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PubMed1997

Differential effects of captopril and nitrates on muscle sympathetic nerve activity in volunteers.

BACKGROUND: The sympathetic nervous system (SNS) is an important regulator of cardiovascular function. Activation of SNS plays an important role in the pathophysiology and the prognosis of cardiovascular diseases such as heart failure, acute coronary syndromes, arrhythmia, and possibly hypertension. Vasodilators such as adenosine and sodium nitroprusside are known to activate SNS via baroreflex mechanisms. Because vasodilators are widely used in the treatment of patients with cardiovascular diseases, the aim of the present study was to assess the influence of clinically used dosages of isosorbide dinitrate and captopril on sympathetic nerve activity at rest and during stimulatory maneuvers. METHODS AND RESULTS: Twenty-eight healthy volunteers were included in this double-blind placebo-controlled study, and muscle sympathetic nerve activity (MSA; with microelectrodes in the peroneal nerve), blood pressure, heart rate, and neurohumoral parameters were measured before and 90 minutes after the oral administration of 40 mg isosorbide dinitrate or 6.25 mg captopril. Furthermore, a 3-minute mental stress test and a cold pressor test were performed before and 90 minutes after drug administration. Resting MSA did not change after captopril and decreased compared with placebo (P < .05 versus placebo), whereas isosorbide dinitrate led to a marked increase in MSA (P < .05). Systolic blood pressure was reduced by isosorbide dinitrate (P < .05), whereas captopril decreased diastolic blood pressure (P < .05). The increases in MSA, blood pressure, and heart rate during mental stress were comparable before and after drug administration regardless of the medication. During cold pressor test, MSA and systolic and diastolic blood pressures increased to the same degree independent of treatment, but after isosorbide dinitrate, the increase in MSA seemed to be less pronounced. Heart rate did not change during cold stimulation. Plasma renin activity increased after captopril and isosorbide dinitrate (P < .05), whereas placebo had no effect. Endothelin-1 increased after placebo and isosorbide dinitrate (P < .05) but not after captopril. CONCLUSIONS: Thus, captopril suppressed MSA despite lowering of diastolic blood pressure but allowed normal adaptation of the SNS during mental or physical stress. In contrast, the nitrate strongly activated the SNS under baseline conditions. These findings demonstrate that vasodilators differentially interact with the SNS, which could be of importance in therapeutic strategies for the treatment of patients with cardiovascular diseases.

Adult↗
PubMed1990

Effects of nifedipine on left ventricular diastolic function in hypertension; echo Doppler study.

Hypertensive cardiac disease shows early alteration of left ventricular diastolic filling, characterized by a longer isovolumetric relaxation period and by an altered E/A ratio on the mitral spectral Doppler. We chose ten hypertensive patients who had left ventricular hypertrophy, but no left ventricular dilatation or mitral valve insufficiency and had a good left ventricular shortening fraction (greater than 26%). After the washout period we studied each of the above-mentioned parameters before and after the acute administration of nifedipine, dinitrate isosorbide, and captopril. While captopril and dinitrate isosorbide induced a prolongation of the isovolumic relaxation time and an impairment of the E/A ratio in mitral spectral Doppler (i.e., left ventricular filling), nifedipine induced an improvement in both parameters. The three drugs also induced a similar reduction in systemic blood pressure values (i.e., similar afterload). We therefore suggest that changes in diastolic function in hypertrophied cardiac fibers, induced by nifedipine, may be the result of a double action: one mediated by hemodynamic changes, the other directly affecting the cellular calcium ion exchange.

Aged↗
PubMed1984

"Maximal" drug therapy is not necessarily optimal in chronic angina pectoris.

