Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparative histochemical and clinical study concerning the state of the intrinsic adrenergic innervation of the human atrial myocardium was carried out, using the glyoxylic acid-induced fluorescence histochemical method. Specimens from the right auricular appendage were obtained during open-heart surgery from patients suffering from 1. ischaemic heart disease (IHD), 2. atrial septal defect of the secundum type (ASD), and 3. left-sided univalvular or multivalvular heart disease (VHD) with or without congestive heart failure (CHF) experienced prior to surgery. In the IHD group the densities of both the perivascular and the "free" myocardial adrenergic nerve net were greater than in the ASD group and especially in the VHD/CHF group. Secondly, the intensity of fluorescence of the adrenergic structures was generally higher in the IHD group than that in the VDH/CHF group. Further, the average size of the varicosities, the number of varicosities per given length of axon, and the proportional share of the large varicosities were greater in the IHD group than in the ASD and VHD/CHF groups. The difference between the IHD and ASD groups was not great but was obvious in any case. In some patients with VHD/CHF fluorescing axons were observed only occasionally, and the tiny varicosities exhibited a hardly discernible fluorescence. Thus the amount of noradrenaline (NA) in the adrenergic fibres in the IHD group seems to be higher than in the ASD and especially VHD/CHF groups. The level of NA in the IHD group is assumed to constitute a contributory factor in both intracellular metabolic changes and the systemic changes typical of myocardial ischaemia and infarction. In one patient with IHD and in six patients with VHD/CHF with significantly higher heart volume (mean+/-SD) compared with the rest of the patients (P less than 0.001), huge local axonal accumulations of NA in the form of "droplet fibres" were found. These enlarged, bulging adrenergic axons are assumed to be a consequence of mechanical trauma with stretching or disruption of the axons due to myodegenerative processes. It is further assumed that these "droplet fibres" are relatively common in those patients with diseased myocardium. They may constitute an extra contributory factor to the tendency to arrhythmiility of non-atuomatic tissue.
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PMID:Studies of auricular catecholamines by fluorescence histochemistry in various heart diseases of man. 14 May 8

The effects of dopamine (DOPA) on haemodynamics, coronary blood flow and myocardial oxygen requirements were compared with those of L-noradrenaline and isoprenaline (isoproterenol) in patients after open-heart surgery, performed because of mitral valvular and congenital heart disease. The patients were in low cardiac output state but not in shock. DOPA increased heart rate less than isoprenaline, averaging 22 and 31 beats/min, and was less arrhythmogenic. DOPA increased mean arterial pressure by an average of 7 mmHg, whereas isoprenaline had little effect; noradrenaline uniformly increased all measurements of arterial pressure. DOPA and isoprenaline increased cardiac index by an average of 1.01 and 0.94 1 min--1 m--2; noradrenaline did not significantly improve peripheral perfusion. DOPA and isoprenaline decreased systemic vascular resistance by an average of 465 and 549 dynes s cm--5; noradrenaline increased resistance in all patients. For similar cardiac outputs average urine flow increased more with DOPA (75 ml/h) than with isoprenaline (28 ml/h). DOPA increased coronary blood flow and myocardial O2 consumption by an average of 28 and 3.60 ml min--1 100 g--1, noradrenaline by 16 and 1.93 and isoprenaline by 62 and 4.25 ml min--1 100 g--1 respectively. Arterial--coronary sinus O2 differences remained unchanged (normal) with DOPA and noradrenaline and decreased with isoprenaline on average by 1.10 ml/100 ml. Myocardial lactate utilization was normal before and during catecholamine administration. It is concluded that, in its haemodynamic effects, DOPA is intermediate between noradrenaline and isoprenaline. The effects of DOPA on coronary blood flow and myocardial O2 consumption are closer to those of noradrenaline than of isoprenaline. DOPA increase coronary blood flow according to myocardial metabolic demand; it is not a potent primary coronary vasodilator. DOPA, although increasing myocardial O2 consumption more than noradrenaline, is by far less O2-demanding than isoprenaline. DOPA appears to be the superior vasoactive agent among the three catecholamines for the treatment of low cardiac output state in patients with preserved coronary reserve.
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PMID:Effects of dopamine on haemodynamics and myocardial energetics in man: comparison with effects of isoprenaline and L-noradrenaline. 74 Oct 96

