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At least 1,783 records · Page 99Linked to original sources
PubMed1998

Increased QT dispersion in patients with vasospastic angina.

BACKGROUND: The risk factors for ventricular arrhythmias in patients with coronary vasospasm have not been identified. We evaluated QT dispersion in patients with vasospastic angina and its relation to susceptibility to ventricular arrhythmias during myocardial ischemia and reperfusion. METHODS AND RESULTS: We assessed the corrected QT (QTc) dispersion before induction of coronary artery spasm by intracoronary injection of acetylcholine (baseline) and 30 minutes after administration of isosorbide dinitrate in 50 patients with vasospastic angina and 50 patients with atypical chest pain. The baseline QTc dispersion was significantly greater in patients with vasospastic angina than in patients with atypical chest pain (mean+/-SD: 69+/-24 versus 44+/-19 ms, 95% confidence interval of mean difference [CI]: 16 to 33 ms; P<0.001). QTc dispersion decreased significantly, to 48+/-15 ms (CI: 15 to 26 ms; P<0.001 versus baseline), after administration of isosorbide dinitrate in patients with vasospastic angina but did not change significantly in patients with atypical chest pain (mean+/-SD: 41+/-17 ms, CI: -3 to 9 ms). During the provocation test, 24 of 50 patients with vasospastic angina experienced ventricular arrhythmias. The baseline QTc dispersion was significantly greater in patients with than without ventricular arrhythmias (mean+/-SD: 77+/-23 versus 61+/-19 ms, CI: 4 to 26 ms; P<0.05). CONCLUSIONS: Patients with vasospastic angina exhibited an increased baseline QTc dispersion compared with patients with atypical chest pain, which suggests that inhomogeneity of repolarization and susceptibility to ventricular arrhythmias are increased in patients with vasospastic angina, even when asymptomatic. The association between increased QTc dispersion and ventricular arrhythmias during the provocation test suggests that measurement of QT dispersion may help predict which patients with vasospastic angina are at high risk for ventricular arrhythmias during ischemia.

Acetylcholine↗
PubMed1997

Smooth muscle cell expression of type I cyclic GMP-dependent protein kinase is suppressed by continuous exposure to nitrovasodilators, theophylline, cyclic GMP, and cyclic AMP.

A key component of the nitric oxide-cyclic guanosine monophosphate (cGMP) pathway in smooth muscle cells (SMC) is the type I GMP-dependent protein kinase (PK-G I). Activation of PK-G I mediates the reduction of cytoplasmic calcium concentrations and vasorelaxation. In this manuscript, we demonstrate that continuous exposure of SMC in culture to the nitrovasodilators S-nitroso-N-acetylpenicillamine (SNAP) or sodium nitroprusside (SNP) results in approximately 75% suppression of PK-G I mRNA by 48 h. PK-G I mRNA and protein were also suppressed by continuous exposure to cGMP analogues 8-bromo- and 8-(4-chlorophenylthio) guanosine-3,5-monophosphate or the cAMP analogue dibutyryl cAMP. These results suggest that activation of one or both of the cyclic nucleotide-dependent protein kinases mediates PK-G I mRNA suppression. Using isoform-specific cDNA probes, only the PK-G I alpha was detected in SMC, either at baseline or after suppression, while PK-G I beta was not detected, indicating that isoform switch was not contributing to the gene regulation. Using the transcription inhibitor actinomycin D, the PK-G I mRNA half-life in bovine SMC was observed to be 5 h. The half-life was not affected by the addition of SNAP to actinomycin D, indicating no effect on PK-G I mRNA stability. Nuclear runoff studies indicated a suppression of PK-G I gene transcription by SNAP. PK-G I suppression was also observed in vivo in rats given isosorbide dinitrate in the drinking water, with a dose-dependent suppression of PK-G I protein in the aorta. PK-G I antigen in whole rat lung extract was also suppressed by administration of isosorbide or theophylline in the drinking water. These data may contribute to our understanding of nitrovasodilator resistance, a phenomenon resulting from continuous exposure to nitroglycerin or other nitrovasodilators.

Animals↗
PubMed1991

Effects of vasodilators on venous tone in vivo in dogs.

