Effects Of Intravenous Nitroglycerin Research Articles

Assessment of Coronary Flow Parameters by Transesophageal Echocardiography in Patients with Isolated Coronary Artery Ectasia: Effect of Intravenous Nitroglycerin

We sought to assess coronary flow parameters in patients with isolated coronary artery ectasia (CAE) as compared to subjects with normal coronaries. Consecutively, we enrolled 30 patients with ectasia of the left anterior descending (LAD) coronary artery (study group), and 10 subjects with normal coronaries (control group). All patients underwent transesophageal echocardiography to visualize the LAD. Spectral recordings of proximal LAD flow velocities were made and velocity time integrals were calculated. The diameter of the proximal LAD was measured and LAD blood flow was calculated. Nitroglycerin (0.3 mg) was administered intravenously and measurements were repeated 5 minutes later. The mean age of the whole series was 48.6 ± 8 years, 39 (97.5%) being males. A significantly higher baseline systolic, diastolic, and total coronary blood flow was found in the study group as compared to the control group (46.1 ± 34.3 vs. 23.1 ± 8.2, 123.9 ± 73.3 vs. 68.1 ± 21.6, 170.1 ± 97.9 vs. 91.1 ± 26.8 cm(3) /min, respectively, P < 0.05 for all). Within the study group, nitroglycerin administration caused a significant decrease in peak diastolic velocity; systolic, diastolic, and total velocity time integrals; and both diastolic and total coronary blood flow (P < 0.05 for all). Meanwhile, within the control group, nitroglycerin administration caused a significant increase in the total coronary blood flow (P < 0.05). Patients with CAE have higher resting coronary blood flow in comparison with subjects with normal coronaries. Intravenous nitroglycerin administration causes significant reduction of coronary blood flow in ectatic coronary arteries.

Effects of intravenous nitroglycerin and noradrenaline on gastric microvascular perfusion in an experimental model of gastric tube reconstruction

Esophagectomy with gastric tube reconstruction is the surgical treatment for cancer of the esophagus. The perfusion of the distal part of the gastric tube depends exclusively on the microcirculation, making it susceptible to hypoperfusion and ischemia. It is unknown whether an increased perfusion pressure can exert a beneficial effect on gastric tissue perfusion.

Effect of intravenous nitroglycerin on the sublingual microcirculation in patients admitted to the intensive cardiac care unit

Nitroglycerin (NTG), a nitric oxide donor with vasodilating effects, is frequently administered to patients with heart failure. We tested the hypothesis of whether the vasodilating effects of NTG could be monitored at the bedside.

Effect of intravenous nitroglycerin on cerebral saturation in high-risk cardiac surgery

To determine whether or not intravenous nitroglycerin (IV NTG) can prevent a decrease in near-infrared spectroscopy (NIRS) values during cardiopulmonary bypass (CPB). We conducted a randomized double-blinded study in a tertiary academic center including 30 patients with a Parsonnet score>or=15 scheduled for a high-risk cardiac surgery. The patients were randomized to receive either IV NTG (initial dose of 0.05 microg.kg(-1).min(-1), followed by 0.1 microg.kg(-1).min(-1)) or placebo after anesthetic induction until the end of CPB. The primary outcome was a decrease of 10% in NIRS values during CPB. Despite the absence of between-group difference in the mean cerebral oxygen saturation during CPB, there was a significant decrease in NIRS values during CPB in the placebo group, whereas mean NIRS values were maintained in the IV NTG group (-16.7% vs 2.3% in the NTG, P=0.019). Major hemodynamic variables were similar at corresponding time periods in both groups, while patients in the IV NTG group had higher CK-MB values and experienced greater blood loss during the first 24 hr postoperatively. Intravenous nitroglycerin administration before and during CPB may prevent a decrease in NIRS values associated with CPB in high-risk cardiac surgery. Further studies are warranted to determine the efficacy and the risks associated with IV NTG infusion for this indication during CPB in high-risk patients.