Beta-adrenergic blocking agents, nitrates and calcium channel antagonists are effective in treating angina pectoris, but much remains unknown about how they act in combination. Consequently, treadmill exercise was used to assess the relative efficacy of nifedipine or isosorbide dinitrate, or both, in 19 patients with stable angina receiving propranolol. Propranolol therapy was continued and either placebo, nifedipine (20 mg), isosorbide dinitrate (20 mg) or both drugs were given randomly 1 1/2 hours before exercise in a double-blind trial. In 16 patients who completed the protocol, heart rate at rest during propranolol therapy was 53.7 +/- 1.9 beats/min (mean +/- standard error of the mean); it increased 4.6 +/- 1.2 beats/min with the addition of nifedipine (p less than 0.01), but was unchanged with isosorbide dinitrate or both combined. Compared with values during treatment with propranolol alone, systolic blood pressure at rest decreased with each vasodilator individually and when combined. Rate-pressure product at maximal exercise was the same with all combinations. Exercise duration was 467 +/- 50 seconds with propranolol, increased to 556 +/- 47 seconds with isosorbide dinitrate (p less than 0.05) and to 636 +/- 50 seconds with nifedipine (p less than 0.001). Exercise duration with all three drugs was 597 +/- 47 seconds (p less than 0.01 compared with propranolol alone). The improvement with nifedipine was greater than with isosorbide dinitrate (p less than 0.05) but exercise duration was not significantly different with the combination of these drugs than when either drug was used alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2002

A long-term transdermal nitric oxide donor improves uteroplacental circulation in women with preeclampsia.

OBJECTIVE: To determine the effects of long-term transdermal administration (range, 4-30 days; mean +/- SD, 11.1+/-7.2 days) of isosorbide dinitrate, a nitric oxide donor, in preeclamptic women. METHODS: We studied uterine and fetoplacental circulation of 12 preeclamptic women with oligohydramnios and an elevated pulsatility index in the uterine arteries. RESULTS: Transdermal isosorbide dinitrate significantly suppressed the blood pressure of patients. Pulsed Doppler ultrasonography revealed that the average pulsatility index in the uterine arteries was significantly reduced by treatment with isosorbide dinitrate (P < .003). The average pulsatility index in the umbilical artery was also significantly reduced (P < .004). Furthermore, the size of the amniotic fluid pocket increased approximately 4-fold by treatment with isosorbide dinitrate. CONCLUSIONS: Long-term transdermal administration of isosorbide dinitrate improves fetoplacental circulation and may be effective therapy for avoiding maternal hypertension and oligohydramnios in some preeclamptic women.

Administration, Cutaneous↗
PubMed1978

Treatment of ruptured interventricular septum with afterload reduction.

Two patients with a ruptured interventricular septum complicating acute myocardial infarction were treated with isosorbide dinitrate. The first patient recovered from cardiogenic shock after sublingual administration of 5 mg of isosorbide dinitrate every two hours and was successfully operated on. The second patient recovered from severe pulmonary edema during the acute stage of the infarction with sublingual isosorbide dinitrate. Moreover, she experienced a considerable symptomatic improvement when a 5 mg sublingual dose of isosorbide dinitrate every three hours was added to her long-term treatment. Analysis of hemodynamic data showed that the most striking change following administration of the drug was the substantial reduction of pulmonary wedge pressure. The striking symptomatic and hemodynamic improvement was achieved by the favorable effect of afterload reduction on left ventricular performance and not by reduction in left to right shunt.

Aged↗
PubMed1983

Drug interactions I: detection of inorganic nitrite in organic nitrate esters under acidic conditions simulating the human stomach.