In 20 normal persons and in 57 patients with heart diseases with functional class I-IV (according to the classification of the New York Heart Association) the 24 hour urinary excretion of the catecholamines adrenaline, noradrenaline and dopamine and of the O2-methylated degradation products metanephrine and normetanephrine was determined. The 3 catecholamines and the 2 O-methylated derivatives were measured simultaneously using chromatographic extraction and purification (Bio-Rex 70) and selective flurometric determination. The following results could be obtained: 1. The urinary excretion of noradrenaline increased with increasing severity of the heart disease. 2. In patients with severe congestive heart failure (functional class IV) in addition the adrenaline excretion in addition the adrenaline excretion increased significantly. 3. There was no relationship between the urinary excretion of dopamine and the severity of the heart disease. 4. The ratio of noradrenaline excretion to dopamine excretion increased with increasing severity of the heart disease, indicating an increased activity of dopamine-mu-hydroxylation in patients with congestive heart failure. 5. The excretion of the O-methylated degradation products metanephrine and normetanephrine in normal persons and in patients with heart diseases paralleled the excretion of the corresponding catecholamines adrenaline and noradrenaline. This indicates, that increased excretion of noradrenaline and adrenaline (Class IV) in patients with heart failure was not due to impaired catecholamine-degradation but indead to increased catecholamine-release indicating increased sympatho-adrenergic activity. These results show in addition that also in patients with heart failure O-methylation represents still the main degradation step for the inactivation of the circulating catecholamines. 6. The relationship of toal excretion of 0-methylated derivates to total excretion of adrenaline and noradrenaline, however, decreased with increasing severity of heart disease, indicating a relative impairment of O-methylation under the condition of severe congestive heart failure.
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PMID:[Urinary excretion of the catecholamines adrenaline, noradrenaline and dopamine as well as the derivatives metanephrine and normetanephrine in heart disease patients]. 101 4

Renal hemodynamics during IABP-assisted pulsatile flow extracorporeal circulation was assessed in terms of measurement values for intraoperative renal blood flow obtained by the local thermodilution method in human clinical patients. In addition, the effect of IABP on renal hemodynamics was investigated in an animal model of renal denervation in a study undertaken to elucidate the action mechanism of IABP. Eighteen patients with acquired heart disease were involved in the study and measured for the renal blood flow (RBF), cardiac output (CO), renal-systemic partition coefficient for blood flow (RBF/CO), renal vascular resistance (RVR) and perfusion pressure. In the pulsatile flow group, the RBF/CO increased as the number of pump runs increased, whole the RVR was conversely reduced with increasing pump runs. The experimental study without extracorporeal circulation was conducted on 19 mongrel dogs. During IABP runs RBF/CO increased, while the RVR decreased. After renal denervation, no noticeable influence of IABP upon renal hemodynamics was observed. Following a loading dose of noradrenaline (Norad), the RVR increased in a Norad concentration-dependent fashion, independently of IABP and renal denervation. These results indicate that IABP reduces the RVR and thereby exerts a favorable action on renal hemodynamics during pump times. The study thus warrants us to surmise that a mechanism involving the renal sympathetic nerves might play an important role in the production of favorable renal hemodynamic effects of IABP-assisted pulsatile flow extracorporeal circulation.
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PMID:[Clinical and experimental study of the production of renal hemodynamic effects of IABP-assisted pulsatile flow extracorporeal circulation]. 156 54

