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)

Peak III phosphodiesterase (PDE) inhibitors have combined positive inotropic and vasodilator effects. We studied 10 patients with chronic heart failure during and after infusion of intravenous (i.v.) ICI 153,110, an investigational peak III PDE inhibitor. Maximum hemodynamic response for the group occurred after cessation of infusion at a lower plasma drug concentration. At maximum hemodynamic response, cardiac index (CI) increased (2.4 +/- 0.5 vs. 3.2 +/- 0.37 L/min/m2, p less than 0.05) with a decrease in mean arterial pressure (MAP 91 +/- 5 vs. 80 +/- 3 mm Hg, p less than 0.05), pulmonary capillary wedge pressure (PCWP 25 +/- 2 vs. 17 +/- 3.1 mm Hg, p less than 0.01), systemic vascular resistance (SVR 1,422 +/- 106 vs. 983 +/- 97 dynes.s.cm-5, p less than 0.05) and pulmonary vascular resistance (PVR 227 +/- 39 vs. 16 +/- 31 dynes.s.cm-5, p less than 0.05). During the infusion, plasma renin activity (PRA) decreased from 6.34 +/- 2.53 to 3.6 +/- 3 ng/ml/h (NS). The five patients with high baseline PRA had a significant decrease (11.2 +/- 2.5 vs. 5.4 +/- 1.67 ng/ml/h, p less than 0.01) that preceded changes in CI and SVR by 1-2 h. These data suggest that reduction in PRA may have contributed to the hemodynamic effects of this peak III PDE inhibitor.
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PMID:Acute neurohormonal and hemodynamic response to a new peak III phosphodiesterase inhibitor (ICI 153,110) in patients with chronic heart failure. 170 Feb 5

Total spinal block was induced by 2% lidocaine in adult mongrel dogs, and its influence on the respiratory, circulatory, endocrine and metabolic systems was studied. HR, MAP, CI and LV dp/dt max during total spinal block decreased significantly compared with those during the control period. The blood gas, Qs/Qt and ETVI were hardly influenced by total spinal block. Regarding the endocrine and metabolic systems, plasma renin activity (PRA) was significantly elevated by total spinal block, while plasma epinephrine and norepinephrine levels showed no changes. Blood levels of lactic acid, pyruvic acid and blood sugar were not influenced by total spinal block.
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PMID:[Changes in respiratory, circulatory, endocrine, and metabolic systems under induced total spinal block]. 177 May 74

The hemodynamics of 18 patients (subgroup A) with severe heart failure (baseline Cl less than or equal to 1.55 l.min-1.m-2), including three patients with cardiogenic shock, and another 22 patients (subgroup B) with moderate heart failure (baseline Cl from 1.55 to 2.5 l.min-1.m-2) were investigated during a 24 h milrinone infusion, combined with investigation of the response of the sympathetic tone (plasma catecholamine levels) and the renin-angiotensin-aldosterone system to the hemodynamic improvement in both subgroups. Cl increased (p less than or equal to 0.001) to 162.7% after 5 min and further to 206.4% of baseline after 30 min of milrinone therapy in subgroup A, and in B to 139.3% and further to 146.4% after 15 min. PCWP decreased (p less than or equal to 0.001) to 83.8% and further to 65.5% of baseline after 30 min in subgroup A, and to 58.4% in subgroup B. Heart rate decreased (p less than or equal to 0.05) from 99.4 to 94.7 bpm in A and showed a decreasing tendency in B. MAP rose in A from 75.5 to 79.4 after 1 h and further to 83.3 mm Hg (p less than or equal to 0.01) after 24 h; in subgroup B, MAP did not change. Plasma noradrenaline level decreased (p less than or equal to 0.001) in A from 1419.5 (B: 782.9) to 838.2 (B: 529.6) after 1 h and further to 655.1 (B: 467.9) pg/ml after 24 h. Plasma renin decreased (p less than or equal to 0.01) in A from 1047.6 (B: 460.2) to 597.4 (B: 222.5) and further to 392.6 (B: 191.7) microU/ml.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of hemodynamic changes in 24-hour milrinone infusion on sympathetic activity and the renin-angiotensin-aldosterone system in patients with severe heart failure]. 186 68