Both unformulated (bulk) and formulated (drugs) organic nitrate esters (isosorbide dinitrate, nitroglycerin, and pentaerythritol tetranitrate) were studied in the presence and absence of hydrochloric acid to determine if they could be sources of nitrite (and therefore lead to nitrosamine formation) under acidic conditions similar to those found in the stomach. The presence and generation of nitrite ion was detected by a modification of the Griess reaction. Bulk isosorbide dinitrate and nitroglycerin were found to be contaminated with 13.8-121.4 mumoles of inorganic nitrite per mole of nitrate ester. In addition, in the presence of hydrochloric acid, these preparations generated 0.52-1.18 mumoles of inorganic nitrite/mole of nitrate ester/min. Unformulated nitroglycerin generated nitrite at a rate roughly twice that of isosorbide dinitrate. In contrast, no evidence for nitrite contamination or generation by pentaerythritol tetranitrate was found. Tablets and capsules of isosorbide dinitrate contained approximately 27-216 mumoles of nitrite/mole of nitrate ester and, in the presence of hydrochloric acid, generated an average of 0.55 mumole nitrite/min. For isosorbide dinitrate, this rate was similar for bulk and formulated drug. In comparison to isosorbide dinitrate, the amount of nitrite initially present in tablets and capsules of nitroglycerin varied more widely (approximately 25-2290 mumoles nitrite/mole of nitrate ester), and in this case nitrite was generated at higher rates than unformulated drug averaging approximately 4.7 mumoles nitrite/mole of nitrate ester/min. Contrary to a literature report, we found that nitrate ion is not reduced to nitrite by hydrochloric acid (pH 1-3).(ABSTRACT TRUNCATED AT 250 WORDS)

Chemistry, Pharmaceutical↗
PubMed1992

Influence of nitrovasodilators on bovine pulmonary histamine release.

The organic nitrates and related nitrovasodilators are relaxants of vascular and airway smooth muscle. Very little information is currently available regarding the influence of nitrates and related nitrovasodilators on pulmonary autacoid release. This study examined the influence of glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside on histamine release from bovine lung mince. Spontaneous histamine release from bovine lung mince was not altered by 0.1 nM to 1 microM glyceryl trinitrate, isosorbide dinitrate or sodium nitroprusside. Glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside produced a concentration-dependent decrease in A23187 (10 microM) stimulated histamine release. Glyceryl trinitrate also inhibited histamine liberation following the addition of compound 48/80. Further studies indicated that the inhibitory action of glyceryl trinitrate was reversed by coincubation with the guanylate cyclase inhibitor, methylene blue (10 microM). These findings indicate that glyceryl trinitrate, sodium nitroprusside and isosorbide dinitrate inhibit non-immunologically stimulated pulmonary histamine release and suggest that alterations in guanylate cyclase activity may influence pulmonary histamine release.

Animals↗
PubMed1988

Coronary artery calibre after direct intra-arterial infusion of epoprostenol (prostacyclin).

Because epoprostenol (prostacyclin) is a prostaglandin that causes vasodilatation and inhibits platelet function it may be of benefit during coronary artery angioplasty. The safety and capacity of intracoronary epoprostenol to dilate coronary arteries were assessed in 16 patients undergoing routine coronary angiography. The view that best displayed the left epicardial coronary arteries was selected as a control for each patient. Intracoronary epoprostenol was then given and the angiogram was repeated in the chosen view. The procedure was repeated twice: once with a higher dose of epoprostenol and once after intracoronary isosorbide dinitrate. Angiograms were coded and analysed by an observer who was unaware of the treatment. The calibre of the arteries was measured from traced projections of the angiograms. The blood pressure, heart rate, and electrocardiogram were recorded throughout. The first two patients were given epoprostenol infusions of 2.5 and 5.0 ng/kg per minute to assess safety, and there were no untoward reactions. The next ten patients had epoprostenol infusions of 5.0 and 7.5 ng/kg per minute followed by intracoronary isosorbide dinitrate. No haemodynamic disturbances occurred and coronary luminal calibre did not change with epoprostenol (mean (SD) luminal diameter: 2.85 (0.62) mm control, 2.80 (0.61) mm at 5.0 ng/kg, and 2.80 (0.54) mm at 7.5 ng/kg), but it did increase significantly with isosorbide dinitrate (to 3.17 (0.36) mm). The last four patients had epoprostenol infusions of 7.5 and 10 ng/kg followed by intracoronary isosorbide dinitrate and two of them became hypotensive (one after epoprostenol and one after isosorbide dinitrate). Coronary luminal calibre did not change significantly (3.5 (0.45) mm control, 2.96 (0.81) mm at 7.5 ng/kg, 3.45 (0.96) mm at 10 ng/kg, and 3.20 (0.61) mm with isosorbide dinitrate). Eight patients developed tall T waves on the electrocardiogram during epoprostenol infusion but none had arrhythmias. The results indicate that clinically tolerable doses of intracoronary epoprostenol do not significantly dilate the epicardial coronary arteries. This route of administration is therefore unlikely to be of use during coronary angioplasty, although the antiplatelet action of intravenous epoprostenol might help to prevent restenosis.