Nitroglycerin Improves Left Ventricular Relaxation by Changing Systolic Loading Sequence in Patients with Excessive Arterial Load

Nitroglycerin abbreviates left ventricular (LV) relaxation through improved hemodynamics as well as by direct actions on the myocardium. The aim of this study was to examine whether the changing systolic loading sequence during nitroglycerin administration affects LV relaxation in patients with excessive arterial load. By use of a conductance catheter with microtip manometer, the effects of intravenous nitroglycerin (0.3-0.5 microg/kg/min) on LV function and hemodynamics were examined in 39 patients with various degrees of LV contractility. Patients were divided into two groups according to LV-arterial coupling, the ratio of end-systolic elastance (Ees) to effective arterial elastance (Ea). In patients with Ees/Ea ratio > 1, nitroglycerin had no effect on the time to peak force or on the time constant of LV relaxation (tau). On the other hand, in patients with Ees/Ea < 1, which represented excessive arterial load, nitroglycerin significantly shortened the time to peak force, shifted the peak of the loading sequence from late to early systole, and significantly decreased tau without any changes in Ees. Thus, nitroglycerin improved LV relaxation in patients with excessive arterial load partly by changing the systolic loading sequence.

Tocolytic effects of intravenous nitroglycerin

Currently available tocolytic agents have shown partial or transient efficacy on uterine contractions delaying delivery for 24 or 48 h without reduction in perinatal morbidity and mortality. These facts led us to study a new tocolytic compound. A double-blind dose finding study of the nitroglycerin tocolytic effect during preterm labor was conducted using a continual reassessment method among six different doses (0.2-1.2 mg/h for 2 h) in pregnant women who were unresponsive, intolerant to salbutamol, or with a contraindication to this therapy. Twenty-five pregnant women were included. The probability of success in stopping uterine contractions reached, for the maximal dose (1.2 mg/h), only a 54% rate (95% CI: 29-79%). Twelve patients complained of headaches and 16 experienced a decrease in arterial blood pressure suggesting that it would not be safe to increase the dose in order to obtain a higher success rate. The present study suggests that nitroglycerin is not as effective as expected in controlling uterine contractions during severe preterm labor in patients where beta2 agonists cannot be used.

Effect of intravenous nitroglycerin on lipid peroxidation after thrombolytic therapy for acute myocardial infarction

Free oxygen radicals are produced after coronary artery occlusion and reperfusion. Polyunsaturated fatty acids are oxidized by free radicals to lipid peroxides. Measurements of plasma malondialdehyde (MDA) formed by the breakdown of lipid peroxides are often used as markers of lipid peroxidation. The effect of intravenous nitroglycerin on plasma MDA levels was studied in 43 patients who received thrombolytic therapy for acute myocardial infarction. Plasma MDA levels in patients were elevated on admission to the hospital compared with healthy controls, and normalized within 48 hours. A greater increase in plasma MDA concentrations after thrombolysis was found in patients with noninvasive signs of reperfusion than in patients judged to have a persistent occlusion. In the 23 patients receiving immediate intravenous nitroglycerin infusion, plasma MDA levels did not change from baseline to 90 minutes (0.92 ± 0.22 and 0.92 ± 0.23 μmol/L, p = 0.99), whereas a significant increase was found in the 20 control patients who did not receive nitroglycerin (from 0.83 ± 0.22 to 1.01 ± 0.30 μmol/L, p = 0.0004) (p = 0.036 for the difference between groups). Successful reperfusion after thrombolytic therapy entails increased lipid peroxidation. Intravenous nitroglycerin reduces lipid peroxidation during myocardial ischemia and reperfusion.

Effects of intravenous nitroglycerin combined with dopamine on intracranial pressure and cerebral arteriovenous oxygen difference in patients with acute subarachnoid haemorrhage.

The effects of intravenous nitroglycerin (NTG) combined with dopamine on intracranial pressure (ICP) and cerebral arteriovenous oxygen difference (AVDO2) were studied in 11 patients with acute subarachnoid haemorrhage (SAH). The study was performed on Days 1 to 3 of SAH after aneurysmal clipping. Treatment consisted of an intravenous drip infusion of NTG in increasing incremental doses of 0.5, 1.0, 1.5, 2.0, and 2.5 micrograms/kg/min at one-hour intervals. Dopamine (5 to 10 micrograms/kg/min) was also given concurrently to maintain systemic blood pressure. ICP values before NTG administration ranged from 7 to 24 mmHg (mean. 11.91 +/- 5.30 mmHg). ICP began to increase immediately after the administration of NTG 0.5 microgram/kg/min and peaked at 14.64 +/- 5.93 mmHg 10 minutes after onset of infusion. Thereafter, ICP gradually returned to pretreatment levels. Increasing the dose of NTG failed to induce further significant rises in ICP. Mean AVDO2 before NTG administration was 4.69 +/- 0.62 ml/dl. This parameter showed no significant change during NTG infusion, although cerebral perfusion pressure decreased to between 75% to 94% of the control value after NTG administration. These results indicate that continuous NTG infusion combined with dopamine does not have adverse effects on ICP (the ICP increase is minimal and transient) and may even have beneficial effects on CBF in patients with acute SAH.