The authors investigated, in vivo, the effects of four vasodilators on venous tone in dogs. Baseline venous tone was determined from the pressure: diameter relationships in the inferior vena cava (VSIVC) and femoral vein (VSFV) as measured during several seconds of occlusion of the proximal inferior vena cava. All of the slopes were nearly linear. All vasodilators were administered in dosages sufficient to lower blood pressure by approximately 20%; these dosages also decreased systemic vascular resistance by 15% to 30%. Isosorbide dinitrate reduced VSIVC from 7.17 +/- 0.81 to 5.81 +/- 0.73 mmHg/mm and VSIVC from 59.4 +/- 13.5 to 37.2 +/- 6.6 mmHg/mm. Neither nifedipine nor nisoldipine altered VSIVC or VSFV. However, prazosin decreased VSIVC from 13.2 +/- 3.3 to 10.7 +/- 2.7 mmHg/mm and VSFV from 43.5 +/- 11.3 to 29.9 +/- 8.8 mmHg/mm. These results suggest that isosorbide dinitrate and prazosin decrease venous tone in vivo, whereas nifedipine and nisoldipine do not.

Animals↗
PubMed1996

Nitrate-induced headache in patients with stable angina pectoris: beneficial effect of starting on a low dosage. 5-ISMN headache study group.

BACKGROUND: Nitrates, although important for the management of angina pectoris, cause significant headache in many patients. METHODS: In a randomized, double-blind, crossover study, 89 patients with stable angina pectoris were studied to compare two different dosage strategies of isosorbide-5-mononitrate (5-ISMN). Patients were randomized to either 60 mg 5-ISMN once daily (od) for two weeks or to 30 mg 5-ISMN od for one week followed by 60 mg 5-ISMN od for one week. Then, there was a two-week placebo washout, after which the alternative treatment was given. The authors assessed the occurrence of angina pectoris and headache by diary cards while taking into account the number of isosorbide dinitrate sublingual puffs and paracetamole tablets required. Data were assessed for carryover and time effects. RESULTS: The two dosage regimens were equally efficient for the relief of angina pectoris without development of tolerance. Thirty percent of the patients never experienced headache from the given dosages. In the remainder of them there was a highly significant time effect: the overall numbers of headache attacks in the first period of active treatment versus the second were 2,380 vs 1,400 (P < 0.003). Yet significantly fewer patients had headache on low dosage than on high dosage (45 vs 57, P < 0.02). CONCLUSIONS: (1) Starting on a low dosage was associated with a reduced frequency and severity of headache and did not notably influence the beneficial effect on angina pectoris. (2) One in 3 patients never experienced headache from the given dosages. (3) The overall number of headache attacks in the first period of active treatment was significantly higher than in the second period irrespective of the dosages given.

Adult↗
PubMed1984

Hemodynamic and metabolic effects of vasodilator therapy for heart failure in acute myocardial infarction.

Hemodynamic effects of vasodilator agents (molsidomine, nitroglycerin, isosorbide dinitrate or prostaglandin I2) were studied in 53 patients with acute myocardial infarction. In 20 of these patients, effect on cardiac metabolism were also studied. Patients were divided into four groups according to the Forrester subset and hemodynamic effects of these agents were evaluated by the cardiac index (CI)-preload (PAEDP) relationship. In patients of Forrester subset II and IV, vasodilators were capable of producing a considerable reduction in preload without a significant decrease in cardiac output. However, in patients of Forrester subset IV, five of six patients had only a minimal improvement in cardiac performance with vasodilator therapy because of a severe pump failure. In these patients, a combination therapy with dopamine was necessary to maintain the cardiac output. In patients with Forrester subset III, vasodilator therapy decreased cardiac index and preload was also reduced. Thus, for these patients vasodilators could not be indicated but volume infusion may be indicated. In patients with Forrester subset I, although vasodilator therapy decreased cardiac output, coronary sinus flow and myocardial oxygen consumption were also decreased, indicating that the vasodilator therapy is also beneficial for patients even without heart failure because of the protective effect of unloading on ischemic myocardium. Three nitrate agents, i.e., molsidomine, nitroglycerin and isosorbide dinitrate, demonstrated the similar effect on hemodynamics; mean blood pressure and PAEDP decreased by 7-10% and 20-29%, respectively, while systemic vascular resistance was not significantly decreased. In contrast to nitrates, PGI2 decreased mean blood pressure and systemic vascular resistance significantly, whereas a decrease in PAEDP was minimal.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1989

Relationship between the coronary diameter and occurrence of vasospastic angina in patients with normal coronary arteries.