Coronary Angiography↗
PubMed1991

[Possibilities of potentiating the antianginal action of nitrates by methionine in patients with stable effort angina pectoris].

When given in a single dose, methionine was studied for its effects on the efficacy of isosorbide dinitrate in 8 patients with coronary heart disease. The antianginal and anti-ischemic effects of the agents were evaluated by treadmill exercise testing that had been performed prior to and repeatedly (1, 2, 3, and 6 hours) following a single application of the drug. Methionine in a dose of 1 g failed to produce antianginal and anti-ischemic effects. The concomitant use of isosorbide dinitrate (10 mg) and methionine (1 g) showed significantly pronounced antianginal and anti-ischemic effect than that of isosorbide dinitrate alone. The methionine-induced increase in the effect of isosorbide dinitrate substantially differed in the patients. Thus, methionine is able to potentiate the antianginal and anti-ischemic effect of isosorbide dinitrate.

Angina Pectoris↗
PubMed1988

Organic nitrates: direct antiplatelet effects and synergism with prostacyclin. Antiplatelet effects of organic nitrates.

Isosorbide dinitrate inhibits platelet function in vivo at concentrations about 10 times lower than in vitro (10(-7)-10(-6) vs. 10(-6)-10(-5) M). We investigated two possible reasons for this difference. Isosorbide dinitrate and its in vivo longer-lived metabolites, isosorbide-2- and isosorbide-5-mononitrate were incubated for 5 min with human platelet-rich plasma or washed platelets; irreversible aggregation was induced with threshold doses of ADP, adrenaline, collagen, arachidonic acid and thrombin, and thromboxane (TX) B2 production was measured by radioimmunoassay. Moreover, the concentration of exogenous prostacyclin required to inhibit platelet aggregation by 50% (IC50) after preincubation with isosorbide dinitrate or vehicle was determined. At 10(-7) M, only isosorbide-2-mononitrate inhibited aggregation (-12%, p less than 0.05) and TX production (-36%, p less than 0.01) by ADP. At 10(-6) M isosorbide-2-mononitrate inhibited aggregation by adrenaline more than the dinitrate (-41% vs. -25%, p less than 0.05). In addition, at supra-threshold doses of all the aggregating agents, isosorbide dinitrate decreased IC50 of prostacyclin from 2.7 +/- 1.2 to 0.36 +/- 0.2 nM. Generation of a platelet-active metabolite and synergism with prostacyclin are new properties of isosorbide dinitrate that may account for antiplatelet effects in vivo.

Adult↗
PubMed1994

Clinical pharmacokinetics of nitrates.

