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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been shown that hydralazine is beneficial in chronic heart failure by virtue of its afterload reducing effect. Nitroglycerin paste results in venodilation and fall in left ventricular filling pressure (LVFP). Thirteen patients with chronic heart failure were given a combination of oral hydralazine and nitroglycerin paste. With oral hydralazine (75 to 100 mg every 8 h), left ventricular stroke work increased and LVFP slightly fell. Following addition of 2% nitroglycerin paste, an additional decline in mean pulmonary artery and LVFP was observed without significant changes in heart rate and arterial pressure. There were no untoward side effects from either therapy. Eight patients followed for three to eight months (mean five months) reported subjective improvement in shortness of breath and other symptoms related to ventricular dysfunction. This study shows that in certain patients with chronic heart failure, hydralazine and nitroglycerin paste combination produces salutary clinical effects on long term probably through afterload and preload reduction, respectively.
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PMID:Non-parenteral combined afterload and preload reduction therapy in congestive heart failure. 11 91

Two types of vasodilators are used for treatment of acute myocardial infarction: Nitrates on the one hand with predominant venodilation and agents like Phentolamie and Nitroprusside on the other hand with venodilation as well as arteriolar vasodilation. Different opinions exist with respect to indication of these vasodilators. They are used for reduction of arterial blood pressure, for reduction of left ventricular filling pressure and for increase of cardiac output. A marked decrease in ejection fraction is the hemodynamic basis of application of vasodilators in the latter indication. By reduction of peripheral vascular resistance emptying of the left ventricle in these patients is enhanced.) As a working hypothesis in clinical situation elevated filling pressure indicates a decreased ejection fraction. The first part of this investigation deals with relation of left ventricular and diastolic pressure to ejection fraction. A good correlation between these two parameters was found in 717 patients with coronary artery disease. However variability was so wide that regression from enddiastolic pressure to ejection fraction in the individual seemed impossible. In 26.6% of patients with ejection fraction over 0.6%, filling pressure was 20 mm Hg or more. On the other hand, in 34.7% of patients with ejection fraction below 0.3% filling pressure was 20 mm Hg or less. As a consequence of practical value, reduced ejection fraction has to be assumed, if a patient presents elevated filling pressure and reduced cardiac output. In the second part, the hemodynamic effects of Phentolamine in 12 patients with acute myocardial infarction and elevated filling pressure (PCV resp. PADP greater than 18 mm Hg) are described. Maximal effects on hemodynamic variables were: reduction of peripheral vascular resistance by 31.4%, of left ventricular filling pressure by 16.2%, and of mean arterial pressure by 17.0%. Cardiac output increased by 25.8% and heart rate rose by 14.8%. At optimal efficacy, stroke volume increased by 23.7%. Further increase of infusion rate with concomitant fall of peripheral vascular resistance resulted in decrease of stroke volume and tachycardia. Most serious side effects consisted in sudden fall of blood pressure. Therefore intraarterial monitoring of blood pressure is demanded. The third part deals with hemodynamic effects of nitrates (Isosorbiddinitrate 10 mg p.o.) in patients with acute myocardial infarction and elevated filling pressure. One hour after application peripheral vascular resistance decrease by 16.5%, filling pressure by 20.8%, and mean arterial pressure by 9.0%. Cardiac output stroke volume and heart rate did not change significantly. No side effects were observed with Isosorbiddinitrate although two cases of nitrate syncope occurred with Nitroglycerin, resulting in bradycardia and hypotension. Indications for vasodilator therapy therefore has to be handled as follows: Nitrates should be given to patients with elevated filling pressure and normal cardiac output...
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PMID:[Hemodynamic guidelines in the treatment of acute myocardial infarction by means of vasodilators]. 16 46

