Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Control of blood pressure in severe pregnancy-induced hypertension has often relied on agents with an unpredictable onset and duration of action. Because intravenous nitroglycerin is a potent, rapidly acting agent with a hemodynamic half-life measured in minutes, we evaluated its cardiovascular effects with and without volume expansion in six patients with severe pregnancy-induced hypertension. Nitroglycerin alone reduced mean arterial pressure by 27.5% without any significant changes in heart rate, central venous pressure, or stroke volume. The pulmonary capillary wedge pressure fell from 9 +/- 3 to 4 +/- 2 mm Hg (p less than 0.05) while the cardiac index decreased from 3.51 +/- 0.67 to 2.87 +/- 0.76 L/min X m2. Oxygen delivery fell significantly (p less than 0.05), from 617 +/- 78 to 491 +/- 106 ml/min X m2. While volume expansion alone had no effect on mean arterial pressure, the combination of blood volume expansion and nitroglycerin resulted in a marked resistance to the hypotensive effect of nitroglycerin. Cardiac index, pulmonary capillary wedge pressure, and oxygen utilization were not significantly different from baseline values when volume expansion preceded nitroglycerin. We conclude that the ease with which nitroglycerin reduces blood pressure is dependent on the individual patient's volume status. Although volume expansion allows one to maintain cardiac index, pulmonary capillary wedge pressure, and oxygen utilization when used in combination with nitroglycerin, this benefit may be offset by a concomitant reduction in hypotensive capability.
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PMID:Cardiovascular alterations in severe pregnancy-induced hypertension: effects of intravenous nitroglycerin coupled with blood volume expansion. 308 2

Nitroglycerin and nifedipine have been suggested as useful agents in the therapy of congestive heart failure. Because of the rapid action and feasability for sublingual administration of both drugs, their comparative hemodynamic and neurohumoral effects were studied in 12 patients with congestive heart failure. After sublingual nitroglycerin, there was a significant decrease in mean arterial pressure (96 +/- 17 to 90 +/- 15 mm Hg, p less than 0.01), left ventricular (LV) filling pressure (30 +/- 12 to 22 +/- 10 mm Hg, p less than 0.01), right atrial pressure (15 +/- 6 to 10 +/- 5 mm Hg, p less than 0.01) and systemic vascular resistance (21.5 +/- 7.7 to 19.3 +/- 6.2 units, p less than 0.05) and an increase in cardiac index (2.2 +/- 0.6 to 2.4 +/- 0.7 liters/min/m2, p less than 0.05) and LV stroke work index (20.4 +/- 7.0 to 24.5 +/- 8.6 gm-m/m2, p less than 0.01). After sublingual nifedipine, there was also a significant decrease in mean arterial pressure (96 +/- 16 to 89 +/- 14 mm Hg, p less than 0.01) and systemic vascular resistance (22.1 +/- 7.1 to 18.0 +/- 6.1 units, p less than 0.01) and an increase in cardiac index (2.1 +/- 0.6 to 2.4 +/- 0.6 liters/min/m2, p less than 0.01); in contrast to nitroglycerin, this was unaccompanied by significant changes in right- or left-sided filling pressures or LV stroke work index.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparative evaluation of hemodynamic and neurohumoral effects of nitroglycerin and nifedipine in congestive heart failure. 310 77

To evaluate the potential value of nitrate therapy in patients with chronic mitral regurgitation, the hemodynamic and angiographic effects of intravenous nitroglycerin were studied in 10 such patients. Nitroglycerin infusion, titrated to reduce mean pulmonary artery wedge pressure at least 20%, resulted in a significant reduction in mean blood pressure (from 91 +/- 12 to 77 +/- 13 mm Hg, p less than 0.0001), mean right atrial pressure (12 +/- 6 to 7 +/- 4 mm Hg, p less than 0.001), left ventricular end-diastolic pressure (22 +/- 7 to 13 +/- 5 mm Hg, p less than 0.0001) and peak V wave of indirect left atrial pressure (34 +/- 9 to 20 +/- 10 mm Hg, p less than 0.001). Changes in systemic vascular resistance (1,986 +/- 468 vs 1,582 +/- 534 dynes s cm-5) and forward stroke volume (39 +/- 14 vs 45 +/- 8 ml) were not statistically significant. Angiographic data showed a decrease in both end-diastolic and end-systolic left ventricular volumes (248 +/- 51 to 216 +/- 54 ml, p = 0.06 and 127 +/- 69 to 99 +/- 48 ml, p less than 0.05, respectively) and an improvement in ejection fraction, from 0.52 +/- 0.15 to 0.55 +/- 0.15 (p less than 0.05). There was no significant change in the group values for mitral regurgitant volume and fraction (from 85 +/- 32 to 72 +/- 32 ml and 67 +/- 10 to 64 +/- 5%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and volumetric effects of venodilation with nitroglycerin in chronic mitral regurgitation. 311 94

