The Effect of Angiocardiographic Contrast Medium on Circulatory Dynamics in Man

Brown, Richard W.; Rahimtoola, Shahbudin H.; Davis, George D.; Swan, H. J. C.

doi:10.1161/01.cir.31.2.234

Cited by 119 publications

(17 citation statements)

References 14 publications

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“…These same investigators 19 studied the effects of 10 and 30 /tg/kg SQ2O,881 in sodium-depleted recumbent subjects, both normal and hypertensive, who had undergone renal arteriography 30 or more minutes previously. In this setting, after 20 minutes, SQ20.881 increased plasma bradykinin in hypertensive but not in normal subjects; the degree to which the findings were modified by the known vascular effects of angiographic contrast medium 30 is uncertain, however. In our study, 3 mg/kg SQ20.881 did not cause a greater reduction of blood pressure or plasma angiotensin II than a dose of 1 mg/kg.…”

Section: Discussionmentioning

confidence: 72%

The effect of converting enzyme inhibition with SQ20,881 on plasma and urinary kinins, prostaglandin E, and angiotensin II in hypertensive man.

Vinci¹,

Horwitz²,

Zusman³

et al. 1979

Hypertension

119

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SUMMARYThe relationship between levels of angiotensin II, kinins, and prostaglandin E and the depressor response to 1 or 3 mg/kg of the conrerting enzyme inhibitor SQ20.88I was studied in recumbent hypertensive subjects during 109 mEq and 9 mEq/day sodium intake. In 13 sodium-replete patients, SQ20,881 decreased angiotensin II from 46.7 ± 9.2 (mean ± SEM) to 31.7 ± 5.1 pg/ml and plasma aldosterone from 6.8 ± 0.9 to 2.9 ± 0.6 ng/dl (p < 0.003) without compensatory elevations of plasma renin activity and angiotensin I. Administration of SQ20.881 had no effect on plasma bradyklnin but it increased mean immunoreactive prostaglandin E from 143 ± 17 to 302 ± 75 pg/ml (p < 0.02) and in some patients it increased urinary kinin excretion. The distribution of the mean 2-hour depressor response was bimodal as four patients had a fall in diastollc pressure of at least 11 torr (mean 14 ± 1 torr) and nine had a minimal depressor response £ 4 torr, (-1 ± 1 torr); patients with a greater decrease in blood pressure showed an increase in urinary kinin excretion rate, whereas the other patients showed a fall (471 ± 121 vs -99 ± 106 ng/hr; p < 0.005); both had similar control levels and responses of plasma angiotensin II, aldosterone, immunoreactive prostaglandin E, and brad} kinin. In nine sodium-depleted patients, SQ20.881 slightly decreased mean angiotensin II from 30.5 ± 4.5 to 22.4 ± 4.3 pg/ml early after drug administration, but because this was accompanied by rapid compensatory elevations of angiotensin I (which increased from < 14 pg/ml to levels as high as 513 pg/ml) and mean plasma renin activity from 43 ± 1.6 to 13.9 ± 43 ng/ml/hr, levels of angiotensin II returned toward control soon after drug administration. We found that SQ20381 had no effect on plasma bradykinin but increased urinary kinin excretion by 203 ± 63 ng/hr (p <0.02) and in some patients increased plasma prostaglandin E. The distribution of the mean 2-hour depressor response in these nine sodium-depleted patients was also bimodal as flve sodium-depleted patients had a depressor response to drug of at least 7 torr (10 ± 1 torr) while four sodium-depleted patients had a minimal response (-1 ± 1 torr). The patients with a greater decrease in blood pressure showed a greater (p < 0.05) increase in both immunoreactive prostaglandin E (248 ± 99 vs 20 ± 12 pg/ml) and urinary kinin excretion (270 ± 69 vs 83 ± 75 ng/hr) whereas decrements in plasma angiotensin II and aldosterone were similar. Thus, the depressor response to SQ20,881 correlated better with alterations in urinary kinins and plasma prostaglandin E than with changes in plasma levels of angiotensin II.

