Improved GLC Determination of Plasma Nitroglycerin Concentrations

Yap, Peter S.K.; McNiff, Edward F.; Fung, Ho‐Leung

doi:10.1002/jps.2600670445

Cited by 68 publications

(19 citation statements)

References 5 publications

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“…Our findings of 0.1 to 1 mm to test the inhibitory effect of SNP and NTG. For NTG, these concentrations are 10-fold higher in the present study are in accordance with this theory for NTG in all the three vasoconstrictor-induced as well as for than the plasma concentrations at an infusion rate of 37-175 mg min −1 [19,20], which is 0.5-2.7 ng ml −1 SNP in ET-1 and PE-induced contraction. In the present study, we have demonstrated that in general the effect of (8.7-7.9-log m units).…”

Section: Discussionsupporting

confidence: 90%

Comparison of nitroprusside and nitroglycerin in inhibition of angiotensin II and other vasoconstrictor‐mediated contraction in human coronary bypass conduits

Yang

1997

Brit J Clinical Pharma

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Aims To compare the effect of nitroprusside (SNP) and nitroglycerin (NTG) on angiotensin II (ANGII), endothelin-1 (ET-1), and a 1 -adrenoceptor ( phenylephrine, PE)-mediated contraction in internal mammary artery (IMA). Methods Human IMA segments (n=120) taken from 37 patients were studied. Concentration-relaxation curves for SNP and NTG were established in IMA precontracted with these vasoconstrictors. Concentration-contraction curves were also constructed in IMA rings incubated with SNP and NTG (0.1 and 1 mm) for 10 min. Results Both SNP and NTG caused full relaxation with similar EC 50 s except NTG was four-fold more potent than SNP in PE-induced contraction (−7.92±0.06 vs −7.32±0.2 log m, mean±s.e. mean, P<0.01; 95% confidence interval for the difference of the means: 0.19, 1.01 log m). Pretreatment with SNP (0.1 and 1 mm) significantly depressed the contraction by ANGII from 56.6±7.7% (of 100 mm K + -contraction) to 18.3±8.6% and 3.9±2.1% (P=0.0001). In four rings treated with SNP, the contraction to ANGII was abolished whereas NTG did not depress ANGII-mediated contraction. Pretreatment with SNP (1 mm), but not NTG, significantly depressed the magnitude of the PE-induced contraction from 4.7±1.2 to 1.7±0.4 g ( P<0.05). Treatment with both SNP and NTG significantly increased the EC 50 (−5.09±0.17 log m, P=0.0007 for SNP and −5.40±0.06 log M, P= 0.02 for NTG). Pretreatment with SNP did not significantly change either the magnitude or the EC 50 of the ET-1-induced contraction. Conclusions SNP may be advantageous compared with NTG in preventing coronary arterial graft contraction. However, once grafts have constricted to ANGII, a 1 -adrenoceptor agonists, and ET-1, NTG may be only marginally advantageous.

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Section: Discussionsupporting

confidence: 90%

Comparison of nitroprusside and nitroglycerin in inhibition of angiotensin II and other vasoconstrictor‐mediated contraction in human coronary bypass conduits

Yang

1997

Brit J Clinical Pharma

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“…These four rings were equilibrated for 5 min [7,20] with vehicle of GTN (0.1% ethanol) or 10 nM, 100 nm, or 30 gM GTN. Those concentrations (10-100 nM) were chosen since they are similar to the optimal plasma concentration reached clinically [22,23] and the supra-clinical concentration (30 gM) was given to study the possible maximal inhibitory effect. A cumulative concentration-contraction curve was then constructed for ET-1.…”

Section: Generalmentioning

confidence: 99%

Interaction between endothelin and vasodilators in the human internal mammary artery.

He¹,

Yang²,

Mack³

et al. 1994

Brit J Clinical Pharma

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1. The internal mammary artery (IMA) is the primary choice as an arterial graft for coronary artery bypass surgery. Endothelin (ET) has been recently measured with an increased release after cardiopulmonary bypass for coronary artery bypass grafting. Threshold concentrations of ET‐1 have been found to amplify specifically contractions induced by noradrenaline and serotonin. This study was designed to investigate the effect of glyceryl trinitrate (GTN) and calcium antagonists on ET‐1 contraction in the human IMA. 2. Human IMA segments taken from 21 patients undergoing IMA‐coronary artery bypass grafting were mounted in an organ bath under the physiological pressure determined from their own length‐tension curves. Four ring segments were allocated into four groups. One served as a control and the others were treated with GTN (10, 100 nM, or 30 microM) for 5 min or nifedipine (20 or 200 nM, or 30 microM) for 25 min before concentration‐contraction curves to ET‐1 were established. In separate experiments, the concentration‐relaxation curves to GTN or nifedipine were established in the IMA rings precontracted with ET‐1 (10 nM). 3. Pretreatment of IMA with GTN for 5 min did not alter the ET‐1‐induced contraction. Pretreatment with 20 or 200 nM of nifedipine slightly but not significantly, altered the maximum contraction induced by ET‐1. Higher concentrations (30 microM) significantly reduced the maximum contraction force (P = 0.008). On the other hand, GTN caused 76.44 +/‐ 6.35% relaxation in ET‐1‐precontracted IMA. In contrast, the nifedipine‐induced relaxation was difficult to establish due to unsustained contraction to ET‐1.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…During each study period, the patients were allowed normal activity without exertion. (Yap, McNiff & Fung, 1978) Mixing was achieved by rapidly injecting the organic solvent into the plasma with a 0.2-ml Kirk pipette affixed to a 1-ml tuberculin syringe. The upper (organic) layer was then removed with a Pasteur pipette.…”

Section: Acute Dosesmentioning

confidence: 99%