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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated cardiopulmonary effects of dopamine in patients with acute respiratory failure. Specifically, we wished to test the hypothesis that left ventricular filling pressure (Pcwp) would increase when cardiac output (CO) increased with dopamine. Dopamine (range, 5.5 to 20 micrograms/kg/min) increased blood pressure (BP) (p less than 0.001) Pcwp, CO, and stroke volume (SV) (p less than 0.005). Mean Pcwp increased (p less than 0.005) 45% with dopamine, from 11 to 16 mmHg. Qs/Qt increased with dopamine in association with an increase in mixed venous O2 tension, and arterial O2 tension remained constant. In 8 of these patients, left ventricular end-diastolic volume (LVEDV) and end-systolic volume (ESV) were measured using scintigraphic techniques. The LVEDV increased (p less than 0.01) in each patient after the administration of dopamine, and the mean change was from 134 to 163 ml. Although BP and LV afterload increased in each patient, there was no consistent change in LVESV after dopamine administration, i.e., ESV decreased in 1 patient, remained constant in 3, and increased in 4. Accordingly, because afterload increased in all patients and ESV did not, dopamine probably increased contractility. Because EDV increased in all patients, we concluded that the increase in SV with dopamine is explained by a combination of inotropic and peripheral vascular effects.
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PMID:Effects of dopamine on cardiopulmonary function and left ventricular volumes in patients with acute respiratory failure. 647 90

To investigate the role of brain catecholamines in the development of spontaneous hypertension, rats were treated with different doses of the neurotoxins 6-hydroxydopamine (6-OHDA) or DSP-4 (N-[2-chloroethyl]-N-ethyl-2-bromobenzylamine hydrochloride). Intracerebroventricular (i.c.v.) 6-OHDA attenuated the development of hypertension in spontaneously hypertensive rats (SHR) and also lowered the systolic blood pressure (BP) in Wistar-Kyoto (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). Norepinephrine was markedly and dose-dependently depleted in brain areas of all three substrains. Dopamine was affected also, although to a lesser extent. Pretreatment with the norepinephrine-uptake inhibitor desmethylimipramine (DMI) did not influence the effect of 6-OHDA on the development of hypertension in SHR. DMI largely antagonized the 6-OHDA-induced depletion of brain norepinephrine, while dopamine depletion was not affected. Specific depletion of brain norepinephrine by treatment with DSP-4 did not alter the rise in BP in SHR. These results suggest that the effect of 6-OHDA on the development of hypertension in SHR may not be mediated through destruction of brain norepinephrine neurons, but that interruption of brain dopaminergic mechanisms is a possibility in this respect.
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PMID:Role of dopamine in the development of spontaneous hypertension. 651 47

The acute metabolic and hemodynamic effects of dopamine, dobutamine (both at 10 micrograms . kg-1 . min), and isoproterenol (at 0.05 or 0.1 micrograms . kg-1. min) were determined in dogs following 20 minutes of normothermic global myocardial ischemia. The catecholamines were started 10 minutes before cardiopulmonary bypass (CPB) was discontinued and were continued for 1 hour after bypass. Regional myocardial and systemic blood flow distribution was measured by means of the radioactive microsphere technique. On bypass all catecholamines sharply increased heart rate, myocardial oxygen consumption, and left ventricular blood flow (p less than 0.01). Because the hearts were unloaded, these data suggest that velocity of contraction is an important component of myocardial oxygen consumption. Although these drugs did not lower myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) levels, the significant rise in oxygen consumption suggested that inotropic treatment on bypass may not be beneficial. Furthermore, renal blood flow was diminished in dobutamine-treated dogs (p less than 0.01) and tended to decrease with isoproterenol infusion. No change was seen with dopamine infusion. After bypass, dobutamine treatment increased cardiac output (p less than 0.01) and stroke volume (p = 0.017) with no change in heart rate, myocardial oxygen consumption, high-energy phosphate levels, and total or transmural distribution of left ventricular blood flow. Dopamine infusion did not change cardiac output but did increase oxygen consumption (p less than 0.01). Isoproterenol showed a slight inotropic effect, but frequent ventricular arrhythmias were present during weaning from bypass. In all treatment groups, blood flow in the other systemic beds (cerebral, gastrointestinal, and renal) was similar to that in control dogs. These data suggest that dobutamine is the most efficient of the drugs tested for support of the heart following global myocardial ischemia but, when given during bypass, it appears to decrease renal blood flow.
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PMID:Comparison of catecholamine effects on canine myocardial metabolism and regional blood flow during and after cardiopulmonary bypass. 670 Feb 52