The pharmacokinetics of organic nitrates are discussed with emphasis on the possible clinical relevance. For glyceryl trinitrate, the measurement of plasma concentrations is very difficult. Its pharmacokinetics are unusual, with a very rapid disappearance from plasma, and large intraindividual and interindividual variations. After oral administration, there seems to be a very extensive first-pass hepatic extraction and the plasma concentrations are often below the detection limit; after sublingual administration, glyceryl trinitrate appears in plasma. With transdermal glyceryl trinitrate controlled-release systems, plasma concentrations of glyceryl trinitrate can be maintained over 24 hours, although with fluctuations and important intraindividual and interindividual variability. After administration of glyceryl trinitrate via different routes, glyceryl dinitrates and mononitrates are present in plasma. The pharmacokinetics of isosorbide dinitrate are somewhat easier to understand. The substance disappears less rapidly from the plasma than does glyceryl trinitrate. After oral administration, there is also a hepatic first-pass extraction; the plasma concentrations can be prolonged by administering slow-release products. Sublingual administration leads to higher plasma concentrations than oral administration. Isosorbide dinitrate is metabolized in the organism to isosorbide 5-mononitrate and isosorbide 2-mononitrate, which both have vasodilator activity: after administration of isosorbide dinitrate, the mononitrates, and mainly the 5-mononitrate, reach very high concentrations in plasma. Isosorbide 5-mononitrate has been studied in its own right as an antianginal agent: it is completely absorbed after oral administration; it has a half-life of around 4 hours, and oral standard and controlled-release formulations have been extensively studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1986

Coronary vasodilation by nitrates is not mediated by the prostaglandin system: a quantitative cineangiographic study.

The possible role of prostaglandins in mediating large coronary artery vasodilation by nitrates was investigated by quantitative magnification coronary angiography. The effects of aspirin (1 g systemically and 100 mg intracoronary) in preventing large coronary artery vasodilation induced by intracoronary isosorbide dinitrate was investigated in 16 patients. Of these, 5 received 0.3 mg (Group 1A) and 11 received 3 mg (Group 1B) intracoronary isosorbide dinitrate, before and 15 minutes after aspirin. Relative to control, 0.3 mg isosorbide dinitrate induced a 19 +/- 9% (mean +/- SD) (p less than 0.01) and 19.5 +/- 11% (p less than 0.01) increase in coronary diameter before and after aspirin, respectively (p = NS). Changes after 3 mg isosorbide were 23 +/- 12% (p less than 0.01) and 26.5 +/- 14% (p less than 0.01), respectively, before and after aspirin (p = NS). In 10 additional patients (Group 2), the effect of the same dose of aspirin on rest coronary artery tone was assessed: changes relative to control were 0.9 +/- 5.5% (p = NS) minutes after aspirin. The intracoronary administration of 3 mg isosorbide dinitrate produced a 24.7 +/- 11% increase in coronary diameter (p = NS versus pre- and postaspirin isosorbide in Group 1B). Urinary 6-ketoprostaglandin-F1 alpha values in urine samples collected in the 8 hours before and the 8 hours after the study in five patients in Group 1B and five patients of Group 2, revealed a 36 +/- 14% (mean +/- SD) reduction in excretion of prostacyclin (p less than 0.01). These data rule out a role for prostaglandins both in mediating dilation of large coronary arteries by nitrates and in affecting their vascular tone at rest.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Induction and circumvention of nitrate tolerance applying different dosage intervals.