Coronary artery diameters were measured after various interventions in 30 patients without angina pectoris (group 1) and in 15 with angina pectoris (group 2: rest, or rest and effort angina) who had normal coronary arteries. The coronary artery diameters were significantly smaller in many coronary segments in group 2 than in group 1 during a control state, after exercise and ergonovine, but became nearly identical after isosorbide dinitrate in both groups. Patients in group 1 had diffuse narrowing but no focal vasoconstriction after ergonovine and all the segments had a diameter of more than 50% of that after isosorbide dinitrate. The change of coronary artery diameter in group 2 patients who had no vasospasm by ergonovine was the same as that in group 1. Patients in whom vasospastic angina was induced had local vasoconstriction or severe diffuse narrowing (less than 45%). These results indicate that angina pectoris patients with normal coronary arteries had an acceleration of coronary arterial basal tone, but vasospastic angina pectoris was not induced just by the general response of the coronary artery to various interventions in addition to the accentuated basal tone. For vasospastic angina to occur, local abnormal response to various interventions must be present.

Adult↗
PubMed1995

The effects of antianginal drugs on energy expenditure during exercise in normal subjects.

The respiratory quotient (RQ = VCO2/VO2) provides important information (ie, the ratio of carbohydrate to fat utilization) concerning energy expenditure. We studied the effects of various antianginal drugs on energy expenditure during steady-state aerobic exercise in 9 healthy adult men. The drugs used were propranolol (a non-selective beta-blocker), metoprolol (a beta-1 selective blocker), amosulalol (an alpha- and beta-blocker), nicardipine (a calcium antagonist) and isosorbide dinitrate. Each drug was administered for 2 weeks, followed by a 2-week washout period. VO2, VCO2 and RQ were measured with an expired gas analyzer during treadmill exercise tests before and during the administration of each drug. Two protocols of constant-load exercise were performed: Protocol 1 lasted for 10 min at a speed of 5.5 km/h and a grade of 0%, (at a level of about 30% peak VO2), while Protocol 2 lasted for 10 min at a speed of 7 km/h and a grade of 0%, (at a level of about 40% peak VO2). RQ during exercise was significantly increased and VO2 was decreased after propranolol, metoprolol and amosulalol (P < 0.05). Neither nicardipine nor isosorbide dinitrate produced significant changes in these values. These data suggest that propranolol, metoprolol and amosulalol increase the efficiency of energy expenditure during ordinary physical activity by increasing the utilization of carbohydrate and by decreasing the utilization of fat.

Adrenergic beta-Antagonists↗
PubMed1997

Flow-mediated vasodilation of a conduit artery in relation to downstream peripheral tissue blood flow during reactive hyperemia in humans.

Arterial conduit vessels dilate in response to increased blood flow stimuli. Our objective was to determine precisely how a change in large arterial diameter results in a change in peripheral tissue blood flow. Using high-resolution ultrasound Doppler echography, we measured the diameter of the right femoral artery at rest, during reactive hyperemia, and after administration of 2.5 mg of sublingual isosorbide dinitrate in 10 healthy young men. Reactive hyperemia was induced by distal circulatory arrest followed by reperfusion of the leg ipsilateral (right) or contralateral (left) to the side of arterial diameter measurements. Femoral arterial blood flow was calculated by simultaneous measurement of femoral arterial diameter and blood velocity. The change in skin blood flow was also analyzed simultaneously by laser Doppler flowmetry. Reactive hyperemia induced a 2-fold increase in femoral arterial blood velocity 30 sec after cuff release. During this flow augmentation, the femoral artery dilated. The peak of skin blood flow was coincident with the peak of femoral arterial vasodilation. The time required for the return of arterial diameter to baseline was longer than that for blood flow in both the conduit artery and the peripheral skin tissue. Equivalent cuff occlusion and release of the contralateral limb had no effect on ipsilateral arterial diameter. Isosorbide dinitrate induced dilation in all subjects, despite the absence of a significant increase in blood velocity. These results indicate that the human femoral artery dilates in response to increased blood velocity, and that the flow-mediated vasodilation of a large conduit artery is involved in the adjustments of blood flow in the downstream peripheral tissue.

Adult↗
PubMed1998

Two cases of hypertrophic cardiomyopathy with coronary vasospasm.