The goal of this study was to determine whether endothelium-dependent responses are impaired in the cerebral microcirculation of stroke-prone spontaneously hypertensive rats (SHRSP). We measured diameters of cerebral arterioles using intravital microscopy in normotensive rats (WKY) and SHRSP (6-8 mo old). Cerebral vasodilator responses to superfusion with adenosine, which is an endothelium-independent agonist, were similar in WKY and SHRSP. In contrast, cerebral vasodilator responses to superfusion with endothelium-dependent agonists were profoundly impaired in SHRSP. Acetylcholine (10(-4) M) increased pial arteriolar diameter 23 +/- 2% (means +/- SE) in WKY and did not change arteriolar diameter in SHRSP (-2 +/- 3%, P less than 0.05 vs. WKY). Serotonin (10(-5) M) increased pial arteriolar diameter 23 +/- 1% in WKY and, in contrast, reduced diameter 11 +/- 1% in SHRSP (P less than 0.05 vs. WKY). Nitroglycerin and acetylcholine produce vasodilatation by activation of guanosine 3',5'-cyclic monophosphate (cGMP). Nitroglycerin was used to determine whether impaired responses of cerebral arterioles in SHRSP were related to altered cGMP activity. We found similar dilatation of cerebral arterioles in WKY and SHRSP in response to nitroglycerin. Thus impaired endothelium-dependent dilatation in SHRSP is not related to alteration of cGMP activity. We speculate that impairment of cerebral vasodilator responses to endothelium-dependent agonists, including vasoactive substances released by platelets, may predispose SHRSP to cerebral ischemia.
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PMID:Impairment of endothelium-dependent responses of cerebral arterioles in chronic hypertension. 312 90

It has previously been shown that nitroglycerin increases the compliance of forearm arteries. The present study investigates whether nitroglycerin reduces the hydraulic load on the heart (as measured by aortic input impedance) by a mechanism compatible with an increase in peripheral arterial compliance. In eight subjects, measurements of aortic flow and pressure were made with a catheter tipped probe before and during intravenous nitroglycerin (6 to 30 micrograms/min) administration. The reduction of aortic systolic pressure (129 +/- 5 to 113 +/- 4 mmHg, P less than 0.001) was due to a decrease in the late systolic pressure peak. There was no change in stroke volume, heart rate or systemic vascular resistance. The lower systolic pressure resulted from a decrease in the amplitude of the first harmonic of input impedance (210 +/- 19 to 143 +/- 11 dyne.s.cm-5, P less than 0.005) yet characteristic impedance (a measure of local aortic distensibility) did not change. The ratio of maxima to minima of the impedance spectrum was reduced (1.02 +/- 0.09 to 0.71 +/- 0.11, P less than 0.05) suggesting a decrease in the amplitude of reflected waves contributing to aortic impedance. Nitroglycerin at doses which have no effect on arteriolar resistance vessels, reduces systolic aortic pressure by diminishing the amplitude of wave reflections returning to the ascending aorta in late systole. This mechanism is compatible with the peripheral arterial effects of nitroglycerin.
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PMID:Effect of nitroglycerin on left ventricular hydraulic load. 313 Jan 71