There is increasing evidence that constant nitrate plasma levels, as induced by at least three-times-daily ingestions of isosorbide dinitrate in sustained-release form, lead to an attenuation or even complete loss of the anti-ischemic effects (nitrate tolerance). Therefore, the dependence of tolerance development on dosage intervals according to once-daily and twice-daily ingestions was assessed. Tablets of isosorbide dinitrate (80 mg) in sustained-release form were administered once-daily at 8 A.M. (dosage interval 24 hours) or twice-daily at 8 A.M. and 8 P.M. (dosage interval 12 hours), as well as at 8 A.M. and 2 P.M., respectively (maximal dosage interval 18 hours). A total of 34 patients with angiographically proven coronary artery disease, a history of stable, exercise-dependent angina pectoris, and a reproducible, exercise-induced ST-segment depression of at least 0.15 mV (1.5 mm), who initially showed a response to 80 mg of isosorbide dinitrate, were enrolled. The anti-ischemic effects of isosorbide dinitrate on exercise-induced ischemia were objectively determined by the measurement of exercise-induced ST-segment depression before as well as two, six, and 12 hours after the ingestion at the first and the 15th day of the studies. Since the dosage interval of 12 hours resulted in constant plasma levels, the initially beneficial anti-ischemic effects of isosorbide dinitrate were considerably attenuated after two weeks of treatment. In contrast, the once-daily regimen with its intermittent peaks and valleys of nitrate plasma levels showed identical anti-ischemic effects at the 15th day as compared with the first day. Ingestions at 8 A.M. and 2 P.M. also circumvented the development of nitrate tolerance, however, combined with an even more pronounced anti-ischemic effect after 12 hours as compared with the once-daily regimen. Thus, the circumvention of nitrate tolerance requires a daily "nitrate-poor" interval. The best compromise between a maximal possible anti-ischemic effect and the circumvention of tolerance development was found for the "eccentric" dosage regimen in which the tablets were ingested in the morning and early afternoon.

Angina Pectoris↗
PubMed1993

Coronary haemodynamics and vasodilatory profile of a potassium channel opener in patients with coronary artery disease.

Previous studies have indicated that nicorandil reduces both preload and afterload, clearly distinguishing nicorandil from conventional nitrates, whose predominant action is that of preload reduction. In association with the decrease in afterload following nicorandil, the contractile responses during isovolumic contraction and relaxation improved significantly, indicating that nicorandil does not demonstrate negative inotropic actions. Furthermore, despite a marked decrease in mean aortic pressure after nicorandil, coronary sinus blood flow remains unchanged. Therefore, coronary vasodilatation must have taken place, while myocardial oxygen consumption decreased significantly. The vasodilatory action of nicorandil on the epicardial coronary artery has also been demonstrated in our previous study. Nicorandil, at a dose of either 20 or 40 mg, induces a significant increase in coronary artery diameter favourably by acting not only on the non-stenotic but also on the stenotic coronary segments. In our recent study, the effects of intracoronary nicorandil (6 mu.kg-1) and isosorbide dinitrate (2 mg) on the epicardial coronary arteries were investigated in patients undergoing coronary angioplasty. In non-stenotic coronary artery segments, the mean coronary diameter increased significantly after either nicorandil (+12%) or isosorbide dinitrate (+17%). In stenotic segments, however, increase in the diameter of the obstructed segment by 20% after intracoronary nicorandil was much more pronounced when compared to that of 8% after isosorbide dinitrate. There was a significant additional increase of 13% in the diameter of the obstructed segment when nicorandil was administered following isosorbide dinitrate, while no such additional effect was observed when isosorbide dinitrate was given after nicorandil.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Sublingual↗
PubMed1981

Effects of nitrates on R-wave variations after exercise in coronary heart disease: differences in patients with and without angina pectoris.

With the purpose of investigating the pathophysiology of changes in the R wave after exercise and its relationship with left ventricular function, we studied 44 patients with coronary heart disease. They were classified into the following three groups: group A, 11 patients with angina pectoris and no prior myocardial infarction; group B, 18 patients with angina pectoris and prior myocardial infarction; and group C, 15 patients with prior myocardial infarction but no angina. All patients performed two exercise tests; one was a control test, and the other was performed after the sublingual administration of 5 mg of isosorbide dinitrate. In group A, variations in the R-wave voltage in control test and in the test after isosorbide dinitrate were 1.5 +/- 0.8 mm and -1.2 +/- 0.9 mm (P less than 0.05), respectively. In group B, results were 1.2 +/- 0.7 mm on the control test and -0.7 +/- 0.6 mm after isosorbide dinitrate (P less than 0.002), and in group C were -1.6 +/- 1.2 mm on the control test and -0.7 +/- 0.7 mm after isosorbide dinitrate (not significant). Thus, the two groups of patients with angina showed an increase of the R-wave after exercise in the control test but a decrease after the administration of nitrates, whereas the patients without angina showed a reduced R-wave after exercise both before and after the administration of nitrates (like normal subjects). This study suggests that ischemic ventricular dysfunction with exercise results in an increase in the R-wave, while exercise after nitrates results in a decrease in the R-wave consistent with less or no ventricular dysfunction due to nitrate therapy.

