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

In nine patients undergoing neurosurgical operation for cerebral aneuryms haemodynamic measurements were made before, during and after continuous intravenous administration of Nitroglycerin at a mean dose of 6.5 micrograms/kg . min. Within 15 min of the start of the infusion mean arterial pressure fell from 94.2 +/- 10.5 to 73.4 +/- 11.1 mm Hg. A further decrease of mean arterial pressure even by a substantial raising of the Nitroglycerin dose was not possible. 15 min after the discontinuation of Nitroglycerin administration mean arterial pressure rose to the preinfusion level. The decrease of stroke volume index from 40.8 +/- 9.9 to 31.0 +/- 7.3 ml/m2 was partially compensated by an increase of heart rate from 65.9 +/- 9.6 to 77.7 +/- 19.4 beats/min. Consequently cardiac index fell only slightly from 2.9 +/- 0.6 to 2.5 +/- 0.5 ml/min . m2. The right atrial pressure decreased to 3.3 +/- 2.9 mm Hg, the mean pulmonary arterial pressure to 6.3 +/- 1.9 mm Hg and the pulmonary capillary wedge pressure to 2.3 +/- 2.1 mm Hg. The significant fall of total peripheral resistance to 983 +/- 194 dyn x s/cm5 (p less than 0.05) and the decrease of left ventricular stroke work index to 34.7 +/- 11.5 g . m/m2 contributed to reduce myocardial oxygen consumption. The authors conclude that, because of its effect on blood pressure, it reversibility of action and its absence of adverse side effects Nitroglycerin is a valuable agent for controlled hypotension.
 ...
PMID:[Haemodynamic measurements during controlled hypotension by nitroglycerin (author's transl)]. 677 44

Nitroglycerin, long known as a safe and effective dilator of the large coronary arteries, has recently been shown to dilate the basilar artery of the dog after experimentally induced vasospasm. In this study we have evaluated the effects of intravenous nitroglycerin on local cerebral blood flow (H2 clearance technique) and intracranial pressure (intracisternal needle monitor) in normal beagle dogs (Group 1). In each of 7 dogs, infusion of nitroglycerin at rates of 3, 5, and 10 microgram/kg/min did not change blood flow in the right and left caudate nucleus, thalamus, frontal and parietal cortex. Autoregulation of cerebral blood flow remained unimpaired and intracranial pressure remained stable during nitroglycerin infusion. The effects of a combination of intravenous nitroglycerin and dopamine on local cerebral blood flow was evaluated in another group of normal beagle dogs (Group 2). Local cerebral blood flow decreased or remained unchanged in response to intravenous infusion of dopamine at low rates, increased in response to moderate rates and again decreased in response to high infusion rates. These dopamine induced changes in blood flow occurred whether or not nitroglycerin was infused simultaneously. When the vasoconstrictor activity of dopamine was blocked by phentolamine or methysergide, local cerebral blood flow increased at moderate and high infusion rates, again whether or not nitroglycerin was infused simultaneously. Our data suggest that nitroglycerin affects mainly the extracerebral capacitance arteries while dopamine affects the smaller intraparenchymal resistance vessels. Nitroglycerin has little effect on cerebral blood flow even when used in combination with dopamine.
Stroke
PMID:Cerebral blood flow and intracranial pressure in the dog during intravenous infusion of nitroglycerin alone and in combination with dopamine. 678 48

The radioactive microsphere technique was used to trace regional blood flow and total cardiac output distribution in rats in heart failure secondary to biventricular volume overload during acute intravenous infusion of nitroglycerin. Data from rats with heart failure (chronic arteriovenous shunt) were compared to data obtained from rats subjected to sham surgical procedures. In both glycerin and normal saline (control). In heart failure, nitroglycerin slightly increased cardiac output at rest and during exercise, increased stroke volume, and reduced systemic vascular resistance at rest but not during exercise. In the heart failure group, exercise reduced flow to the renal, gastrointestinal, and cutaneous circulations but had little or no effect in the sham group. Nitroglycerin dramatically increased renal, gastrointestinal, and cutaneous blood flow during exercise in the heart failure group but had minimal effects on active hyperemia in the skeletal muscle bed. In the sham group, nitroglycerin decreased blood flow in the renal, gastrointestinal, and cutaneous beds and had no effect on skeletal muscle blood flow. Thus, in the renal, gastrointestinal, and cutaneous circulations during exercise, nitroglycerin increased flow in the heart failure group and decreased flow in the sham group to the extent that the respective values in the two groups were equal.
 ...
PMID:Mechanism of action of nitroglycerin during exercise in a rat model of heart failure. Improvement of blood flow to the renal, splanchnic, and cutaneous beds. 678 98