Twelve patients with severe persistent cardiogenic shock complicating acute myocardial infarction underwent single crossover treatment with intravenous dopamine and salbutamol to determine the more beneficial therapy. Salbutamol (10 to 40 microgram/min) reduced systemic vascular resistance and progressively increased both cardiac index and stroke index. Heart rate increased from 95 to 104 beats/min. Changes in mean arterial pressure and pulmonary artery end-diastolic pressure were small and insignificant. Dopamine infusion at rates of 200 and 400 micrograms/min also increased cardiac index and stroke index. Systemic vascular resistance fell slightly but mean arterial pressure rose from 57 to 65 mm Hg. Heart rate increased from 95 to 105 beats/min. Changes in pulmonary artery end-diastolic pressure were again small and insignificant. Dopamine infusion at 800 micrograms/min caused an appreciable increase in systemic vascular resistance; a further increment in mean arterial pressure was observed, though cardiac index fell slightly. Heart rate and pulmonary artery end-diastolic pressure rose steeply. Salbutamol, a vasodilator, increased cardiac output in patients with cardiogenic shock complicating acute myocardial infarction but did not influence blood pressure. If correction of hypotension is essential dopamine in low doses may be the preferred agent. Doses of 800 microgram/min, which is within the therapeutic range, worsen other manifestations of left ventricular dysfunction.
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PMID:Comparison of haemodynamic responses to dopamine and salbutamol in severe cardiogenic shock complicating acute myocardial infarction. 677 74

An evaluation has been made on the effectiveness and feasibility of the individualized fluid replacement programme based on intensive haemodynamic monitoring using a Swan-Ganz catheter. Twenty-one extensively burned patients with an average burn of 60.8 per cent BSA were resuscitated with lactated Ringer's and colloid solutions. The rate of fluid administration was adjusted to maintain the optimal ranges of the various haemodynamic parameters including cardiac index and left ventricular stroke work index. Two patients failed to respond to fluid resuscitation possibly due to inadequate emergency procedures given before arrival at our institute. The remaining patients survived the shock phase, with the amount of fluid given to the 18 adult patients being (3.38 /+- 1.02 ml/kg) x (percentage burn) for the first 24 hours. A negative correlation existed between the amounts of lactated Ringer's solution and colloid solution used for the fluid resuscitation. Dopamine was effective in 4 out of 5 patients who showed depressed myocardial function. The individualized fluid programme was shown to be effective and reliable for the management of critically burned patients.
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PMID:Individualized fluid resuscitation based on haemodynamic monitoring in the management of extensive burns. 706 23

The hemodynamic effects of dopamine were measured during the immediate postoperative period in five infants with low cardiac output following repair of congenital cardiac defects. Dopamine was administered at doses of 5, 10, 15, 20 and 25 micrograms/kg/minute. Heart rate, systemic arterial pressure, and cardiac index increased significantly at a dose of 15 micrograms/kg/minute or greater. There were no significant changes in right atrial pressure, left atrial pressure, pulmonary artery pressure, pulmonary vascular resistance, systemic vascular resistance, or stroke volume. These data support the hypothesis that inants respond to dopamine in a fashion qualitatively and quantitatively different from that in adults.
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PMID:The hemodynamic effects of dopamine in infants after corrective cardiac surgery. 735 65

Twenty post-open heart surgery patients with low output syndrome were given dopamine, sodium nitroprusside (SNP) alone and in combination. Dopamine alone (3--4 mcg/Kg/min) caused an increase of cardiac output (CO) from 3.2 to 4.6 L/min/M2 (p less than 0.001), SNP (1--1.5 mcg/Kg/min) raised the CO to 3.7 L/min/M2 (p less than 0.005). While the combination of the 2 drugs elevated the CO to 5 L/min/M2 (p less than 0.001). The mean pulmonary artery wedge pressure dropped moderately with dopamine and significantly with SNP and combined drugs. The diastolic pulmonary artery pressure fell significantly with either drug and in combination. The stroke index increased significantly with dopamine and combined therapy. All patients survived. It is concluded that in post-open heart surgery patients with low output syndrome substantial hemodynamic improvement results with the combined use of dopamine and SNP more than with either agent alone.
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PMID:Simultaneous dopamine and sodium nitroprusside therapy following open heart surgery. 740 14