Single beat estimation of the slope of the end-systolic pressure-volume relation assumes symmetric left ventricular pressure increase and decay and requires extrapolation of peak isovolumic developed pressure (Pmax) from the left ventricular pressure curve of an ejection contraction. To test the sensitivity of this slope to positive inotropic stimuli, biplane cineangiocardiography and simultaneous high-fidelity left ventricular pressure measurements were performed in 50 patients with heart disease. The end-systolic pressure-volume relations were assessed under baseline conditions and during norepinephrine infusion (n = 19) or after postextrasystolic potentiation (n = 24), or both (n = 7). Norepinephrine did not change left ventricular end-systolic volume despite significant elevations of end-systolic pressure. Postextrasystolic potentiation significantly decreased end-systolic volume in association with an unaltered left ventricular end-systolic pressure. The potentiation significantly decreased the pressure half-time of contraction, an index of the speed of the left ventricular pressure increase, while it increased the pressure half-time of relaxation, an index of the speed of the pressure decline, indicating asymmetric pressure increase and decay. The slope of the end-systolic pressure-volume relation increased from 3.3 to 4.4 mm Hg/ml/m2 (p less than 0.001) during norepinephrine infusion. In contrast, despite an augmented contractility, the slope decreased significantly from 3.2 to 2.4 mm Hg/ml/m2 (p less than 0.0001) after the potentiation. The slope showed a high correlation with Pmax (r = 0.86, p less than 0.0001, n = 107). Thus, the slope of the end-systolic pressure-volume relation derived from single beat analysis is not always sensitive to inotropic interventions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Slope of the end-systolic pressure-volume relation derived from single beat analysis is not always sensitive to positive inotropic stimuli in humans. 158 71

Twenty-six infants and children with congenital heart disease (CHD) undergoing cardiac surgery were investigated for alterations in myocardial beta-adrenoceptor density. The patients were divided into three groups according to type and severity of CHD: group I consisted of 6 patients with acyanotic shunt lesions of moderate severity; group II comprised 13 children with severe acyanotic shunt and valve lesions and group III included 7 children with cyanotic CHD. The myocardial beta-adrenoceptor density was determined using (-)3-[125I]Iodocyanopindolol [( 125I]ICYP) and was reduced by approximately 50% in severe acyanotic CHD (33.6 fmol/mg protein) and cyanotic CHD (35.3 fmol/mg protein) in comparison with the group with less severe acyanotic shunt defects (64.4 fmol/mg protein). The affinity dissociation constant (Kd.ICYP) did not differ statistically between the groups. The proportion of beta 1- and beta 2-subpopulations was evaluated by ICI 118,551-[125I]ICYP competition studies. In group II (61.5%) and group III (69.1%) significant lower portions of beta 1-adrenoceptors were found compared with group I (78.2%). This shift of subpopulations was due to a decreased beta 1-receptor density while beta 2-receptor density was unchanged in all groups. While the plasma noradrenaline levels of group I were similar to those of a control group of 13 healthy children, respective values of group II and III were significantly elevated. A significant negative correlation was found between plasma noradrenaline levels and myocardial beta-adrenoceptor density. It is concluded that exposure of these receptors to increased circulating catecholamines, due to an enhanced sympathetic tone, leads to a reduction of their density.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial beta-adrenoceptor density and the distribution of beta 1- and beta 2-adrenoceptor subpopulations in children with congenital heart disease. 164 67

Sympathetic regulation of myocardial performance has been shown to be altered in congestive heart failure. Right atrial tissue of children with severe acyanotic and cyanotic congenital heart disease (CHD) showed a significantly lower beta-receptor density than that of children with less severe defects. Since mononuclear leukocytes (MNL) contain a homogeneous population of beta 2-adrenoceptors which have similar properties to those of cardiac beta 2-adrenoceptors, they are frequently used for studying the beta-adrenergic system. In a group of 37 children with CHD of different types and severity who underwent cardiac surgery, we compared the MNL beta-adrenoceptor density to the type and severity of CHD and looked for a possible relationship to plasma catecholamine levels and to the right atrial beta-adrenoceptor density. Membranes of MNL and myocardial cells were radiolabeled with (-)3-[125I]Iodocyanopindolol [( 125I]ICYP). A significantly higher beta-adrenoceptor density on MNL was found in patients with moderate acyanotic CHD (group I) than in those with severe acyanotic (group II) and cyanotic CHD (group III). Patients of group I showed approximately 50% higher myocardial beta-receptor density than those of groups II and III. ICI 118.551-[125I]ICYP competition studies revealed that in groups II and III significantly lower proportions and densities of beta 1-receptors were found compared to group I. Noradrenaline (NA) plasma levels in group II and group III were significantly higher than those in group I. The adrenaline plasma levels were found to be very high in all children with CHD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-adrenoceptor density on mononuclear leukocytes and right atrial myocardium in infants and children with congenital heart disease. 166 27