Effects of intravenous nitroglycerin and nitroglycerin and metoclopramide on intravariceal pressure: a double blind, randomized study.

Effects of intravenous nitroglycerin and nitroglycerin and metoclopramide on intravariceal pressure: a double blind, randomized study.

Effects of intravenous nitroglycerin and nitroglycerin and metoclopramide on intravariceal pressure: A double blind, randomized study : Sarin SK, Saraya AS. Am J Gastroenterol. 1995;90(1):48–53

Effects of intravenous nitroglycerin and nitroglycerin and metoclopramide on intravariceal pressure: A double blind, randomized study : Sarin SK, Saraya AS. Am J Gastroenterol. 1995;90(1):48–53

Effect of intravenous nitroglycerin on heparin dosage requirements in coronary artery disease

Patients admitted to the coronary care unit who received both intravenous nitroglycerin and heparin were studied to evaluate heparin dosage requirements. Physicians ordered all nitroglycerin and heparin doses as well as coagulation studies without knowledge of this study. Activated partial thromboplastin time (APTT) values obtained during steady-state heparin administration were considered therapeutic if the ratio of APTT/APTT-baseline was ≥1.5. Sixty patients with myocardial infarction or unstable angina were included in the study. The initial therapeutic heparin dose of 1,014 ± 151 units/hour produced an APTT ratio of 2.0 ± 0.5. At the time of the initial therapeutic dose, the nitroglycerin dose was 110 ± 108 μg/min. There was a significant correlation between the initial therapeutic dose and both total (r = 0.56; p = 0.0001) and lean (r = 0.26; p < 0.05) body weight. Comparison of patients with nitroglycerin doses < and ≥100 μg/min revealed a significant difference in the initial therapeutic dose (971 ± 147 vs 1,077 ± 136 U/hour, p < 0.01), but not the initial therapeutic dose standardized to total body weight (14.0 ± 2.5 vs 13.5 ± 2.7 U/kg/hour). Similarly, analysis of variance revealed a significant difference in the initial therapeutic dose (p < 0.05), but not the initial therapeutic dose standardized to weight among 5 different nitroglycerin dosage ranges (10 to 533 μg/min). Neither aspirin use, thrombolytic therapy nor decreasing or discontinuing the nitroglycerin dose significantly affected heparin requirements. Thus, contrary to prior reports, clinically significant heparin resistance induced by nitroglycerin was not found.

Interventricular Septal Excursions and Velocities During Experimental Myocardial Ischemia. Effects of Nitroglycerin Infusion

The effects of intravenous nitroglycerin on the excursions and velocities of the interventricular septum were evaluated by use of ultrasound in 20 open-chest dogs during experimental myocardial ischemia. In 10 dogs with acute septal ischemia the systolic and diastolic excursions and velocities of the interventricular septum were reduced (p&lt;0.01), but with the use of nitroglycerin, they increased as follows, although they did not return to the preischemia levels: Systolic septal excursion (p&lt;0.01), systolic septal velocity (p&lt;0.01), diastolic septal excursion (p = 0.01) and diastolic septal velocity (p&lt;0.01). In 10 dogs with acute posterior wall ischemia, the mobility of the interventricular septum increased (p&lt;0.01). This compensatory hyperactivity increased even more with the use of nitroglycerin as follows: Systolic septal excursion (p = 0.05), systolic septal velocity (p = 0.02), diastolic septal excursion (p = 0.05), and diastolic septal velocity (p&lt;0.01). The measurements were obtained using the recently described method of the specific points. Possible mechanisms for these effects include increased regional blood flow, reduced afterload, and mechanical pulling of the ischemic myocardium.