Nitroglycerin (NTG) has recently been suggested to decrease myocardial ischemia and enhance cardiac pump function during acute myocardial infarction (AMI). To evaluate the sublingual agnet in this condition, the hemodynamic effects of 0.4 mg NTG administered to 16 supine patients during the first 72 hours of AMI were determined serially 5, 10 to 15, and 20 to 30 minutes post-NTG. Data were evaluated for the entire group, as well as for six patients with normal pulmonary artery wedge pressure (PAW) (less than or equal to 12 mm Hg; mean 7) who formed group I and for ten patients with elevated PAW (greater than 12 MM Hg; mean 19) who comprised group II. In the 16 patients, NTG resulted in significant decreases in PAW (14 TO 7 MM Hg; P less than .01), mean systemic arterial pressure (MAP) (95 TO 82 MM Hg; P less than .01), cardiac index (CI) (1.79 TO 1.46 L/min/m-2; P less than .02), stroke index (SI) (24 TO 18 CC/M-2; P less than .01) and stroke work index (SWI) (27 TO 20 GM TIMES M/M-2; P less than .01). These alterations were significant in both subgroups, with the decline in PAW greater (P less than .05), while there was no change in group II. There was no significant change in total peripheral vascular resistance (TPVR) for the entire group or in the two subgroups. This study demonstrates that, regardless of initial left ventricular filling pressure, sublingual NTG given in the acute phase of AMI results in rapid fall in PAW, concomitant with decreases in systemic blood pressure, cardiac output and SWI, without changes in TPVR and with little or no effect on heart rate. Since TPVR was unaltered, the decline in MAP was due to fall in cardiac output. Thus, the principal action of sublingual NTG in AMI appears to be systemic venodilation with consequent reduction of ventricular preload. This effect is translated into decline ofpump output even in patients with high initial filling pressures. Although NTG may rapidly relieve pulmonary congestion and lower myocardial oxygen consumption, use of the agent sublingually is limited in AMI because these salutary effects are accomppanied by potentially deleterious fall in cardiac output and systemic blood pressure.
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PMID:Hemodynamic effects of nitroglycerin in acute myocardial infarction. 80 94

Hemodynamic and electrocardiographic analysis during rapid right atrial stimulation was performed before and one, two, and four hours after oral application of longacting nitroglycerin (5 mg) and isosorbide dinitrate (20 mg) in 11 and 9 patients, respectively with coronary heart disease. Atrial stimulation without nitrate induced significant ischemic ST segment depression. Cardiac output showed a small decrease and the mean arterial, pulmonary artery, and pulmonary wedge pressure increased. Isosorbide dinitrate reduced the ischemic reaction by 40% from the first to the fourth hour after application. Cardiac output, stroke volume, aterial, pulmonary artery, and pulmonary wedge pressure also decreased continuously. Nitroglycerin caused a similar reduction of ischemic ST segment depression for two hours. Systolic, diastolic, and mean arterial pressure decreased significantly. Cardiac output, stroke volume, and pulmonary artery pressure remained unchanged. It was concluded that the applied dose of isosorbide dinitrate showed a more extensive longacting effect.
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PMID:[Hemodynamic and electrocardiographic prolonged nitrate effect during frequency load in coronary disease]. 82 Jan 4

The effects of an intravenous infusion of nitroglycerin were studied in 20 acutely hypertensive patients during coronary-artery surgery. Eight patients had histories of essential hypertension and six had been treated for it. They were anesthetized with morphine, diazepam, N2O, O2, pancuronium, and enflurane. Control measurements were obtained after sternotomy. Nitroglycerin was then administered until the blood pressure returned to normal, and the measurements then repeated. The mean dose of nitroglycerin was 80.0 +/- 4.7 mug/min, or 0.96 mug/kg/min. This produced significant decreases (P less than .05) in systolic, diastolic, and mean arterial blood pressures, central venous pressure, pulmonary capillary wedge pressure, systemic vascular resistance, and left ventricular stroke work index. Cardiac index, stroke index, and heart rate were unchanged. Two indices of myocardial oxygen demand (rate-pressure product and tension-time index) were significantly decreased by nitroglycerin (P less than .005). Fifty per cent of the patients had improvement in ST-segment depression on the electrocardiogram. These findings demonstrate that nitroglycerin can be safely administered intravenously during operation, and suggest that nitroglycerin decreases myocardial oxygen demand and relieves myocardial ischemia.
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PMID:Nitroglycerin infusion during coronary-artery surgery. 82 Feb 17