In 20 infarct patients, whose age varies from 43 to 78 years (m 59.6), continuous hemodynamic measurements were made to determine the cardiovascular effects of propranolol without and during a simultaneous infusion treatment with nitroglycerin. In cases of compensated ventricular function and pulmonary wedged pressures of 15 mm Hg or less (N = 10), a mean intravenous propranolol dose of 6.1 +/- 1.3 mg led to a significant reduction of the LVSWI and a simultaneous increase of the PCP by 31% of the control value (P less than or equal to 0.005). A simultaneously performed infusion treatment with nitroglycerin at a mean dose of 3.0 +/- 1.6 mg/h resulted in totally cutting off the propranolol-induced PCP increase, whereas a decrease of the heart rate and the LVSWI due to a beta-receptor-blockade remained completely unchanged. In the case of pre-existing congestion insufficiency of the left ventricle (N = 10) and of a pulmonary wedged pressure of above 15 mm Hg, the administration of a mean dose of propranolol of 5.8 +/- 1.1 mg for protection of the myocardium resulted in a partly disquieting decrease of the volume of cardiac output (P less than or equal to 0.005) which was 28% of the control value for the CI an 12% for the SVI. Correspondingly the left ventricular stroke work decreased to 18%. Nitroglycerin has a reducing influence on these changes, but not down to the initial level. In cases of sufficient ventricular function, propranolol has a favorable influence on the myocardial O2-metabolism via its depressor effect on heart rate and contractility. By means of nitroglycerin, an increase of the pulmonary wedged pressure occurring under this condition can be inhibited. However, in the case of a pre-existing congestion insufficiency, propranolol can lead to a partly disquieting depression of the circulation, which, apart from the hemodynamic risks, makes a rather unfavorable influence on the myocardial O2-metabolism seem likely.
 ...
PMID:[The treatment of acute myocardial infarctions with beta-receptor-blockers. II. Hemodynamic effects of propranolol with and without combination therapy with nitroglycerin (author's transl)]. 679 41

Glyceryl trinitrate (GNT, 0.8 mg) was administered in a spray to 15 coronary patients of whom 7 had a pulmonary wedge pressure (PWP) greater than 16 mm Hg on exercise (subgroup I) and the others (subgroup II) had a normal PWP at rest and during exercise. At rest, GNT increased heart rate and decreased cardiac output, systolic index, stroke work index, right atrial pressure, pulmonary wedge and mean systemic pressures in all patients. Peripheral resistances did not change. During exercise, GNT lowered PWP, systemic arterial pressure and peripheral resistances in all cases. It increased cardiac output as well as systolic and stroke work indices only in patients of subgroup I. In subjects with coronary disease, no overt cardiac failure but elevated PWP on exercise, GNT in a spray can quickly improve exercise capacity and hemodynamic reserves and increase anginal threshold.
 ...
PMID:Hemodynamic response to glyceryl trinitrate in a spray at rest and during exercise in a sitting position. 680 31

The hemodynamic effects of standard dose of Nitroglycerin (NTG) ointment (23 +/- 4 mg) and oral Isosorbide Dinitrate (ISDN) 10 mg were compared in the treatment of left ventricular failure. Ten patients, 8 males and 2 females (mean age 59 +/- 9 years), affected by acute myocardial infarction (7 cases). Ischemic cardiomyopathy (2 cases) and hypertensive cardiomyopathy (1 case) were submitted to right heart catheterization by triple lumen Swan-Ganz catheter. Heart Rate (HR), mean Arterial Pressure (AP), Right Atrial Pressure (RAP), mean Pulmonary Artery Pressure (PAP), Pulmonary Wedge Pressure (PWP), Stroke volume (SV), Cardiac Index (CI), Stroke Work Index (SWI), Systemic Vascular Resistances (SVR), Pulmonary Total Resistances (PTR) were controlled every 30 minutes until the disappearance of the hemodynamic effects. ISDN did not produce any statistically significant changes; on the contrary NTG ointment caused significant changes in: (formula: see text). Decrease of RAP, PAP, PWP, PTR and increase of SV, CI, SWI were statistically significant from 30 until 180 minutes after NTG ointment administration. These changes were statistically different from those produced by ISDN (p less than 0,05). Thus NTG ointment, at this dose, improved cardiac performance, while oral ISDN 10 mg did not. It is concluded that the hemodynamic effects of NTG ointment are prompt and sustained.
 ...
PMID:[Comparison between the hemodynamic effects of nitroglycerine ointment and oral isosorbide dinitrate in the treatment of left ventricular failure (author's transl)]. 680 18