The goal of this study was to determine whether responses of cerebral arterioles to products released by platelets are impaired in stroke-prone spontaneously hypertensive rats (SHRSP). The diameter of pial arterioles was measured during suffusion with adenosine 5'-diphosphate (ADP), serotonin, and the thromboxane analogue U-46619, using intravital microscopy in normotensive Wistar-Kyoto rats (WKY) and SHRSP (7-10 months old). Responses of cerebral arterioles to ADP and serotonin were profoundly impaired in SHRSP. ADP (10(-5) M) increased pial arteriolar diameter 17 +/- 3% (mean +/- SE) in WKY and only 4 +/- 1% in SHRSP. Serotonin (10(-5) M) increased pial arteriolar diameter 15 +/- 2% in WKY and, in contrast, reduced the diameter 13 +/- 1% in SHRSP. Nitroglycerin produced a similar dilatation of cerebral arterioles in WKY and SHRSP, suggesting that impairment of dilatation in SHRSP in response to ADP and serotonin was not related to nonspecific impairment of vasodilatation in SHRSP. The thromboxane analogue U-46619 produced a similar constriction of arterioles in WKY and SHRSP. We also examined the possibility that impaired dilator responses of cerebral arterioles in SHRSP in response to ADP and serotonin may be related to production of a cyclooxygenase vasoconstrictor substance. Indomethacin (10 mg/kg i.v.) partially restored dilator responses to ADP and serotonin in SHRSP, without altering responses in WKY. Thus, we speculate that vasoactive substances released by platelets may release a prostanoid constrictor substance from cerebral vessels of SHRSP and thereby predispose SHRSP to cerebral ischemia and, perhaps, stroke.
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PMID:Responses of cerebral arterioles to adenosine 5'-diphosphate, serotonin, and the thromboxane analogue U-46619 during chronic hypertension. 320 60

Nitroglycerin improves perfusion to ischemic myocardial regions and therefore has theoretical advantages over sodium nitroprusside to treat hypertension (mean arterial pressure [MAP] greater than 95 mm Hg) following coronary bypass operation. Thirty-three hypertensive patients were randomized to an initial infusion of either nitroglycerin or nitroprusside in a crossover trial designed to reduce MAP to 85 mm Hg. Thermodilution cardiac output measurements permitted calculation of left ventricular stroke work index (LVSWI), and nuclear ventriculograms permitted estimation of left ventricular ejection fraction, left ventricular end-diastolic volume index (LVEDVI), and left ventricular end-systolic volume index (LVESVI). Coronary sinus blood flow was measured by the continuous thermodilution technique, and arterial and coronary sinus lactate measurements permitted calculation of myocardial lactate flux (MVL). Both nitroglycerin and nitroprusside reduced MAP (-25 +/- 12 mm Hg and -20 +/- 10 mm Hg, respectively; not significant [NS]). Nitroglycerin reduced LVSWI more than did nitroprusside (-15 +/- 13 gm-m/m2 and -7 +/- 9 gm-m/m2, respectively; p less than 0.01). Both agents increased left ventricular ejection fraction (nitroglycerin, +8 +/- 8%, and nitroprusside, +10 +/- 7%; NS), and decreased LVEDVI (-20 +/- 22 ml/m2 and -11 +/- 17 ml/m2, respectively; NS) and LVESVI (-13 +/- 14 ml/m2 and -10 +/- 12 ml/m2, respectively; NS). Coronary sinus blood flow decreased with both drugs (NS), but MVL increased with nitroglycerin (+0.02 +/- 0.14 mmol/min) and decreased with nitroprusside (-0.02 +/- 0.02 mmol/min) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of nitroglycerin and nitroprusside: I. Treatment of postoperative hypertension. 391 59