Chest pain in patients with hypertrophic cardiomyopathy seems to be caused by relative myocardial ischemia due to the left ventricular outflow pressure gradient and myocardial hypertrophy. However, in 2 cases of hypertrophic cardiomyopathy chest pain was associated with coronary vasospasm. Thus, chest pain in these cases was decreased not by a beta-blocker but by isosorbide dinitrate and a calcium antagonist. Because beta-blockers are commonly used for hypertrophic obstructive cardiomyopathy and chest pain may be aggravated by beta-blockers in patients with coronary vasospasm, a combination of beta-blocker, isosorbide dinitrate and calcium antagonist was necessary for this hypertrophic cardiomyopathy with variant angina.

Adrenergic beta-Antagonists↗
PubMed1996

Evaluation of nitric oxide formation from nitrates in pig coronary arteries.

To clarify the hypothesis that organic nitrates are converted to nitric oxide (NO) via nitrite ion (NO2-) by glutathione S-transferase, the metabolic conversion of four nitrates was examined in pig coronary arteries and compared with that in rat liver. Nitrates caused the relaxation of the artery muscles with the order of nitroglycerin > isosorbide dinitrate > nicorandil > or = nipradilol, whereas the order of NO formation in the arteries was nitroglycerin > isosorbide dinitrate > nipradilol > nicorandil. The same order of NO formation from the nitrates was also observed in liver cytosol. Nicorandil may cause more relaxation than nipradilol by both NO releasing and other (unknown) actions. Although the order of the potency in NO2- formation from the nitrates in liver cytosol was the same as that seen in NO formation, NO2- was not detected in pig coronary arteries. Thus NO2- formation from the nitrates correlated with NO formation in liver cytosol but not in pig arteries. When nonenzymatic and enzymatic NO formations from nitroglycerin were examined in the arteries, the enzymatic NO formation, which was not inhibited by glutathione S-transferase inhibitors, was 13% of the total NO. These results indicate that in pig coronary arteries, nitrates release NO mostly through a nonenzymatic manner, although there is a slight amount of enzymatically produced NO, and glutathione S-transferase may not contribute to the enzymatic NO formation.

Animals↗
PubMed1995

Differences in ischemic threshold and nitrate efficacy between normotensive and hypertensive patients with stable angina pectoris.

The coexistence of ischemic heart disease with hypertension makes antihypertensive therapy essential, since relief of hypertension may ameliorate the coronary disease. On the other hand, the effect of antianginal nitrate therapy in patients with stable angina pectoris and systemic arterial hypertension is not fully understood. This study assessed the effects of hypertension on the ischemic threshold and the time to moderate angina, measured as parameters of nitrate efficacy. In this double-blind, parallel-group study, 141 patients with stable angina pectoris were randomly assigned to receive 5 mg, 10 mg or 20 mg isosorbide-5-mononitrate or matching placebo bid for 21 days. Ninety-three normotensive and 48 hypertensive patients were compared with regard to the time to moderate anginal pain and the ischemic threshold before and after nitrate treatment on the first day of the study. The acute nitrate effect 2 h after drug administration was substantially attenuated in hypertensives at both 10 and 20 mg of isosorbide-5-mononitrate, with the time to moderate anginal pain being significantly shortened. Impaired vasodilatator response of the arterial vasculature to organic nitrates, probably due to impaired biotransformation of organic nitrates to nitric oxide in hypertensive patients, is suggested as a possible mechanism for the diminished nitrate effect. Thus, oral nitrate therapy does not have the same beneficial antianginal effect in hypertensive patients as it does in normotensives. Dose adjustment based on the pretreatment blood pressure, and the administration of higher doses of oral nitrates should therefore be considered in hypertensive patients suffering from stable angina pectoris.

Aged↗
PubMed1994

A characteristic change in ventilation mode during exertional dyspnea in patients with chronic heart failure.

Although exertional dyspnea is an important symptom limiting daily lives in patients with chronic heart failure, there is no objective assessment of this symptom. To characterize the exertional dyspnea, ventilatory responses to exercise were studied in relation to exertional dyspnea. Gas exchange data were obtained during a maximal bicycle exercise in 43 patients with chronic heart failure and 20 normal subjects. In addition to standard ventilatory variables, the ventilation mode was assessed from the tidal volume-ventilation rate (VT-f) relationship. The exercise was performed again after sublingual administration of 5 mg of isosorbide dinitrate. In normal subjects, the f and VT increased almost proportionally with exercise intensity. In 17 (85 percent) of 20 patients with exertional dyspnea, the VT-f relationship abruptly lost linearity at the onset of exertional dyspnea. This change resulted from an inadequate increase in VT and a further increase in f. In 8 of these 17 patients, isosorbide dinitrate improved exertional dyspnea with normalization of the VT-f relationship; however, in 9 patients whose dyspnea was not improved, the abnormal VT-f relationship was unaltered. Only 2 (9 percent) of 23 patients without exertional dyspnea showed the abnormal VT-f relationship. Other ventilatory variables were not different between patients with and without dyspnea. Thus, exertional dyspnea is characterized by simultaneous appearance of rapid and shallow ventilation. The VT-f relationship appears to be a simple and useful objective assessment of exertional dyspnea in patients with chronic heart failure.