Effects of Intravenous Nitroglycerin on Hemodynamics in Neonates with Refractory Congestive Heart Failure of PFC

(1) Continuous intravenous infusion (2-10 micrograms/kg/min) of nitroglycerin (TNG) was administered to 20 neonates consisting of 17 with refractory congestive heart failure and 3 with PFC (Persistent Fetal Circulation). (2) At doses of 2-4 micrograms/kg/min, there were no significant changes in heart rate or systemic blood pressure. (3) At doses of 2-4 micrograms/kg/min, the CVP was significantly reduced and urinary output increased. (4) Echocardiograms revealed a significant decrease in LVS at 4-5 micrograms/kg/min. In addition, the EF and cardiac output were significantly increased at 2-5 micrograms/kg/min. (5) The right ventricle systolic time interval (STI) was reduced significantly at 2 micrograms/kg/min. The left ventricle STI was not reduced below doses of 4 micrograms/kg/min. (6) In the dose range 2-5 micrograms/kg/min, TNG is an effective and safe vasodilator in the treatment of refractory congestive heart failure or PFC in neonates.

Left Ventricular Excursions and Velocities During Coronary Arterial Ligation. Effects of Nitroglycerin Infusion in an Experimental Model

To determine the effects of intravenous nitroglycerin on the velocities and excursions of the acutely ischemic myocardium, 20 open-chest dogs were studied by use of ultrasound. In 10 dogs with acute septal ischemia, the posterior wall excursion during contraction (B-C excursion), the mean systolic posterior wall velocity, and the posterior wall excursion remained unaltered. Nitroglycerin, however, increased all these parameters (P less than 0.01). In 10 dogs with acute posterior wall ischemia the B-C excursion (aneurysmal bulging) increased (P less than 0.01), but the mean systolic posterior wall velocity and posterior wall excursion decreased (P less than 0.01). Nitroglycerin increased even more the aneurysmal bulging (P less than 0.01) and the other parameters (P less than 0.01). Increased regional blood flow, reduced afterload, and mechanical pulling of the ischemic myocardium seem to be a possible mechanism. The measurements were obtained using the recently described method of the specific points.

Comparable Effects of Intravenous Nitroglycerin and Intravenous Nitroprusside in Acute Ischemia

Forty patients with unstable angina were randomized to therapy with intravenous nitroglycerin (NTG) or nitroprusside (NTP). Invasive hemodynamic measurements were compared in both treatment groups and were used in concert with serial radionuclide monitoring of left ventricular function as patients were titrated to a therapeutic dose. Of the 22 patients randomized to intravenous NTG, there were 18 responders. Cardiac output significantly increased 28%, from 5.0 to 6.5 L/min at maximum effect. Mean pulmonary capillary wedge pressure (PCWP) decreased from 19 to 12 mm Hg. Mean arterial pressure decreased 10% and heart rate was unchanged (82 beats/min pre-treatment, 81 beats/min post-treatment). Radionuclide determined ejection fraction (EF) increased an average of 0.13, from 0.45 to 0.58. Peak filling rate paralleled increases in EF, increasing from 2.2 to 3.4 EDV/sec at peak level. Hemodynamic and radionuclide responses in the intravenous NTP group were compared to those with NTG. Of 18 patients randomized to NTP, 15 responders increased cardiac output from 5.1 to 6.8 L/min, a 35% increase. PCWP was 18 mm Hg at baseline and 10 mm Hg at peak effect. Mean arterial pressure decreased 13%, which was not significantly different from the NTG group. Heart rate response was identical to that in the NTG group. Ejection fraction increased an average of 0.17, from 0.43 to 0.60. Similar improvements were seen in peak filling rate (2.09 to 3.3 EDV/sec). There were no baseline differences between the NTG and NTP groups. In these patients NTG and NTP demonstrated equal efficacy, with the majority of patients showing substantial improvement in acute hemodynamics and left ventricular function with either agent.(ABSTRACT TRUNCATED AT 250 WORDS)

Reduced thiols and the effect of intravenous nitroglycerin on platelet aggregation

Nitroglycerin inhibits platelet aggregation in vitro and this effect may be important in its overall mechanism of action. In addition, its use has been associated with prolonged bleeding times and hemorrhagic complications. Despite these experimental and clinical observations, no significant antiplatelet effect of nitroglycerin has been observed ex vivo during intravenous nitroglycerin administration to patients. Because the in vitro antiplatelet effects of nitroglycerin have been shown by one of the investigators participating in this study to depend on the presence of sufficient stores of reduced intracellular thiol—which are readily depleted ex vivo by nitroglycerin in the formation of S-nitrosothiols—an attempt was made to unmask nitroglycerin-mediated inhibition of platelet aggregation by exposing platelets taken from patients treated with nitroglycerin to the reduced thiol N-acetylcysteine ex vivo. The obtained data demonstrate that platelets taken from patients treated with intravenous nitroglycerin manifest attenuated aggregation responses ex vivo when thiol stores are repleted. It is therefore proposed that the mechanism of action of nitroglycerin is mediated in part by its antiplatelet effect and that this effect depends on the adequacy of reduced intracellular thiol stores.

