The hemodynamic and metabolic effects of acetate were studied in rats in vivo and in the isolated perfused heart. Hemodynamic parameters, myocardial phosphagens, inorganic phosphate, and adenosine were measured in vivo. Acetate uptake, coronary flow, O2 consumption, parameters of the cellular energy state, and hypoxanthine compounds and their washout were measured in heart perfusion experiments. Heart rate (HR), cardiac output, and the peak derivative of the left ventricular pressure rise (dP/dtmax) increased significantly during acetate infusion in vivo, but mean arterial pressure, systolic arterial pressure, and systemic vascular resistance decreased. Heart muscle ATP concentrations decreased after 7 min of acetate infusion. In vivo cardiac work load (HR.(peak left ventricular pressure] showed a positive correlation with tissue adenosine concentration and a negative correlation with phosphorylation potential. Acetate uptake in the perfused hearts was about 2.5 mumol/min per gram wet weight. Acetate perfusion increased O2 consumption and coronary flow concomitantly with a decrease in tissue ATP concentration. Tissue AMP and perfusate effluent adenosine concentration and adenosine output increased significantly, perfusate adenosine showing a non-linear positive correlation with coronary flow. The results demonstrate that acetate induces considerable changes in hemodynamics and metabolism in the heart.
OBJECTIVES: There is increasing evidence that blood coagulation factors can influence blood pressure. In the present study, we tested the hypothesis that the beta fragment of human coagulation factor XIIa (beta-FXIIa) induces adrenal catecholamine-mediated pressor and chronotropic responses via bradykinin generated from the plasma kallikrein-kinin system. METHODS AND RESULTS: In anaesthetized bioassay rats with blocked autonomic reflexes, in the Brown Norway strain a bolus injection of beta-FXIIa (1 microg/kg, administered intravenously) elicited a 170-fold rise in plasma epinephrine (from 0.12 +/- 0.02 to 20.58 +/- 2.42 nmol/l; P
Laboratory of Biochemistry and Endocrinology of Aging, Institute of Children and Adolescent Health Protection, Academy of Medical Science, 50-Let VLKSM av., 52A, 61153, Kharkov, Ukraine. firstname.lastname@example.org
In order to investigate the possible reasons for age-related decrease in myocardium resistance to stress, we carried out a study of lipid peroxidation (LPO) stimulation features in the myocardium of adult (10-12 months) and aged (22-25 months) male Wistar rats during immobilization stress. In our studies of ascorbate-dependent LPO and induced chemiluminescence, we found that immobilization stress is accompanied by decreased efficiency in the induction of free radical processes in the heart of aged rats. An important cause of this phenomenon may be age-dependent changes in the catalytical properties of the cytosolic superoxide dismutase. The pathophysiological consequences of stress-related, age-dependent decreased efficiency of induction of free radical processes in the heart are discussed.
The effect of chronic ethanol intake and warm acclimation on the heat tolerance of rats under the influence of alcohol was studied. The animals were divided into two groups: Group 1 received water as their fluid intake and, group 2 received a 10% ethanol solution, and both groups were exposed to a temperature of 30 degrees C for 4 weeks. Excretion of urinary catecholamines was measured prior to warm exposure at 22 degrees C and once a week during warm exposure at 30 degrees C. After warm acclimation a dose of alcohol 2 g/kg was injected in the rats intraperitoneally (i.p.), and then they were exposed to a heat stress of 40 degrees C for 45 min. During warm acclimation, the controls consumed more fluid and they excreted more norepinephrine into the urine than the alcohol-fed animals during the first week. After the period of acclimation there were no significant differences in urinary excretion of catecholamines between the groups. Colonic temperature of the controls was 0.7 degrees C higher than in the alcohol-fed animals. Acute alcohol administration (2 g/kg) increased the colonic temperature of the alcohol-fed animals during a heat stress of 40 degrees C more than in the controls. After heat stress, the concentration of catecholamines in the blood was significantly higher in the controls. The results show that the hyperthermic effect of ethanol was more considerable in the rats whose drinking water during warm acclimation was an ethanol solution.
Cardiovascular arousal is associated with patterned cortical activity changes. Head-down-tilt bed rest (HDBR) dimishes the baroreflex-mediated cardiac control. The present study tested the hypothesis that HDBR deconditioning would modify the forebrain organization for heart rate (HR) control during baroreflex unloading. Heart rate variability (HRV), blood pressure and plasma hormones were analysed at rest, whereas HR and cortical autonomic activation patterns (functional magnetic resonance imaging) were measured during graded and randomly assigned lower body negative pressure treatments (LBNP, -15 and -35 mmHg) both before (Pre) and after (Post) a 24 h HDBR protocol (study 1; n = 8). An additional group was tested before and following diuretic-induced hypovolaemia (study 2; n = 9; spironolactone, 100 mg day(-1) for 3 days) that mimicked the plasma volume lost during HDBR (-15% in both studies; P
The modifying effect of aminoguanidine (a histaminase inhibitor) and heparin (a histaminase liberator) on anaphylactic shock in guinea pigs was studied using ovalbumin as an antigen and trigger. The animals died of the shock, the time to death remaining unaltered by the drugs. Serum histamine and cortisol values were high after shock, but were reduced by heparin. Both noradrenaline and adrenaline in plasma were also elevated after shock, the final concentration of the latter being lowered by heparin. The lungs were dilated, indicating bronchoconstriction. The results confirm the role of histamine in anaphylactic shock and its potential value for the diagnosis in this kind of rapid death, in which morphological signs are scarce or lacking. Its diagnostic value still requires confirmation, however, which only autopsy studies can supply. It also appears that pretreatment of the animals with heparin affected the blood cortisol and catecholamines, which are involved in the shock mechanism as countermeasures, although aminoguanidine did not have any effect.