The treatment of postoperative hypertension with nitroglycerin or nitroprusside reduces cardiac filling, and volume loading is required to maintain hemodynamic and metabolic stability. Postoperative hypertension (mean arterial pressure greater than 95 mm Hg) developed in 33 patients who were randomized to an initial infusion of nitroglycerin or nitroprusside in a crossover trial. Volume loading (a rapid infusion of 250 to 500 ml of colloid to raise the left atrial pressure 2 to 4 mm Hg) was instituted prior to hypertension and again following the crossover trial during the infusion of nitroglycerin (11 patients) and nitroprusside (13 patients). Volume loading increased left ventricular end-diastolic volume index (LVEDVI) as documented by nuclear ventriculography, cardiac index (CI), and left ventricular stroke work index (LVSWI). Although CI was higher (p less than 0.01) with nitroprusside at any level of LVEDVI, myocardial performance (the relation between LVSWI and LVEDVI) was not different. Diastolic compliance (the relation between left atrial pressure and LVEDVI) was increased (p less than 0.01) with nitroglycerin. Myocardial metabolism was assessed by calculating myocardial lactate flux (MVL), the product of myocardial lactate extraction and coronary sinus blood flow by the thermodilution technique. Volume loading increased MVL during nitroglycerin therapy and decreased (p less than 0.01) MVL during nitroprusside therapy. Volume loading restored preload and increased CI with both nitroglycerin and nitroprusside. Only nitroglycerin improved myocardial lactate utilization. Nitroglycerin is the preferred vasodilator when ischemia is suspected after coronary bypass operations.
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PMID:A comparison of nitroglycerin and nitroprusside: II. The effects of volume loading. 391 60

Left ventricular performance was assessed in ten patients with acute myocarditis during the acute stage (within the first 3 days after the onset of cardiac symptoms) and during the convalescent phase (3-5 weeks later). In nine, the diagnosis was confirmed by endomyocardial biopsy during the acute stage, when left ventricular function was markedly reduced, i.e., cardiac index 1.53 +/- 0.33 l/min/m2 (mean +/- SD), left ventricular stroke work index 14.1 +/- 3.9 g/beat/m2, pulmonary capillary pressure 25.9 +/- 4.3 mm Hg, and systemic vascular resistance 27.9 +/- 9.4 R units. During convalescence, seven patients improved clinically with normal cardiac function and in three it remained impaired. Cardiovascular response to nitroglycerin ointment in three patients and a combination of dopamine and nitroglycerin ointment in five were compared. Nitroglycerin ointment reduced pulmonary capillary pressure by an average of 28.5% (P less than 0.05) and systemic vascular resistance by 26.8%, while the cardiac index increased by 34.1% (P less than 0.05) and left ventricular stroke work index by 30.3% (P less than 0.01). The combined therapy was more effective, with a reduction of pulmonary capillary pressure by 30.4% (P less than 0.05) and systemic vascular resistance by 27.5% (P less than 0.05), accompanying an increase in cardiac index by 53.5% (P less than 0.005) and left ventricular stroke work index by 63.5% (P less than 0.01), with little change in the double products. This study suggests that serial hemodynamic monitoring accurately evaluates cardiac function, selection of appropriate therapy, and the hemodynamic effects of treatment in patients with acute myocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic studies and response to a combined therapy of nitroglycerin ointment and dopamine in patients with acute myocarditis. 393 46

Nitroglycerin (NTG) in a transdermal therapeutic system (TTS) was evaluated in 16 patients with severe chronic heart failure. Eight patients were given NTG TTS with an in vivo release rate of 5 mg/24 h. No significant changes in heart rate or blood pressure were observed. Pulmonary capillary wedge (PCW) pressure was reduced significantly from a control value of 29 +/- 4 mm Hg to 17 +/- 2 mm Hg after 1 h (p less than 0.01), and significant reduction was maintained for 24 h. The system was then removed and PCW pressure rose to 27 +/- 2 mm Hg after 2 h. NTG TTS, 10 mg/24 h, was applied and PCW pressure was again reduced significantly. Significant reduction in systemic vascular resistance and increases in cardiac and stroke volume indices occurred on the first day at 4 h but were not maintained. In another eight patients, the haemodynamic effects of NTG TTS (5 mg/24 h), oral isosorbide dinitrate (20 mg), and topical NTG ointment (1 inch) were compared. Significant reductions in PCW pressure were achieved with each method of treatment, but no significant alterations in other haemodynamic measurements were observed. Haemodynamic reevaluation of 10 patients treated with NTG TTS for 3 months showed partial attenuation of the reduction in PCW pressure compared with the initial response.
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PMID:Nitroglycerin in a transdermal therapeutic system in chronic heart failure. 619 16


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