Effects of three representative vasodilators on peripheral and cardiac hemodynamics were studied in 20 patients with heart failure due to acute myocardial infarction (PCWP greater than 18 mmHg, C1 greater than 2.20 L/min/m2) using venous occlusion plethysmography and a Swan-Ganz catheter. Sublingual isosorbide dinitrate (ISDN) significantly increased calf venous capacitance (CVC) from 5 to 60 min (p less than 0.01) and calf blood flow (CBF) in the initial 15 min (p less than 0.05), while simultaneously lowering PCWP (p less than 0.05) and central venous pressure (p less than 0.05). Calf vascular resistance (CVR), cardiac index, blood pressure, and total systemic peripheral resistance (TSPR) were not affected significantly. Nitroglycerin ointment (NGO) significantly decreased CVR (p less than 0.05) and increased CVC (p less than 0.05) from 60 to 240 min, simultaneously with lowering of PCWP (p less than 0.01), central venous pressure (p less than 0.05), and TSPR (p less than 0.05). Oral prazosin (Pz) increased CBF (p less than 0.01) and CVC (p less than 0.05) from 60 to 240 min, simultaneously with significant lowering of PCWP (p less than 0.01) and TSPR (p less than 0.05), resulting in increased stroke work index (p less than 0.05). These data confirm that ISDN predominantly causes capacitance vessel dilatation and reduce excessive venous return, while Pz and NGO dilate not only capacitance vessels but also resistance vessels, consequently reducing systemic vascular resistance and resulting in increased peripheral blood flow and cardiac performance. It was observed that the higher the base-line calf vascular resistance rose, the better the response to the vasodilator treatment appeared in terms of a decrease in calf vascular resistance.
 ...
PMID:Unloading effects of vasodilators on peripheral circulation and cardiac hemodynamics in patients with acute myocardial infarction. 681 69

The coronary and systemic hemodynamic effects of the novel nitrate ester ITF 296 were investigated in conscious, resting dogs and compared with nitroglycerin and nicorandil. ITF 296 at 1-25 micrograms/kg i.v. elicited selective, long-lasting, and dose-dependent increases in large epicardial coronary artery diameter (CD) without affecting coronary blood flow (CBF) or coronary vascular resistance (CVR). Blood pressure (BP) and heart rate (HR) were also unaltered. At 125 micrograms/kg, ITF 296 further increased CD but simultaneously reduced CVR and mean aortic pressure and increased CBF and HR. Nitroglycerin 1-25 micrograms/kg induced a shorter and less selective dilatation of large coronary conductance arteries, as it was accompanied by a decrease in CVR at all doses used. Nicorandil produced a selective increase in left circumflex CD only at the lowest dose used (10 micrograms/kg), whereas higher doses were effective on both CD and CVR. ITF 296 significantly reduced left ventricular end-diastolic pressure and increased stroke volume (SV) and cardiac output (CO) at doses that did not alter HR or BP, indicating an increase in cardiac efficiency. In contrast, the increases in CO produced by nitroglycerin and nicorandil were dependent on the augmentation of HR, because SV was unchanged at all doses used. Nitroglycerin dose-dependently decreased BP, whereas ITF 296 reduced BP only at the highest dose used. In conclusion, ITF 296 induces a selective, flow-independent dilatation of large coronary conductance arteries without affecting the tone of small coronary resistance vessels or systemic hemodynamics over a broad range of doses. An equally selective effect was elicited by nicorandil only at the lower dose used, whereas no selective effect of nitroglycerin on the diameter of coronary conductance arteries was seen at the doses utilized in this study.
 ...
PMID:Effect of the new nitrate ester ITF 296 on coronary and systemic hemodynamics in the conscious dog: comparison with nitroglycerin and nicorandil. 883 21