It was demonstrated recently that a local renin-angiotensin system (RAS) exists in the heart and coronary vessels, and the angiotensin converting enzyme inhibitors can protect the heart from ischemia. Eight patients with NYHA class II-IV subjected to valve replacement were studied in protecting the heart from global ischemia with captopril during open heart surgery. After the ascending aorta was clamped, 500-1000 ml 4 degrees C modified St. Thomas No 1 cardioplegic solution containing 0.058-0.23 mmol/L captopril was perfused into coronary arteries under pressure until the electrocardiogram showed disappearance of myocardial electroactivity. The cardioplegic perfusion was repeated every 30 minutes thereafter during cardiopulmonary bypass (CPB). All the hearts rebeat after reperfusion either spontaneously or from defibrillation without any trouble. Three patients developed an A-V dissociation which returned to sinus rhythm or atrial fibrillation after a tiny dose of dopamine or isoprenaline intravenously. All the patients weaned from the CPB easily with a stable heart rate and a reasonable MAP. None of them needed inotropic support, even those with severe heart failure before operation did not either, and all recovered uneventfully.
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PMID:Captopril as a component of cardioplegia in protecting the myocardium from global ischemia during open heart surgery. A preliminary clinical report. 187 3

We have shown previously that both sinoaortic denervation (SAD) and high renin hypertension in the rat produce a pronounced alteration in the pattern of pressure change during sleep, namely from unchanged to a rise in pressure during synchronized sleep (SS) and from a slight rise to a marked fall during desynchronized sleep (DS). Since acute SAD also produces overactivity of the renin-angiotensin system (RAS), we investigated if this overactivity is essential for the development of the alterations. In rats studied 1 day after SAD (138 +/- 1.0 mm Hg) the MAP rose during SS (+14 +/- 0.7 vs. +1.0 +/- 0.16 mm Hg in the controls) and fell during DS (-27.2 +/- 1.5 vs. 4.9 +/- 0.6 mm Hg in the controls). Captopril-treated rats, studied 1 day after SAD (89 +/- 1.2 mm Hg), also exhibited rise in pressure during SS (+12.3 +/- 0.6 mm Hg) and fall during DS (-12.8 +/- 1.7 mm Hg). Similar alterations were observed in rats studied 10 days after SAD (116 +/- 0.7 mm Hg) when RAS activity was normal (PRA: 1.3 +/- 0.2 vs. 10.4 +/- 2.7 ng AI/ml/h for SAD-1 day); the MAP rose during SS (+6.5 +/- 0.3 mm Hg) and fell during DS (-5.0 +/- 0.9 mm Hg). These data indicate that impairment of the baroreceptor function per se determines the typical alteration in the pattern of pressure change during sleep in the rat.
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PMID:Alteration in baroreceptor function in rats produces typical pressure changes during sleep. 245 78

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

Plasma angiotensin converting enzyme (ACE) activity was studied during the development and the reversal of one-kidney, one clip (1K1C) renal hypertension in rats (RHR). Plasma ACE activity was measured in RHR 1 (n = 11), 3 (n = 8), 6 (n = 12), 14 (n = 7), and 80-120 days (n = 17) after clipping. Plasma ACE activity (nmol/min/ml) was elevated (p less than 0.05) in chronic RHR (80-120 days; mean arterial pressure, MAP: 216 +/- 9 mmHg), being 142 +/- 14 (n = 17) vs. 100 +/- 3.2 (n = 20) for normotensive control rats (MAP: 116 +/- 3 mmHg), whereas no significant differences were observed at earlier times. Overactivity of the renin-angiotensin system (RAS) was demonstrated indirectly by the reduction of MAP (greater than 15 mmHg) in response to captopril (10 mg/kg, i.v.) only during the first 3 days after clipping and in chronic severely hypertensive rats. In another experiment, ACE activity in chronic RHR was measured serially before and 1, 6 and 24 hours after unclipping. Serial measurements of plasma ACE showed a progressive decrease from 145 +/- 26 to 122 +/- 21, 24 hours after unclipping (n = 7, p less than 0.05, paired Student t-test) when MAP was reduced from 204 +/- 15 to 113 +/- 7 mmHg. There was essentially no change during 24 hours from the initial values of RHR-sham (MAP: 206 +/- 5 mmHg, ACE: 140 +/- 19, n = 8) and normal rats-sham (MAP: 115 +/- 2 mmHg, ACE: 96 +/- 3, n = 6). These data provide further evidence that chronic renal hypertension is associated with important changes in the metabolism of vasoactive peptides.
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PMID:Changes in plasma ACE activity during the development and reversal of one-kidney, one clip hypertension in rats. 253 27