To study neurohumoral control mechanisms of the hemodynamic response to ventricular tachycardia, arterial blood pressure, plasma atrial natriuretic peptide (ANP) and catecholamine levels were monitored during simulated ventricular tachycardia before and after administration of beta blockade. Tachycardia was simulated by ventricular pacing at 150 beats/min for 150 seconds in 9 patients without and 14 with angiographically demonstrable coronary artery disease (CAD). The effects of intravenous propranolol (0.15 mg/kg) were evaluated in 7 control subjects and in 13 patients with CAD. Arterial blood pressure decreased to its minimum within 5 seconds after onset of pacing in all patients, the decrease being 27 and 30% (p = not significant) in the groups without and with CAD, respectively. Propranolol did not affect the initial decline, but blunted subsequent recovery. The ANP baseline levels were similar in both groups, increasing by 60% (p less than 0.05) and 71% (p less than 0.02) in the groups without and with CAD, respectively, during ventricular pacing. After administration of propranolol the increase in ANP was 180% in both groups. Rapid ventricular pacing did not affect catecholamine levels before propranolol, but after propranolol norepinephrine increased by 71 (p less than 0.02) and 97% (p less than 0.01) in patients without and with CAD, respectively. There was a significant correlation (r = 0.53, p = 0.001) between pacing-induced ANP and norepinephrine changes, but changes in arterial blood pressure did not correlate with those in either of these hormones. Thus, beta-adrenergic blockade blunts blood pressure recovery during simulated ventricular tachycardia. However, this is partly counterbalanced by increased circulating norepinephrine levels.(ABSTRACT TRUNCATED AT 250 WORDS)
By means of ultra and cytochemical study the catecholamine inserts in erythrocytes look like dark lumps and beads the size and quantity of which being directly proportional to the sympathetic adrenaline system functional state. Under the conditions of catecholamine shortage the inserts reducing to fragments occurs and under catecholamine growth the increase in inserts size takes place. In both cases the erythrocyte structure disorder has been observed. Cytochemical method of catecholamine detection in erythrocytes also allows simultaneously to determine the erythrocyte morphological state.
Myocardial ischemia, electrolyte changes, and fluctuations in autonomic tone may play an important role in the presentation of malignant ventricular arrhythmias. beta-Adrenoceptor blocking agents have been shown to decrease the incidence of ventricular fibrillation and sudden cardiac death in patients with coronary artery disease. Therefore we investigated the changes in myocardial metabolism and transcardiac electrolytes during simulated ventricular tachycardia before and after beta-adrenergic blockade. Six patients with normal coronary arteries (group 1) and 12 patients with documented coronary artery disease (group 2) were included in the study. The right ventricle was paced with electrode catheters to a constant cycle length of 400 msec for 3 minutes. Blood samples were withdrawn simultaneously from the coronary sinus and femoral artery to determine the transcardiac differences in metabolic variables and electrolytes before the pacing, at the end of the pacing, and 2 minutes thereafter. After pacing, the patients were given intravenous propranolol (0.15 mg/kg), and the protocol was repeated. Intraarterial blood pressure and electrocardiogram were monitored continuously. There was a rapid decline of the mean arterial blood pressures after initiation of the pacing in both study groups, whereafter the pressures began to rise. Propranolol somewhat blunted the blood pressure recovery, especially in group 2. Norepinephrine levels increased during the pacing in both patient groups, and the increase was accentuated by beta-adrenergic blockade. The femoroarterial coronary sinus difference in lactate turned negative, and pH, PCO2 and potassium differences increased in group 2 during pacing. However, the myocardial energy state remained relatively good as estimated from the nonsignificant change in the transcardiac differences of the plasma adenosine catabolites. There were no changes in the metabolic variables or transcardiac electrolytes in group 1 patients during pacing. Propranolol did not prevent the metabolic ischemia, but it did prevent the pacing-induced decrease in coronary sinus potassium and increase in transcardiac potassium difference. Propranolol also decreased arterial levels of free fatty acids and their extraction in group 2 patients during pacing. In conclusion, blood pressure decay during simulated ventricular tachycardia is followed by instantaneous sympathoadrenergic activation. In patients with coronary artery disease, this process is accompanied by metabolic ischemia and net transfer of extracellular potassium into the intracellular space. The metabolic and electrolyte changes may result in alterations of electrophysiologic millieau, thereby also modifying the clinical characteristics of ventricular tachycardia. Propranolol decreases arterial levels of free fatty acids and prevents changes in transcardiac electrolytes observed in coronary artery disease patients during simulated ventricular tachycardia. These effects of propranolol may be of clinical significance.