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Section: Discussionmentioning

confidence: 72%

The effect of converting enzyme inhibition with SQ20,881 on plasma and urinary kinins, prostaglandin E, and angiotensin II in hypertensive man.

Vinci¹,

Horwitz²,

Zusman³

et al. 1979

Hypertension

119

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“…10 The left ventriculograms were performed before the coronary arteriograms to avoid the hemodynamic and cardiac effects of accumulated contrast material." [1][2][3][4][5][6][7][8][9][10][11][12][13] The left ventricular cineangiograms were analyzed by a combination of the technic of Greene and Bunnell and the area-length method for calculation of volume of Dodge and Sandler, as previously reported.9 14 15 When premature ventricular contractions were induced by injection of contrast material, the second normal cycle following an extrasystole was the first one employed in the volume calculations. During normal rhythm, the ventricular cavity on each frame was traced and the area measured by planimetry.…”

mentioning

confidence: 99%

Systolic and Diastolic Abnormalities of the Left Ventricle in Coronary Artery Disease

1970

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SUMMARYLeft ventricular volume and circumference were calculated from cineangiocardiograms at 60 frames/sec in 15 patients with arteriographically proven coronary artery disease (CAD) and five control subjects. The patients with CAD had no mitral regurgitation and had an average end-diastolic volume equivalent to that reported by others in normal subjects and to that of the control group. The average end-diastolic pressure was higher in CAD and was often abnormal, despite lack of increase in enddiastolic volume.

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“…The exercise tests were per formed after the coronary angiography. Al though 25 min were allowed for an adequate dissipation of the injections of contrast me dium, which is the time interval usually rec ommended [18], a masking effect of the dye on coronary vasodilation induced by SIN-1, cannot be excluded. Another methodological problem is the fact that the exercises were performed in supine position.…”

Section: Discussionmentioning

confidence: 99%

Exercise-Induced Angina Alleviated by Intracoronary SIN-1<sup>1</sup>

Berkenboom

Unger²,

Jottrand³

et al. 1987

Cardiology

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To investigate the mechanism of action of nitrovasodilators in exercise-induced angina, 15 patients with chronic stable angina underwent a symptom-limited supine exercise test (exercise 1). After recovery, in 10 patients (group I) a coronary vasodilator, SIN-1 (the active metabolite of molsidomine) was injected into the most diseased coronary artery (80 µg in 4 min). In the remaining 5, a placebo was injected (group II). Immediately thereafter, the same exercise (exercise 2, identical workloads and exercise duration) was repeated. In group I, after intracoronary injection of SIN-1, the control values at rest (including pulmonary wedge pressure) did not significantly change. Heart rate, blood pressure and cardiac index rose in a similar way during exercises 1 and 2 (61, 20, 26 and 62, 21, 35%, respectively). However, 3 patients were angina-free without ST-changes during exercise 2. In the remaining 7, the ST/heart rate slope was reduced (60%; p < 0.02), the increase in pulmonary wedge pressure was less pronounced (p < 0.01) and ST-depression at end-exercise 2 was smaller: 1.3 ± 0.3 versus 2.1 ± 0.3 mm (p < 0.01) for identical work loads and double products. In group II, exercise 2 was identical to exercise 1 and the ST/heart rate slopes were quite reproducible. Therefore, these results argue for an improvement in coronary blood supply after intracoronary SIN-1 and suggest that the beneficial action of nitro vasodilators could be related to direct effects on the coronary circulation. However, the magnitude of this mechanism seems variable from one patient to another.

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The Effect of Angiocardiographic Contrast Medium on Circulatory Dynamics in Man

Cited by 119 publications

References 14 publications

The effect of converting enzyme inhibition with SQ20,881 on plasma and urinary kinins, prostaglandin E, and angiotensin II in hypertensive man.

The effect of converting enzyme inhibition with SQ20,881 on plasma and urinary kinins, prostaglandin E, and angiotensin II in hypertensive man.

Systolic and Diastolic Abnormalities of the Left Ventricle in Coronary Artery Disease

Exercise-Induced Angina Alleviated by Intracoronary SIN-1<sup>1</sup>

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