The pharmacologic profiles of nicorandil in the cardiovascular system have been characterized by K-channel opening and nitrate activities. However, the effects of nicorandil on acute heart failure have yet to be elucidated. To investigate the effects of nicorandil under such pathophysiologic conditions, we administered nicorandil intravenously to dogs with acute ischemic heart failure induced by coronary embolization and compared the results with those induced by cromakalim and nitroglycerin. The heart failure in this experiment was demonstrated by a reduction of mean blood pressure (MBP) from 143+/-3 to 129+/-2 mm Hg (p < 0.01); cardiac output (CO) from 2.18+/-0.10 to 1.06+/-0.05 L/min (p < 0.01); stroke volume (SV) from 12.7+/-0.6 to 6.8+/-0.3 ml/min (p < 0.01); Vmax, an index of the contractility of the left ventricle, from 105.5+/-4.4 to 49.9+/-1.8 1/s (p < 0.01), and an increase in right atrial pressure (RAP) from 2.9+/-0.3 to 5.3+/-0.3 mm Hg (p < 0.01); left ventricular end-diastolic pressure (LVEDP) from 2.5+/-0.4 to 26.0+/-1.4 mm Hg (p < 0.01); and T, time constant of left ventricular relaxation, from 38.3+/-0.8 to 62.4+/-2.8 ms (p < 0.01). Furthermore, plasma renin activity (PRA) and plasma atrial natriuretic peptide (ANP) increased (from 1.72+/-0.29 to 5.03+/-0.68 ng AngI/ml/h, p < 0.01; from 103.9+/-5.8 to 411.5+/-29.4 pg/ml, p < 0.01, respectively), whereas brain natriuretic peptide (BNP) remained unchanged (from 23.1+/-2.2 to 26.9+/-1.4 pg/ml). Nicorandil (10-40 microg/kg/min, i.v. infusion for 20 min for each dosing) or cromakalim (0.25-1 microg/kg/min) decreased MBP, systemic vascular resistance (SVR), RAP, and LVEDP, and increased CO, SV, and Vmax. However, the reduction of RAP in cromakalim was significantly smaller than those of nicorandil and nitroglycerin in comparison at similar hypotensive doses. Nitroglycerin (2.5-10 microg/kg/min) decreased MBP, RAP, and LVEDP, and increased Vmax but did not change CO or SV. Increased plasma ANP levels, an index of cardiac filling pressure after induction of acute ischemic heart failure, were decreased significantly by cromakalim and tended to decrease by nicorandil or nitroglycerin. Plasma BNP levels and PRA were not influenced by any of these drugs. These results suggest that nicorandil produces the reduction of both preload and afterload followed by an improvement of cardiac contractility in this model. The increase in CO may be mediated mainly by the drug's K-channel opening activities and the reduction of venous tone by its nitrate properties. Nicorandil may prove to be useful in the treatment of acute ischemic heart failure.
 ...
PMID:Hemodynamic and hormonal responses to nicorandil in a canine model of acute ischemic heart failure: a comparison with cromakalim and nitroglycerin. 989 Apr 2

Venodilatation with consequent reduction in left ventricular filling and end-diastolic wall stress is an important mechanism for the beneficial effects of nitroglycerin in ischemic heart disease and in left ventricular failure. The effects of sublingual nitroglycerin on arterial pulsatile hemodynamics are less well defined. Doppler echocardiography and the calibrated subclavian artery pulse tracing were used to assess hemodynamics in subjects with sustained arterial hypertension (n = 25) before and 5 to 10 minutes after sublingual deposition of 0.5 mg glyceryl trinitrate. Aortic characteristic impedance was calculated by averaging the modulus of the input impedance (ratio of pressure to flow) at high frequencies and by calculating the ratio of pressure and flow increments during upstroke. The pressure wave was split into forward and backward components, and the reflection coefficient (the ratio of backward to forward pressures) was calculated. Parameters of the arterial bed were estimated by using 2- and 3-element Windkessel models. Nitroglycerin delayed the return of arterial wave reflections by 17% (P =.02) and increased aortic characteristic impedance by 20% (P =. 01), but it did not influence total arterial compliance. Mean arterial pressure decreased 7% (P =.0001), but pulse pressure did not change. Stroke volume and the acceleration time of aortic root flow decreased by 13% (P =.0001) and 8% (P =.01), respectively. Cardiac output decreased 7% (P =.01), despite an increase in heart rate of 10% (P =.0001). Peripheral resistance tended to decrease (4%, P =.06). Thus, in subjects with sustained hypertension, sublingual nitroglycerin dilates peripheral, predominantly muscular arteries with a subsequent delayed return of reflected pressure waves. Reflex activation of the sympathetic nervous system with consequent increased acceleration of left ventricular ejection seems to counteract the effect of reduced mean arterial pressure (distending pressure) with respect to the "stiffness" of the aorta.
 ...
PMID:Sublingual nitroglycerin delays arterial wave reflections despite increased aortic "stiffness" in patients with hypertension: a Doppler echocardiography study. 1111 78


<< Previous 1 2 3 4 5 Next >>