To assess further the effects of atrial natriuretic factor on autonomic nervous system reflexes in normal humans, the hemodynamic and neurohormonal responses to lower body negative pressure were measured at control and during infusions of atrial natriuretic factor and nitroglycerin in nine normal male subjects. The control -20 mm Hg lower body negative pressure was characterized by significant reductions in right atrial and pulmonary wedge pressures, as well as stroke volume and cardiac output. This was associated with a reflex increase in forearm vascular resistance and plasma norepinephrine. During the infusion of atrial natriuretic factor, the same -20 mm Hg lower body negative pressure produced a larger decrease in mean arterial pressure of 7.9 +/- 3.9 mm Hg (p less than 0.05), as well as a larger decrease in stroke volume (41.3 +/- 4.2 ml/beat) and cardiac output (2.0 +/- 0.3 L/min). Atrial natriuretic factor infusion did not affect the increase in forearm vascular resistance during lower body negative pressure, but did attenuate the increase in plasma norepinephrine. To control for nonspecific vasodilator actions, lower body negative pressure was also repeated during nitroglycerin infusion. Nitroglycerin infusion did not significantly change the responses of blood pressure, cardiac output, stroke volume, forearm vascular resistance, or plasma norepinephrine during lower body negative pressure. Thus, these data demonstrate that atrial natriuretic factor infusion can attenuate sympathetic nervous system reflexes evoked during lower body negative pressure. These inhibitory effects on the sympathetic nervous system may contribute to many of the observed hemodynamic actions of atrial natriuretic factor.
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PMID:Atrial natriuretic factor attenuates sympathetic reflexes during lower body negative pressure in normal men. 170 79

Thirty-five non-selected, consenting patients were studied during induction of anesthesia before coronary artery bypass grafting. Anesthesia was induced with diazepam, thiopentone and fentanyl, followed by pancuronium. Before induction, 200 MBq Tc 99 m - HSA was given i.v. and ejection fraction (EF) of the left ventricle was measured with a collimated single-crystal probe. The patients were allocated to five groups (seven patients in each) treated with: Group A: nitroglycerin i.v. bolus 4 micrograms x kg-1 given 30-60 s before laryngoscopy; Group B: nitroglycerin i.v. in continuous infusion, 1 micrograms x kg-1 x min-1 started before induction; Group C: two-stage topical anesthesia of the vallecula region and larynx with lidocain; Group D: a combination of nitroglycerin and topical anesthesia (as in Group B and C); and Group E: propranolol i.v. 0.01 mg x kg-1 given 5 min before intubation. All groups reacted in the same way during induction of anesthesia up to the point of laryngoscopy. End-diastolic volume and systemic arterial pressure decreased while cardiac index remained unchanged and EF increased. During laryngoscopy and intubation, however, differences between the groups were evident. Nitroglycerin i.v. as a bolus effectively prevented a reduction in EF and an increase in left ventricular volume. In addition to these beneficial hemodynamic effects, there was a moderate increase in heart rate and a reduction of stroke index. Continuous infusion of nitroglycerin and propranolol i.v. had no effect, since EF fell and left ventricular volume increased. Patients receiving topical anesthesia demonstrated a blunted response to endotracheal intubation with a moderate decrease in EF and an unchanged (Group C) or slightly increased (Group D) left ventricular volume.
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PMID:A comparative study of five different techniques to reduce left ventricular dysfunction during endotracheal intubation. 178 39

