Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.11.18 (MAP)
7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac and circulatory function (cardiac output, stroke volume, heart rate, mean arterial pressure = MAP, total peripheral resistance = TPR), further renal function (PAH- and inulin clearance, filtration fraction, urinary excretion, renal sodium- and potassium excretion) were measured on 15 patients undergoing cardiac surgery to whom Dopamine and Orciprenaline were administered in increasing doses of 100 mug - up to 500 mug/min (Dopamine) and 10 mug - to 20 mug/min (Orciprenaline). An infusion of Dopamine up to 250 mug/min caused a dosis-related increase of the cardiac output up to 31% (2P less than 0.001) without essential increasing of the MAP and of the heart rate. Dopamine caused a decrease of the TPR up to 24%. Doses of Dopamine over 250 mug/min cause an increase of the MAP and of the heart rate without a real increase of the cardiac output. Renal function improved under increasing doses of Dopamine, effective renal plasma flow (ERPF) up to 74%, urinary excretion up to 130%, sodium and potassium excretion up to 60% respectively. After administering Orciprenaline in a dosis of 20 mug/min cardiac output increases up to 28%, MAP and heart rate up to 12% and 17% respectively. After the administration of Orciprenaline (20 mug/min) and Dopamine (500 mug/min) frequent extra systoles were observed without any increase of the cardiac output; MAP increased by 12%, TPR decreased by 16% after 20 mug/min of Orciprenaline. ERPF decreased slightly after Orciprenaline. Urinary excretion was reduced by a half.
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PMID:[Comparing studies on the influence of dopamine and orciprenaline on cardiac and renal function of patients after cardiac surgery (author's transl)]. 108 62

The purpose of this study was to assess the physiologic training effects of functional electrical stimulation leg cycle ergometer (FES-LCE) exercise in persons with spinal cord injury (SCI) who were previously untrained in this activity. Ten persons with quadriplegia (C5 to C7) and eight with paraplegia (T4 to T11) performed FES-LCE training on an ERGYS I ergometer 10 to 30 minutes per day, 2 or 3 days per week for 12 to 16 weeks (36 total sessions). Training session power output (PO) ranged from 0.0W (no external resistance) to 30.6W. Each subject completed discontinuous graded FES-LCE and arm crank ergometer (ACE) tests before and after training for determinations of peak lower and upper extremity metabolic, pulmonary, and hemodynamic responses. Compared with pretraining, this SCI group exhibited significantly (p less than or equal to .05) higher posttraining peak PO (+45%), oxygen uptake ([O2], + 23%), pulmonary ventilation (+27%), heart rate (+11%), cardiac output ([Qt], + 13%) and significantly lower total peripheral resistance ([TPR], - 14%) during FES-LCE posttests. There were no significant changes in peak stroke volume (+6%), mean arterial pressure ([MAP], - 5%), or arteriovenous oxygen difference ([a-vO2diff], + 10%) during posttraining FES-LCE tests. In addition, no significant differences were noted for the peak level of any monitored variable during ACE posttests after FES-LCE training. The rise in total vascular conductance, implied by the significant decrease in posttraining TPR during FES-LCE tests, denotes that a peripheral circulatory adaptation developed in the persons with SCI during FES-LCE exercise training.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Physiologic effects of electrical stimulation leg cycle exercise training in spinal cord injured persons. 158 Jul 76