To estimate the pumping function of the left-sided heart in patients with "latent" left-sided heart failure due to heart disease which primarily affected the left-side of the heart (former NYHA class I and II), we measured (i) the increase of peripheral venous pressure in response to supine mild leg exercise (delta VP), and (ii) the increase of plasma noradrenaline (NA) concentration due to phentolamine (PH) injection (delta NAPH). We divided the patients into well-functioning left-sided heart group (delta CI/delta PAW greater than 0.180 L.min-1.M-2.mmHg-1) and poorly-functioning left-sided heart group (delta CI/delta PAW less than or equal to 0.180 L.min-1.M-2.mmHg-1) on the basis of a ratio (delta CI/delta PAW), relating the increase in cardiac index (delta CI) in response to exercise to the concomitant increase in mean pulmonary artery wedge pressure (delta PAW). This diving line (delta CI/delta PAW = 0.180 L.min-1.M-2.mmHg-1) correlated with delta VP (diving line: delta VP = 35 mmH2O) and with delta NAPH (diving line: delta NAPH = 0.353 ng/ml). Our results suggest that delta VP and delta NAPH reflected the pumping function of the left-sided heart with considerable accuracy.
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PMID:[Plasma noradrenaline response to phentolamine in "latent" left-sided heart failure]. 232 18

Catecholamine-induced cardiopathy accompanied with pheochromocytoma in a 28-year-old female including two other cases are reported and the relationship between pheochromocytoma and cardiac change was also discussed. In the first case, catecholamine in the tumor tissue showed extremely high values; 94.22 micrograms/g of adrenaline and 6,332.42 micrograms/g of noradrenaline. Histologically, myocardial degeneration and inflammatory cell infiltration between myocardial fibers were noted. In the second case, hypertrophied heart showed focal degeneration of myocardial fibers with a few inflammatory cells in the stroma. The third case showed increase of heart weight, but neither myocardial degeneration nor inflammatory infiltration was noted except for moderate myocardial hypertrophy. Although the cause of difference in degree of myocardial changes is not yet clear, it may be attributed to the blood catecholamine level and/or duration of disease and/or area examined. A relative hypoxia theory is accepted for the mechanism of catecholamine-induced cardiopathy. This theory is supported by more severe lesions being noted near to the cardiac apex corresponding to peripheral coronary circulation.
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PMID:Catecholamine-induced cardiopathy accompanied with pheochromocytoma. 295 67

To determine whether altered vascular reactivity could contribute to hypertension after repair of coarctation, the change in forearm and calf vascular resistances to small intra-arterial infusions of norepinephrine were measured in six patients who had undergone surgical correction of coarctation of the aorta but still had upper extremity hypertension and compared with similar measurements made in five normotensive patients with mild heart disease. Only the mean upper extremity pressure was significantly greater in the group that underwent repair of coarctation (102 +/- 11 vs 83 +/- 5 mm Hg, p less than .05, for mean arm pressures and 96 +/- 13 vs 83 +/- 7 mm Hg for mean leg pressures in patients who had coarctation vs normotensive patients, respectively). Forearm and calf blood flows were measured in the right arm and leg with a mercury-in-plastic strain-gauge plethysmograph. Forearm and calf vascular resistances were calculated by dividing mean arterial pressure of the appropriate extremity by the blood flow of that extremity. Norepinephrine was infused into the right brachial and femoral arteries of the patients at doses of 0.02, 0.05, 0.1, 0.2, 0.3, 0.5, and 0.7 microgram/min. Resting forearm and calf vascular resistances were similar in both groups of patients. The norepinephrine dose-response curves showed that control patients required more than three times the norepinephrine to produce the same percent increase in forearm vascular resistance (after 0.2 microgram/min forearm vascular resistance increased by 55% in the coarctation group, while the resistance in the control group increased by only 3%, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased forearm vascular reactivity in patients with hypertension after repair of coarctation. 397 23


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