Dyspnea↗
PubMed1991

The day-long antianginal effectiveness of nitroglycerin patches. A double-blind study using dose-titration.

This study was designed to determine the day-long antianginal effectiveness of nitroglycerin patches in the nitrate-exposed patient, as well as the doses required. Eight men with chronic stable angina, a positive treadmill test, and demonstrated responsiveness to long-term oral isosorbide dinitrate were studied after they had been taking effective doses of isosorbide dinitrate three times a day for at least two weeks. Treadmill exercise bouts were performed every 1 to 2 hours over 1 day, after the 8 am application of active nitroglycerin patches in a previously titrated dose, and on another day after application of placebo patches. Mean necessary effective patch dose was 125 sq cm (60 to 220 sq cm). Mean exercise duration to angina rose from 271 to 480 s (p less than 0.001) 1 hour after active patches, while resting systolic blood pressure fell from 122 mm Hg to 100 mm Hg (p less than 0.001). (After placebo patches: +19 s and -2 mm Hg, respectively.) Active patches were superior to placebo throughout the day, but in declining degree (by 94 s at 7 pm, p less than 0.05). Thus, nitroglycerin patches can provide a significant day-long antianginal effect in the patient with long-term exposure to nitrate. However, the need for large doses and individual titration may make this therapy impractical.

Administration, Cutaneous↗
PubMed1998

Effects of intravenous administration of L-arginine on autonomic nervous activities. Analysis of heart rate variability.

We studied the differences between isosorbide dinitrate (ISDN) and L-arginine (L-Arg), the precursor of nitric oxide, regarding autonomic nervous function by assessing changes in heart rate variability and blood levels of various vasoactive substances. Healthy volunteers received infused L-arginine (L-Arg group) or isosorbide dinitrate (ISDN group). ECGs were monitored and analyzed. Blood levels of catecholamines, endothelin, renin activity, angiotensin, human atrial natriuretic peptide, aldosterone, arginine, and citrulline were examined. Time-domain analyses of heart rate variability showed no significant changes in occurrence of R-R variability or coefficient of R-R variability, indicators of parasympathetic activity, after administration of ISDN. By contrast, both measures showed significantly more variation following administration of L-Arg. Frequency-domain analyses showed that high frequency power, an indicator of parasympathetic activity, was significantly elevated in the L-Arg group, whereas there was no significant change in the ISDN group. The blood levels of the measured vasoactive substances in L-Arg and ISDN groups were significantly different. The differences in autonomic nervous function and various kinds of vasoactive substances between the L-Arg and ISDN groups suggest that L-Arg had other actions on humoral factors in addition to vasodilation. Thus, arginine/nitric oxide may act as a neurotransmitter, altering parasympathetic nervous tension.

Adult↗
PubMed1991

Chronopharmacology of oral nitrates in healthy subjects.

The pharmacokinetics and the hemodynamic effects (blood pressure, heart rate) of oral organic nitrates have been investigated in healthy subjects after oral single-dose application either in the morning or in the evening. Isosorbide-5-monitrate (IS-5-MN, 60 mg) was administered as an immediate-release tablet or as a slow-release formulation. Isosorbide dinitrate (ISDN, 20 mg) was ingested as an immediate-release tablet. After administration of IS-5-MN as an immediate-release tablet, the drug was more rapidly absorbed in the morning (tmax of 0.9 h) than in the evening (tmax of 2.1 h). The rapid absorption led to more pronounced effects in the morning, at which time maximum drug concentrations occurred at the same time as peak effects were observed. After evening administration, however, peak effects were in advance of the maximum drug concentrations. No chronokinetics were observed after application of the slow-release formulation of IS-5-MN. In accordance with the results of the immediate-release formulation, peak effects of the slow-release preparation occurred significantly earlier than peak drug concentrations after evening than after morning dosing. ISDN bioavailability was higher after morning than after evening administration and hemodynamic effects were more pronounced in the evening than in the morning. These results show that daily variations in pharmacokinetics and/or hemodynamic effects can be observed with oral nitrates. In addition, galenic formulation can influence the time-specified pharmacokinetics of IS-5-MN.