The influence of different rates of dopamine and dobutamine on the cardiovascular depression during a standard halothane anesthesia was studied in dorsally recumbent ventilated ponies. Haemodynamic and respiratory responses were investigated by means of cardiac output (CO) determination (thermodilution technique), mean systemic (MAP) and pulmonary artery pressure (MPAP) (direct intravascular method) and arterial blood analysis (blood gases and packed cell volume). An important cardiopulmonary depression characterized by decreases (55% of the standing values) in CO, cardiac index (CI), MAP, MPAP and other cardiovascular related parameters occurred in the dorsally recumbent anaesthetized ponies after a stabilization period of 30 minutes. Dopamine at 2 different infusion rates (2.5 and 5.0 micrograms/kg/min) induced few changes of the cardiopulmonary parameters (non-significant increases in MAP, CI, left ventricular work [LVW], stroke volume [SV]; non-significant decrease in total peripheral resistance [TPR]). Several minor time related influences were also observed (increases in MPAP and total pulmonary resistance [TpR]). Arterial blood gases did not change during the different dopamine infusions. Low doses of dobutamine (1.25 micrograms/kg/min) were efficient to counteract the cardiovascular depression. Significant increases in CO, CI, MAP, MPAP and SV were observed. TPR and TpR tended to decrease but non-significantly. Heart rate and blood gases remained constant. The higher doses of dobutamine (2.5 and 5.0 micrograms/kg/min) accentuated these changes but a significant increase in heart rate with even periods of severe tachycardia and an increase of the packed cell volume were also observed. Apparently, low doses of dobutamine were indicated for the management of the cardiovascular depression during anaesthesia in the dorsally recumbent ventilated horse.
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PMID:Influence of dopamine and dobutamine on the cardiovascular depression during a standard halothane anaesthesia in dorsally recumbent, ventilated ponies. 195 Feb 40

In closed-chest rats, isoproterenol (ISO, 25 mg/kg), 5 hours after subcutaneous administration, increased heart rate by 53%, left ventricular (LV) dP/dtmax by 80%, and cardiac output by 37%. LV systolic pressure (LVSP, -10%), mean arterial pressure (MAP, -12%), and total peripheral resistance (TPR, -36%) were diminished. In separate experiments, continuous intravenous infusion of adenine (50 mg/kg/hr) for 5 hours reduced heart rate (-11%), LVSP (-16%), MAP (-20%), TPR (-33%), and LV dP/dtmax (-20%). Cardiac output was increased (+20%). Inosine has been shown to have similar effects, except for a decline in cardiac output. Adenine (50 mg/kg/hr) attenuated the ISO-induced increase in heart rate and LV dP/dtmax and aggravated the decline in LVSP, MAP, and TPR. The increase in cardiac output was not changed. Inosine (200 mg/kg/hr) modified the ISO effects to a similar extent. Ribose (200 mg/kg/hr) added to the adenine infusion did not have functional effects. However, it aggravated the modifying influence of inosine on LVSP, LV dP/dtmax, and MAP. ISO reduced the cardiac ATP content (mumol/g) from a control value of 5.02 +/- 0.06 (n = 12) to 3.51 +/- 0.13 (n = 10). Adenine (3.56 +/- 0.21, n = 7) and ribose (3.64 +/- 0.11, n = 9) alone did not affect it, but inosine attenuated it (4.33 +/- 0.08, n = 8). Adenine and inosine in combination with ribose abolished the ISO-induced ATP decline (5.18 +/- 0.23, n = 7, and 4.76 +/- 0.10, n = 8, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nucleotide precursors modify the effects of isoproterenol. Studies on heart function and cardiac adenine nucleotide content in intact rats. 195 77

The cardiac and hemodynamic effects of 3 doses (0.1, 0.3 and 1 mg/kg, iv) of spiraprilat, the diacid active metabolite of the new angiotensin I converting enzyme inhibitor spirapril, have been investigated and compared to those of saline in chronically implanted conscious dogs at rest. Under a normal sodium diet, spiraprilat, 1 mg/kg, induced significant (at least P less than 0.05) decreases in mean arterial pressure (MAP, -11%), total peripheral resistance (TPR, -21%), left ventricular end diastolic pressure (LVEDP, -15%) and increases in heart rate (HR, +12%) and cardiac output (CO, +16%) whereas dP/dtmax remained unchanged. Spiraprilat-induced tachycardia was not modified by propranolol pre-treatment but was abolished by previous administration of the propranolol-N-methylatropine combination. Spiraprilat, 0.1 mg/kg, did not affect any parameter, but spiraprilat, 0.3 mg/kg, showed intermediate effects. Finally, sodium depletion strongly potentiated spiraprilat effects on MAP, TPR, LVEDP, HR and CO. We conclude that: a), in conscious dogs under normal sodium diet, spiraprilat reduces TPR and MAP through peripheral vasodilating properties; b), spiraprilat-induced tachycardia is mainly related to parasympathetic tone withdrawal, possibly in relation with high and low pressure baroreceptors deactivation; and c), sodium depletion considerably potentiates spiraprilat cardiac and hemodynamic effects.
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PMID:Hemodynamic and cardiac effects of spiraprilat in normal and sodium depleted conscious dogs. 228 46

