The effects of dipyridamole on blood flow and oxygen handling in the acutely ischaemic and normal canine myocardium

Marshall, Richard; Parratt, J. R.

doi:10.1111/j.1476-5381.1973.tb17249.x

Cited by 64 publications

(20 citation statements)

References 14 publications

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“…As diazepam is widely used in patients with ischaemic heart disease, further investigation of this aspect of diazepam action is warranted since direct coronary vasodilatation such as that produced by adenosine, dipyridamole, dilazep, hexabendine and lidoflazine has been considered to compromise perfusion of ischaemic areas by 'coronary steal', i.e. diversion of blood away from poorly perfused, but maximally dilated areas (Marshall & Parratt, 1973).…”

Section: Discussionmentioning

confidence: 99%

Potentiation of the Effects of Adenosine on Isolated Cardiac and Smooth Muscle by Diazepam

Clanachan

Marshall

1980

British J Pharmacology

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Adenosine (10−7 to 3 times 10−4 m) or 2‐chloroadenosine (10−8 to 10−5 m) produced concentration‐dependent inhibition of the responses of the rat isolated vas deferens to electrical field stimulation. In electrically driven (2 Hz) guinea‐pig isolated left atria, adenosine (10−6 to 10−3 m) or 2‐chloroadenosine (10−8 to 10−7 m) produced concentration‐dependent decreases in isometric tension. Diazepam (10−6 and 10−5 m) had no direct effect per se, but significantly potentiated the inhibitory action of adenosine on both tissues without altering the inhibitory effect of 2‐chloroadenosine. The adenosine uptake inhibitors, hydroxynitrobenzylthioguanosine (HNBTG, 10−5 m) and dipyridamole (10−5 m) also potentiated the inhibitory actions of adenosine in rat vas deferens, but not those of 2‐chloroadenosine. Following adenosine uptake inhibition in rat vas deferens by HNBTG (10−5 m), diazepam (10−5 m) failed to produce any significant further potentiation of the inhibitory action of adenosine. It is concluded that the potentiation of adenosine by diazepam is possibly due to an inhibition of adenosine uptake.

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Section: Discussionmentioning

confidence: 99%

Potentiation of the Effects of Adenosine on Isolated Cardiac and Smooth Muscle by Diazepam

Clanachan

Marshall

1980

British J Pharmacology

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“…For comparative purposes, the selective coronary dilator drug dipyridamole was administered. This drug has been shown to increase flow to the normal myocardium considerably and to leave flow in the ischaemic zone unchanged (Marshall & Parratt, 1973b Although decreased temperature in both regions of the heart was the usual response to practolol, a different effect was obtained when the thermocouples Time Figure 4 The effects of practolol on both normal (0) and ischaemic (0) myocardial muscle temperature in the deep subendocardial layers of the canine left ventricle.…”

Section: Methodsmentioning

confidence: 99%

Comparative Effects of Propranolol and Practolol in the Early Stages of Experimental Canine Myocardial Infarction

Marshall

Parratt

1976

British J Pharmacology

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I The effects of propranolol and practolol, at equivalent myocardial P-adrenoceptor blocking doses, (as assessed by the degree of shift of isoprenaline dose-response curves) were investigated in anaesthetized greyhounds before and after acute coronary artery ligation. 2 When administered intravenously to the intact closed-chest dog, propranolol (0.1 mg/kg) and practolol (0.5 mg/kg) caused similar decreases in heart rate, left ventricular dP/dt max, myocardial blood flow and cardiac output. Only propranolol increased peripheral vascular resistance. 3 When administered 2-3 h after acute coronary artery ligation, propranolol (0.1 mg/kg) significantly decreased blood flow in both normally perfused and ischaemic regions of the heart. There was also electrocardiographic evidence of further deterioration after propranolol; two out of seven animals died following this treatment. 4 Practolol (0.5 mg/kg) when administered after coronary artery ligation also decreased normal myocardial blood flow but flow in the ischaemic area remained unchanged. Evidence was obtained from electrocardiographic, myocardial temperature, myocardial 02 consumption and lactate measurements that the administration of practolol, in contrast to propranolol, benefited the ischaemic myocardium. SAnalysis of the results suggests that this beneficial action of practolol may be related to at least two mechanisms. Firstly the ability of practolol to increase the period during diastole when perfusion of the subendocardium is possible, without decrteing the transventricular pressure during this period. Secondly that practolol does not unnu;k a-adrenoceptor vasoconstriction in the ischaemic region.

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“…Although it is generally recognized that dipyridamole increases the coronary blood flow in the area perfused by normal coronary arteries, there are conflicting reports (10)(11)(12)(13) concerning the absolute flow change in the jeopardized area. Our data on the changes in collateral flow due to dipyridamole were in agreement with those described in a study by Becker et al (1).…”

Section: Discussionmentioning

confidence: 98%

Effects of dipyridamole on collateral flow and regional myocardial function in conscious dogs with newly developed collaterals

et al. 1990

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Studies were conducted on six conscious dogs instrumented for measurement of subendocardial segment lengths in the area perfused by the left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCCA), LCCA flow, and left ventricular pressure. Externally inflatable occluders were placed around the proximal LAD and LCCA. Collateral channels sufficient for the resting metabolic demands in the occluded LCCA perfusion territory were induced by repeated, brief LCCA occlusions. Dogs were then subjected to two consecutive brief periods of LAD occlusion. Dipyridamole (0.25 mg/kg) was injected intravenously 3 min prior to the second LAD occlusion. The collateral blood flow from the LCCA to the occluded LAD area was measured as the stepwise decrease in LCCA flow upon release of the LAD occlusion. During LAD occlusion after dipyridamole treatment collateral blood flow velocity decreased to 3.8 +/- 1.1 cm/s (+/- standard error) compared with a value of 4.9 +/- 0.9 cm/s measured during LAD occlusion without dipyridamole treatment. Percentage systolic segment shortening in the collateral dependent zone significantly deteriorated from 14.3 +/- 5.2 to 9.7 +/- 5.0% (p less than 0.05). Electrocardiograms taken simultaneously from endocardial ultrasonic transducers in the ischemic segment revealed significant increases in ST-segment level from 4.2 +/- 0.6 to 5.4 +/- 0.6 mV. These findings indicate that dipyridamole adversely affects the extent of myocardial ischemia in the collateral-dependent zone.

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The effects of dipyridamole on blood flow and oxygen handling in the acutely ischaemic and normal canine myocardium

Cited by 64 publications

References 14 publications

Potentiation of the Effects of Adenosine on Isolated Cardiac and Smooth Muscle by Diazepam

Potentiation of the Effects of Adenosine on Isolated Cardiac and Smooth Muscle by Diazepam

Comparative Effects of Propranolol and Practolol in the Early Stages of Experimental Canine Myocardial Infarction

Effects of dipyridamole on collateral flow and regional myocardial function in conscious dogs with newly developed collaterals

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