開心術後急性期の心筋代謝におけるニトログリセリンの効果

開心術後急性期の心筋代謝におけるニトログリセリンの効果

Role of Intravenous Nitroglycerin in the Treatment of Severe Pregnancy-Induced Hypertension Complicated by Pulmonary Edema

Intravenous nitroglycerin would appear to be an ideal agent for the treatment of severe pregnancy-induced hypertension complicated by cardiogenic pulmonary edema. Nitroglycerin infusion effectively reduces preload by venous dilatation and, at higher doses, results in arterial vasodilatation. Because of these pharmacologic properties, the effects of intravenous nitroglycerin were studied in three patients with severe pregnancy-induced hypertension complicated by pulmonary edema. The major cardiovascular effects of nitroglycerin were to reduce the mean pulmonary capillary wedge pressure from 27 +/- 4 to 14 +/- 6 mm Hg, which result in a change in the colloid osmotic pressure to pulmonary capillary wedge pressure gradient from -10 to 2 mm Hg. No significant changes occurred in heart rate, central venous pressure, or cardiac index. Analysis of oxygen-related parameters revealed a significant (p less than 0.05) increase in oxygen delivery and extraction accompanied by a 53% increase in oxygen consumption. The changes in oxygen-related variables appeared to be secondary to a fall in mixed venous oxygen tension from 39 +/- 4 to 33 +/- 1 torr. These changes occurred without any significant improvement in arterial oxygen tension. We conclude that while intravenous nitroglycerin expeditiously corrects the hydrostatic derangements of pulmonary edema seen in pregnancy-induced hypertension, a rapid improvement in arterial oxygenation does not occur.

Role of intravenous nitroglycerin in the treatment of severe pregnancy-induced hypertension complicated by pulmonary edema

Intravenous nitroglycerin would appear to be an ideal agent for the treatment of severe pregnancy-induced hypertension complicated by cardiogenic pulmonary edema. Nitroglycerin infusion effectively reduces preload by venous dilatation and, at higher doses, results in arterial vasodilatation. Because of these pharmacologic properties, the effects of intravenous nitroglycerin were studied in three patients with severe pregnancy-induced hypertension complicated by pulmonary edema. The major cardiovascular effects of nitroglycerin were to reduce the mean pulmonary capillary wedge pressure from 27 ± 4 to 14 ± 6 mm Hg, which result in a change in the colloid osmotic pressure to pulmonary capillary wedge pressure gradient from −10 to 2 mm Hg. No significant changes occurred in heart rate, central venous pressure, or cardiac index. Analysis of oxygen-related parameters revealed a significant (p < 0.05) increase in oxygen delivery and extraction accompanied by a 53% increase in oxygen consumption. The changes in oxygen-related variables appeared to be secondary to a fall in mixed venous oxygen tension from 39 ± 4 to 33 ± 1 torr. These changes occurred without any significant improvement in arterial oxygen tension. We conclude that while intravenous nitroglycerin expeditiously corrects the hydrostatic derangements of pulmonary edema seen in pregnancy-induced hypertension, a rapid improvement in arterial oxygenation does not occur

Dose-Related Prolongation of the Bleeding Time by Intravenous Nitroglycerin

The effects of intravenous nitroglycerin (NTG) upon the bleeding time, platelet aggregation response, and plasma 6-keto-PGF1 alpha concentration were measured in 17 patients about to undergo coronary bypass grafting. NTG produced a dose-related prolongation of the bleeding time that correlated with the accompanying decrease in systolic blood pressure. Platelet aggregation was not affected and measurements of 6-keto-PGF1 alpha failed to reveal detectable levels (less than 10 pg/ml) either before or after NTG infusion. This suggests that the prolonged bleeding time associated with NTG infusion may be due to vasodilation and increased venous capacitance, rather than altered vascular-platelet interaction.