Dopamine and norepinephrine fluorescence in the nucleus caudatus and putamen and cerebral cortex was markedly depleted along with rCBF reduction in symptomatic stroke-prone spontaneously hypertensive rats (SHRSP) with bilateral carotid artery ligation under light pentobarbital anesthesia. An accumulation of fluorescence at the intima of blood vessels, especially in the nucleus caudatus and putamen, was noted in some SHRSP under the same experimental conditions. These changes were hardly seen in deeply anesthetized SHRSP, as well as in normotensive Wistar-Kyoto (WK) rats. It may be possible, therefore, that released cerebral amines in acute brain ischemia accelerate the vasoconstriction and permeability of cerebral arteries, which further decreases the blood supply to these areas. Also, a barbiturate protective effect against the release of central dopamine and norepinephrine during acute brain ischemia was noted in deeply anesthetized SHRSP.
Stroke
PMID:Role of central aminergic fibers in experimental cerebral ischemia in stroke-prone SHR. Relation to anesthetic effect. 741 67

Dobutamine, a new synthetic catecholamine, has been developed as a more specific inotrope and is reported to have less effect on heart rate and peripheral vascular resistance than other catecholamines. Reports of its effects after cardiotomy have cast doubt on this idea. We have compared the haemodynamic effects of dobutamine with isoprenaline (Group I) and with dopamine (Group II) in early postcardiotomy patients. In both groups a dose response curve was evaluated (dopamine and dobutamine were given at 1.25, 2.5, 5.0 and 10.0 microgram/kg/min; isoprenaline at 0.005, 0.01, 0.02 and 0.04 microgram/kg/min). In Group I both drugs caused significant increases in cardiac index at the highest dose level only. At that level isoprenaline was associated with a significantly higher heart rate than dobutamine and a significantly lower systemic vascular resistance. Similarly, in Group II, both drugs caused significant increases in the cardiac index only at the highest dose level. However, the heart rate at this dose was significantly higher with dobutamine. Dopamine caused no changes in heart rate at any dose level. Neither drug was associated with any alteration of systemic vascular resistance. No changes in stroke volume, left atrial pressure or pulmonary vascular resistance were found in either group. The rise in cardiac output was caused mainly by tachycardia.
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PMID:Dobutamine, isoprenaline and dopamine in patients after open heart surgery. 745 24

Dopamine seems theoretically to be a rationale choice when adrenergic support is needed to counter undesired cardiovascular depressant effects of isoflurane. Although the cardiovascular effects of isoflurane (ISO) and exogenous dopamine (DA) are well documented, there are no reports on their pharmacological interaction. The effects of ISO 1.4% (MAC 1.0) on the cardiovascular response to exogenous DA were studied in dogs during chloralose anesthesia. Instrumentation included catheterizations of the femoral artery (for aortic pressures and heart rate, HR), the pulmonary artery (for thermodilution cardiac output, CO, and pulmonary arterial pressures) and the left ventricle (for tip-manometer measured left ventricular end-diastolic pressure, LVEDP). ISO per se decreased HR (-16%), mean arterial pressure (MAP; -33%), CO (-29%), left ventricular dP/dt (LV dP/dt; -51%), and increased pulmonary artery occlusion (PAOP; +64%) and LVEDP (+28%). Prior to ISO, DA increased MAP, CO stroke volume (SV), LV dP/dt and LV dP/dt/SAP (systolic arterial pressure) at the dose 10 micrograms.kg-1.min-1. At the dose 20 micrograms.kg-1.min-1 DA, besides these effects, increased PAOP and mean pulmonary artery pressure (MPAP). During ISO, DA at the dose 10 micrograms.kg-1.min-1 restored MAP, CO, and SV to pre-ISO control levels, while LV dP/dt was increased to +96% above the pre-ISO control level. At the dose 20 micrograms.kg-1.min-1, DA increased MAP (+33%), LV dP/dt (+172%), PAOP (+132%) and MPAP (+50%) above pre-ISO control levels. The cardiac effects of DA were similar to when it was given alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Are the cardiovascular actions of dopamine altered by isoflurane? 757 20


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