Administration, Topical↗
PubMed1995

Interaction of intravenous heparin and organic nitrates in acute ischemic syndromes.

We evaluated whether a drug interaction between intravenous nitroglycerin or isosorbide dinitrate and heparin exists. Ninety-six patients with a diagnosis of acute myocardial infarction, unstable angina, or other thromboembolic disorders were divided into 3 groups: group I (control group, n = 35) received intravenous heparin alone; group II (n = 31) received combined intravenous nitroglycerin and heparin; and group III (n = 30) received combined intravenous isosorbide dinitrate and heparin. We determined the mean of 2 separate measurements of heparin dosage requirement, antithrombin III activity, and the dose of intravenous nitroglycerin or isosorbide dinitrate at the time that the ratio of activated partial thromboplastin time (aPTT) to baseline aPTT was 1.5 to 2.0. The mean therapeutic heparin dose standardized to total body weight of each group was 13.8, 15.4, and 15.5 U/kg/hour, respectively. At that time, patients were receiving intravenous nitroglycerin at doses of 58.8 +/- 38.6 micrograms/min or intravenous isosorbide dinitrate at doses of 3.7 +/- 2.0 mg/hour. The mean antithrombin III activity of each group was 22.2, 22.8, and 21.3 mg/dl, respectively. The overall results for groups I, II, and III, and results for the subgroup of patients with acute ischemic syndromes in those groups, did not differ significantly. The heparin dose did not show a significant correlation to the dose of intravenous nitroglycerin (r = -0.26, p > 0.05) nor to that of isosorbide dinitrate (r = 0.30, p > 0.05).

Acute Disease↗
PubMedDate not supplied

Pharmacokinetic activity of nitrites evaluated by digital pulse volume recording.

Evaluation of the pharmacological properties of vasoactive drugs using routine pharmaco-chemical methods is often complex, time consuming and expensive. We used finger plethysmography for the evaluation of the bioactivity of two long-acting nitrite preparations. Eight healthy male volunteers were exposed to four different drugs: (1) Nitroglycerin; (2) Placebo; (3) Isosorbide dinitrate as Isotard Forte; (4) Isosorbide dinitrate as Cordil-40 SR. Digital pulse volume recording (PVR) was monitored for twelve hour periods. The shape of the PVR curve was used to calculate the diastolic amplitude response intensity, an indication of the vasoactive effect of the drug. There was no measurable response to the administration of placebo. The effect of nitroglycerin was maximal one hour after administration and disappeared after three hours. The long term effect of the two long-acting nitrite preparations was clearly demonstrated as compared to nitroglycerin. Noninvasive measurements of peripheral blood flow can serve as a convenient and accurate tool for pharmacokinetic studies of vasoactive drugs.

Adult↗
PubMed1995

Comparison of the vasorelaxing effect of different nitrovasodilators in conductive arterial and venous blood vessels.

We tested classically used organic nitrovasodilators such as s-nitroso-n-acetyl-D,L-penicillamine, 3-morpholino-sydnonimine, pentaerythrityl-tetranitrate, isosorbide-dinitrate, isosorbide-mononitrate, glyceryl-trinitrate on different isolated conductive arterial and venous blood vessels of the same species (rabbit). We found an up to two orders of magnitude more pronounced venoselectivety in the systemic-circulation as compared to the lung-circulation. ISMN and PETN were most venoselective nitrovasodilators, with PETN being the most potent drug in all vessels studied.

Animals↗