. This must be considered in evaluating interventions which may alter collateral flow. (CircRes 54: 204-207, 1984) IN the event of coronary artery occlusion, collateral vessels can provide an alternate source of blood flow. Little is known, however, about the functional physiology of immature collateral vessels. If a partially stenosed major coronary artery is suddenly totally obstructed, the integrity of the myocardium will become entirely dependent upon the functional adequacy of the collateral vessels. It is important, therefore, to determine whether immature collateral vessels function to deliver a fixed maximal amount of flow immediately after total occlusion of the stenosed coronary, or if blood flow to the collateraldependent area can be augmented by prior brief episodes of total occlusion, or by drug administration.In order to carry out these studies, a model was developed in our laboratory in which collateral vessel growth was stimulated by partial stenosis of the left circumflex coronary artery. In our model, the blood flow to a region of myocardium was supplied by both the partially stenosed circumflex artery, and by immature but developing collateral vessels. During complete temporary occlusion of the circumflex artery, the immature collaterals were the primary source of flow to this area of myocardium.The primary aim of the study was to determine whether (after a brief occlusion of a major coronary artery and reperfusion), a second occlusion would elic...

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Section: Resultsmentioning

confidence: 70%

“…Regional transmural myocardial blood flow was measured with 9 ± 1-jzm microspheres (Minnesota Mining and Manufacturing Co.) labeled with six different 7-emirting radionuclides, as has been described previously (Swain et al, 1979).…”

Section: Methodsmentioning

confidence: 99%

Increase in collateral blood flow following repeated coronary artery occlusion and nitroglycerin administration.

Brazzamano¹,

Mays²,

Rembert³

et al. 1984

Circulation Research

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“…In contrast, Neichi et al (39) (42)(43)(44)(45). NTG may also relieve angina by causing relaxation of coronary artery spasm (46), and by shifting blood flow from normally perfused to ischemic myocardium in the absence of peripherally mediated hemodynamic changes (47). We have shown that intact monolayers of human endothelial cells in vitro release PGI2 in response to clinically attainable concentrations of NTG.…”

Section: Discussionmentioning

confidence: 86%

Nitroglycerin Stimulates Synthesis of Prostacyclin by Cultured Human Endothelial Cells

Levin¹,

Jaffe²,

Weksler³

et al. 1981

J. Clin. Invest.

255

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A B S T R A C T Nitroglycerin (NTG), the agent most commonly used to treat acute angina pectoris, is a vasodilator whose mechanism of action remains unknown. We hypothesized that NTG might induce endothelial cells to synthesize prostacyclin (PGI2), a known vasodilator and inhibitor ofplatelet aggregation. Therefore, cultured human endothelial cells were incubated with NTG at various concentrations for 1-3 min. PGI2 biologic activity in the endothelial cell supernates was assayed by inhibition of platelet aggregation in vitro. The concentration of 6-keto-PGFie, the stable hydrolysis product of PGI2, was measured by specific radioimmunoassay.NTG alone significantly inhibited platelet aggregation and thromboxane A2 synthesis only at suprapharmacologic concentrations (.1 ,ug0ml). However, when NTG at clinically attainable concentrations (0.1-10 nglml) was incubated with endothelial cells, the endothelial cell supemates inhibited platelet aggregation in a dose-dependent manner. The inhibitor was heat labile. Radioimmllunoassay of the endothelial cell supernates for 6-keto-PGF,i, demonstrated that NTG elicited dose-dependent increments in the synthesis of PGI2 by endothelial cells, ranging from 13% at NTG 10 pg/ml to 63% at NTG 10 ng/ml (P < 0.01, n = 10). Pretreatment of endothelial cells with either aspirin (50 ,uM for 120 min) or the prostacyclin synthetase inhibitor 15-hydroperoxyarachidonic acid

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“…The flow (cm3/min) of each sample was divided by the sample weight (grams) and expressed as cm3/min per g of tissue (12). The microsphere method described above has been shown in our laboratory to be adequate to test for differences in segmental atrial blood flow (13).…”

Section: Methodsmentioning

confidence: 99%

Regional atrial blood flow in dogs. Effect of hypertrophy on coronary flow reserve.

Bauman

Rembert²,

Greenfield³

1989

J. Clin. Invest.

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Little is known regarding regional atrial blood flow responses during varying hemodynamic states in both the normal and hypertrophied atria. This study was undertaken to develop a canine model of chronic atrial hypertrophy and to define in both this group and in normal dogs the regional blood flow response to acute atrial fibrillation and to measure coronary flow reserve. In the 12 dogs with atrial but not ventricular hypertrophy the mean left and right atrial weights were 75 and 47% respectively greater than in the normal group. Blood flow in the normal dogs was less in the appendage than in the nonappendage region for both atria and increased significantly during atrial fibrillation. Similar findings were noted in the hypertrophy group except that during control conditions the left atrial appendage flow was similar to the nonappendage flow. Minimal vascular resistance for the hypertrophy group, 39±3 was significantly (P < 0.05) greater when compared to the normal group 28±2 mmHg/cm3 per min per g. Thus, significant regional blood flow differences occur in both the normal and hypertrophied atria. In addition, atrial hypertrophy does not alter the autoregulatory capacity to the hemodynamic stress of atrial fibrillation but does reduce coronary flow reserve.

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Effects of Nitroglycerin and Propranolol on the Distribution of Transmural Myocardial Blood Flow during Ischemia in the Absence of Hemodynamic Changes in the Unanesthetized Dog

Cited by 37 publications

References 24 publications

Increase in collateral blood flow following repeated coronary artery occlusion and nitroglycerin administration.

Increase in collateral blood flow following repeated coronary artery occlusion and nitroglycerin administration.

Nitroglycerin Stimulates Synthesis of Prostacyclin by Cultured Human Endothelial Cells

Regional atrial blood flow in dogs. Effect of hypertrophy on coronary flow reserve.

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