We studied the hemodynamic changes produced in conscious, chronically instrumented rabbits during steady-state administration of atrial natriuretic peptide (ANP). We administered synthetic alpha-human ANP intravenously (i.v.) at progressively increasing doses of 1, 2, and 4 micrograms/min, each for 30 min. In different experiments in each rabbit, we determined the effects of the peptide under closed-loop conditions in the intact animal and the "direct" circulatory effects of the peptide after "total" blockade of the autonomic nervous system (TAB) and after combined neurohumoral blockade (NHB), where in addition the vascular effects of vasopressin and angiotensin II were also prevented. In intact rabbits, ANP produced a dose-related reduction in mean arterial pressure (MAP, -3 to -14%), which was entirely due to a fall in cardiac output (CO, -14 to -20%), and there was a small rise in total peripheral resistance (TPR 5-12%). Heart rate remained unchanged. In rabbits subjected to TAB and NHB, all hemodynamic effects of ANP were attenuated. There were dose-related falls in left and right atrial pressures which reached maxima of -3.3 +/- 0.9 and -1.8 +/- 0.2 mm Hg, respectively. There was a reversible rise in hematocrit, probably owing to a shift of approximately 8% in blood volume. These effects occurred mainly through direct actions of the peptide, and there was no evidence of systemic vasodilatation. The magnitude of reflex autonomic effects appeared to be less than expected for the observed fall in MAP, suggesting that ANP also inhibited cardiovascular reflexes.
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PMID:Direct and neurohumoral cardiovascular effects of atrial natriuretic peptide. 246 43

In conscious dogs, we examined the hypothesis that the effects of atrial natriuretic peptide (ANP) are mediated by cyclic GMP and tested whether stimulation of the intracellular pathway beyond the ANP receptor level still exerts ANP-like effects during tolerance to ANP in heart failure. We studied the hemodynamic, renal, and hormonal effects of the cyclic GMP analogue 8-bromo-cyclic GMP (8-Br-cyclic GMP) in conscious dogs before and after induction of congestive heart failure by right ventricular pacing. In healthy dogs, 8-Br-cyclic GMP (1-100 micrograms/kg/min) dose-dependently decreased mean arterial pressure (MAP -19% by 100 micrograms/kg/min) and total peripheral resistance (TPR -22%) with no change in cardiac output (CO) and right atrial pressure, increased urine flow (UF 52%), and sodium excretion (UNaV 135%). Plasma renin (62%) and norepinephrine (NE 24%) were increased. In dogs with heart failure, 8-Br-cyclic GMP induced a similar arteriolar dilation (MAP -16%, TPR -23%) with no change in CO and preload. However, the effects on renal excretory function were abolished or markedly attenuated (UF -4%, UNaV 7%). Plasma renin (163%) and aldosterone (40%) were increased. Our findings support the hypothesis that the renal effects of ANP are mediated by cyclic GMP in vivo. The attenuation of renal effects of 8-Br-cyclic GMP in heart failure does not prove but is in agreement with the hypothesis that an intracellular defect beyond cyclic GMP production might be involved in the tolerance to ANP in heart failure.
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PMID:Hemodynamic, renal, and hormonal effects of 8-Br-cyclic GMP in conscious dogs with and without congestive heart failure. 247 97