Peak filling rate is an indicator of left ventricular (LV) diastolic function. It is influenced by heart rate, loading conditions, sympathetic nervous system activity, ejection fraction and other factors. To determine the effect of altered loading conditions on peak filling rate, independent of heart rate and sympathetic nervous system activity, 12 patients were studied 3 weeks after orthotopic heart transplantation. Plasma catecholamine level, heart rate and ejection fraction were not changed by any maneuver. Nitroglycerin caused a decrease in pulmonary artery wedge pressure (9 +/- 2 to 6 +/- 1 mm Hg, p less than 0.001) and in absolute peak filling rate (46.0 +/- 3.0 to 42.8 +/- 2.5 kcts/s, p less than 0.01), but no change in normalized peak filling rate. Volume infusion increased pulmonary artery wedge pressure (9 +/- 2 to 12 +/- 2 mm Hg, p less than 0.001) and absolute peak filling rate (46.0 +/- 3.0 to 51.5 +/- 5.3 kcts/s, p less than 0.01), but peak filling rate normalized to stroke volume was unchanged. During nitroglycerin and volume infusions, there was a high correlation between changes in pulmonary artery wedge pressure and absolute peak filling rate (r = 0.82, p less than 0.001). With normalization of peak filling rate, these variables correlated less well. With methoxamine, 4 patients demonstrating systolic dysfunction had a decrease in absolute and normalized peak filling rate despite a large increase in pulmonary artery wedge pressure. The other 8 patients without systolic dysfunction had an increase in pulmonary artery wedge pressure with increased absolute but unchanged normalized peak filling rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of acute alterations in left ventricular loading conditions on peak filling rate in the denervated (transplanted) ventricle. 190 17

It has recently been shown that early left ventricular filling is a multifactorially determined phenomenon, the characteristics of which are highly dependent on relative changes in any of its determinants (left ventricular end-systolic volume, the constant of isovolumic left ventricular pressure decay, left atrial pressure at the onset of mitral valve flow, and left ventricular and left atrial compliance). Thus changes in the pattern of filling do not necessarily reflect changes in diastolic properties; they might instead simply reflect changes in loading conditions. To define a clinically implemented approach where the contribution of each of the covariates of early filling to the filling process and their modification by load manipulation could be assessed, nine patients with ischemic heart disease underwent simultaneous assessment of micromanometer left ventricular pressure and two-dimensional echo-guided Doppler mitral flow velocity before and after administration of nitroglycerin (0.2 mg intravenously). Nitroglycerin induced a significant reduction in the early-filling E wave (from 41 +/- 5 cm/sec to 32 +/- 7 cm/sec; p less than 0.002), whereas the late-filling A wave did not change (from 51 +/- 12 cm/sec to 55 +/- 9 cm/sec; p = 0.15), so that the E/A ratio decreased 27 +/- 16% (p = 0.016). End-systolic volume, the constant of isovolumic left ventricular pressure decay, and left atrioventricular pressure crossover at the onset of mitral flow decreased (from 49 +/- 37 to 43 +/- 38 ml [p = 0.016], from 52 +/- 14 to 47 +/- 13 msec [p = 0.016], and from 19 +/- 10 to 12 +/- 7 mm Hg [p = 0.08], respectively), whereas left atrial compliance (defined as stroke volume/atrioventricular pressure crossover) and left ventricular compliance (computed as change in volume/change in pressure at early and late diastole) did not change (p = 0.15 and p = 0.38, respectively); the diastolic pressure-volume relationship, however, was displaced slightly leftward and markedly downward, suggesting relief of pericardial constraint. A multilinear regression analysis, performed with pooled data at baseline and during infusion of nitroglycerin in each patient, identified left atrioventricular pressure crossover at the onset of mitral flow as the only significant predictor (p less than 0.02) of peak E wave velocity in the circumstances considered. Thus the interaction among covariates of early left ventricular filling and the relationship between filling and diastolic left ventricular and left atrial properties can be addressed with relative ease by means of this clinically implemented approach, in an effort to sort out the contribution of each cofactor to such a complex event.
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PMID:Early left ventricular filling: an approach to its multifactorial nature using a combined hemodynamic-Doppler technique. 190 74

We used a combination of transcranial Doppler ultrasonography and single-photon emission computed tomography to noninvasively assess changes in the diameter of the middle cerebral artery induced by sublingual nitroglycerin in 10 healthy subjects. Nitroglycerin reduced mean blood flow velocities without concurrently changing regional cerebral blood flow in the perfusion territory of this vessel. Our results strongly suggest that nitroglycerin causes vasodilatation of the basal intracranial arteries.
Stroke 1989 Dec
PMID:Effect of nitroglycerin on cerebral circulation measured by transcranial Doppler and SPECT. 251 93


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