Administration, Oral↗
PubMed2004

Effects of nitric oxide on gastric ulceration induced by nicotine and cold-restraint stress.

AIM: Stress induces gastric ulceration in human and experimental animals. People tend to smoke more cigarettes when under stress. Nitric oxide (NO) and nicotine have opposing effects on gastric integrity. The present study examined the possible therapeutic benefit of NO in nicotine-treated rats with stress-induced gastric ulceration. METHODS: Rats drank a nicotine solution while control rats drank tap water for 20 days. The alkoloid was then replaced by water with or without supplementation of isosorbide dinitrate (NO donor) for an additional 10 days. Isosorbide dinitrate was given twice shortly before experiments (acute) or three times daily by oral gavages for 10 days after the rats stopped drinking nicotine solution. At the end of experiments, ulcer index, gastric adhesion mucus content and MPO activity were measured and analysed. RESULTS: Nicotine treatment decreased gastric mucus content and intensified stress-induced gastric ulcer. A higher ulcer index persisted even after the rats stopped drinking nicotine solution for 10 days. Acute NO donor showed no benefit on both mucus and ulcer index in nicotine treatment or/and stress condition. Chronic NO donor treatment reversed the worsening action of nicotine in stomach. Stress increased gastric mucosal myeloperoxidase (MPO) activity, which was antagonized by chronic NO treatment. However, nicotine was unlikely to change mucosal MPO activity. CONCLUSION: The intensifying action of nicotine on stress-induced gastric ulceration persists for 10 days after cessation. Nicotine treatment significantly decreases gastric mucus content that can be restored by chronic NO donor treatment. The present study suggests that NO antagonizes the ulcerogenic action of nicotine through a cytoprotective way.

Animals↗
PubMed1982

Vasodilators and prostaglandin inhibitors in primary pulmonary hypertension.

Ten women with primary pulmonary hypertension had resting hemodynamic measurements taken before and after the nonparenteral administration of various vasodilators and prostaglandin inhibitors. Only sublingual isoproterenol, alone or combined with sublingual isosorbide dinitrate, effected a substantial (greater than 20%) drop in pulmonary vascular resistance; this decrease was accompanied by little change in pulmonary artery pressure. Isosorbide dinitrate was the only drug that elicited any reduction in pulmonary artery pressure; pulmonary vascular resistance decreased modestly. The oral administration of diazoxide, hydralazine, phentolamine, and tolazoline elicited little change in pulmonary artery pressure or resistance. Except for tolazoline, all these agents significantly decreased systemic blood pressure and resistance. Prostaglandin inhibition by indomethacin (acute and chronic dosing) increased pulmonary and systemic vascular resistances and reduced cardiac output. Aspirin combined with dipyridamole elicited no changes. The vasodilators and prostaglandin inhibitors studied evoked little improvement in resting pulmonary hemodynamic abnormalities in primary pulmonary hypertension.

Adolescent↗
PubMed2002

Effect of a nitric oxide donor on the ophthalmic artery flow velocity waveform in preeclamptic women.

OBJECTIVE: To evaluate the effects of an antihypertensive agent on the orbital circulation of preeclamptic women. METHODS: We studied the ophthalmic arteries of 10 healthy pregnant women and 10 women with severe preeclampsia by pulsed Doppler ultrasonography and evaluated the effect of transdermal isosorbide dinitrate, a nitric oxide donor, on preeclamptic women. RESULTS: The average pulsatility index and resistive index were significantly lower, whereas the average end-diastolic velocity, time-averaged mean peak velocity, and peak ratio, which quantifies characteristic changes in the ophthalmic artery flow velocity waveform, were higher in preeclamptic women. Transdermal isosorbide dinitrate significantly reduced the average end-diastolic velocity (P < .05) and peak ratio of the ophthalmic artery (P < .01), whereas it did not significantly affect other indices. CONCLUSIONS: Orbital circulation was altered in preeclamptic women. A nitric oxide donor affected orbital circulation. Peak ratio was a sensitive index for evaluating orbital circulation in preeclampsia.

Administration, Cutaneous↗