Esmolol infusion at rates of 200, 300, and 400 micrograms.kg-1.min-1 was used to potentiate hypotension (mean arterial pressure = 60 mm Hg) induced with sodium nitroprusside (SNP) in 10 male patients undergoing radical cancer surgery during nitrous oxide-oxygen and fentanyl anesthesia. Heart rate (HR), blood pressure (radial arterial catheter), and plasma levels of renin activity (PRA), norepinephrine (N), epinephrine (E), and dopamine (D) were measured: 1) while patients were awake; 2) after induction of anesthesia (nitrous oxide, 60% in oxygen, fentanyl = 5 micrograms/kg followed by an infusion at 10 micrograms.kg-1.hr-1); 3) after surgery had begun; 4) after 20 minutes of SNP-induced hypotension; 5) after 20 minutes of esmolol at each of the above infusion rates; and 6) after the completion of surgery. Compared to awake values, SNP-induced hypotension (mean infusion rate = 3.1 micrograms.kg-1.min-1 +/- 0.6 SE) during surgery resulted in significant (P less than 0.05) increases in heart rate, PRA, N, and D. Infusion of esmolol resulted in significant (P less than 0.05) dose-dependent reductions in SNP requirement to maintain MAP = 60 mm Hg. At 200 micrograms.kg-1.min-1, SNP requirement was 2.1 micrograms.kg-1.min-1 +/- 0.4, at 300 micrograms.kg-1.min-1, it was 1.0 micrograms.kg-1.min-1 +/- 0.2, and at 400 micrograms.kg-1.min-1, was 0.5 micrograms.kg-1.min-1 +/- 0.3. Concomitant with the decrease in SNP requirement, there were significant reductions in HR and PRA at all infusion rates of esmolol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Esmolol for potentiation of nitroprusside-induced hypotension: impact on the cardiovascular, adrenergic, and renin-angiotensin systems in man. 256 49

The present study evaluated a protocol for drawing large volumes of blood over an acute time frame in conscious cannulated rats with blood from cannulated donor rats simultaneously infused to maintain isovolemia. During time control (n = 6), three successive 1.5-ml blood samples were drawn at 10-min intervals with equal volumes of donor blood infused simultaneously. One milliliter of blood was drawn quickly and saved for analysis followed by an additional 3 ml of blood withdrawal to total a 15-ml/kg hemorrhage. Two subsequent 1.5-ml samples were replaced with autologous (hemorrhage) blood. During hypoxia inspired O2 was decreased to 10% after the first sample-transfusion. The sampling-transfusion protocol (time control) had no effect on blood pressure (MAP), hematocrit (Hct), blood gases, renin, or adrenocorticotropic hormone (ACTH). Hemorrhage resulted in a significant decrease in MAP, Hct, base excess, and arterial PCO2 and an increase in arterial PO2, renin activity, and ACTH. Ten percent O2 resulted in significant hypoxemia, respiratory alkalosis, and a small degree of hypotension at the 20-min sample with no change in renin and a moderate increase in ACTH. The consistency of the results with previous studies confirms the utility and efficiency of large sample-transfusion protocols for the study of blood gas and endocrine dynamics in conscious rats.
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PMID:Evaluation of a blood sample-transfusion protocol in rats: blood gases, renin, and ACTH. 284 65

Patients with untreated essential hypertension had significantly higher plasma atrial natriuretic factor (ANF) levels (92.9 +/- 12.9 pg/ml, mean +/- SE) than those of age-matched controls (37.8 +/- 6.0 pg/ml; p less than 0.01). Plasma ANF levels in essential hypertensive patients showed a significant positive correlation with mean arterial pressure (MAP; r = 0.46, p less than 0.05) and an inverse correlation with plasma renin activity (PRA; r = -0.43, p less than 0.05). Plasma ANF levels after medication showed significant correlation with the decrease in MAP (r = 0.565, p less than 0.05). Patients with primary aldosteronism had significantly higher plasma ANF levels (122.4 +/- 30.2 pg/ml, n = 8) than those of controls (p less than 0.05). The levels returned to normal after extirpation of adrenal tumors. The response of plasma ANF levels in patients with primary aldosteronism to volume expansion with infusion of 2 L of physiological saline in 2 hours was greater than in controls. Such exaggerated response disappeared after surgical treatment. Infusion of angiotensin II (Ang II; 20 ng/kg/min) or norepinephrine (200 ng/kg/min) for 30 minutes to normal volunteers (n = 5) resulted in a rise in MAP (24.9 +/- 3.3 and 15.8 +/- 4.4 mm Hg, respectively) and a twofold increase in plasma ANF level. Infusion of the Ang II antagonist [Sar1, Ile8]Ang II (600 ng/kg/min) for 30 minutes, resulted in a rise in MAP (18.8 +/- 2.1 mm Hg) and more than a twofold increase in plasma ANF level in patients with essential hypertension (n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor in essential hypertension and adrenal disorders. 296 1


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