In a porcine endotoxin shock model employing a continuous intravenous administration of Salmonella abortus equi endotoxin the cardiorespiratory and metabolic parameters were studied with main emphasis on the effect of hemofiltration (HF) as the only therapeutical measurement on the enhancement of survival time. Arachidonic acid (AA) metabolites Thromboxan B2 and 6-Keto-PGF 1-alpha could be lowered significantly by hemofiltration. Measuring the inadequacy of the supply and delivery systems in terms of O2-uptake, CO2 production, lung mechanics, TPR, CO, heart rate and MAP the control group seemed to be more severely compromised than the hemofiltrated groups, although the final outcome as for survival time could not be increased significantly. HF can nonselectively counteract some toxic effects of shock mediators without depriving the organism of beneficial components of a protective system being stimulated at the same time. Once the AA cascade is initiated, pharmacologic inhibition is of limited value as long as a direct specific therapeutic manipulation is still not available. Elimination of mediators by HF helps to combat the overstimulation of host defense mechanisms in ET shock which represents the ultimate threat to the host.
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PMID:Can hemofiltration increase survival time in acute endotoxemia--a porcine shock model. 250 78

We studied reflex responses to pressure changes at arterial and cardiopulmonary baroreceptors in five awake dogs with atrioventricular block before and after baroreceptor denervation. We changed ventricular pacing rate and blood volume to vary cardiac output and arterial (MAP) and central venous pressure (CVP). We determined peripheral resistance (TPR) and atrial rate (HRA) as responses. In the intact animal, regression analysis showed an average relationship across dogs of TPR = 169-0.69 MAP-1.952 CVP + error. Correlation (r) between observed and predicted TPR was 0.83. For HRA, regression indicated HRA = 291.66-2.319 MAP + 8.144 CVP + error (r = 0.899). TPR and MAP are percent of control at 90 beats/min; CVP is in mmHg; HRA, in beats/min. Although its coefficient is smaller, MAP explains approximately 69% of the variation in TPR. After arterial baroreceptor denervation, effects of MAP on TPR were insignificant and the coefficient for CVP increased. Subsequent vagal block eliminated all reflex responses. Effects from the two receptor sites sum linearly. They act cooperatively with changes in blood volume, but oppose one another with cardiac output changes.
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PMID:Cardiovascular control by arterial and cardiopulmonary baroreceptors in awake dogs with atrioventricular block. 260 88

In a controlled study on 24 dogs with severe damage to the lungs HFJV was compared to CPPV on the basis of selected cardiorespiratory parameters. The pulmonary damage was produced by injection of oleic acid (OA) into the right atrium under conventional mechanical ventilation (IPPV). After the damage, the dogs were randomly allotted into one of two groups. Twelve dogs (group I) were ventilated for 5 hours with a PEEP of 10 cm H2O (1 kPA), 12 animals (group II) for 5 hours with HFJV. The oleic-acid-induced damage results in the known hypoxaemia with an increase in the intrapulmonary shunt. After changing to CPPV, the PaO2, which fell from 27.2 +/- 3 kPa to 10.8 +/- 2.9 kPa, rises to 20.3 +/- 7.7 kPa, but shows no further significant alteration until the end of the experiment. In contrast to the clearly improved oxygenation, essential cardiocirculatory parameters (CI, SVI, RVSWI, LVSWI, TCO2) are partially reduced by more than 50% of the initial values. PAP, PCWP, HR, TPR and PVR increase significantly, MAP remaining nearly unchanged. After changeover to HFJV, there is first a further fall of PaO2 from 11.1. +/- 3.0 kPa to 9.1 +/- 1.4 kPa following OA, then, however, until the end of the experiment, a continuous elevation to 15.6 +/- 2.4 kPa with a mean airway pressure that is by 75% lower. The haemodynamic parameters show no significant changes as compared to the initial values, overall, however, they lie significantly below or above those of group I. The results from our investigations allow to draw the conclusion that, despite haemodynamic advantages, HFJV in consequence of deterioration of the arterial oxygenation currently is no alternative superior to CPPV in ventilating the severely damaged lung.
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PMID:[A comparison between high-frequency jet ventilation (HFJV) and conventional positive end-expiratory pressure ventilation (CPPV)--an experimental study on dogs with acute lung damage]. 264 93


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