[Autonomic nervous system--physiology and diagnosis].
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Autonomic Nervous System↗
Biomedical subjects
L Kaijser
Publications and source records attributed to L Kaijser.
Release of prostacyclin into the coronary venous blood in patients with coronary arterial disease.
Voluntary patients with a history of myocardial infarction and with typical effort angina underwent catheterization of the coronary sinus and a brachial artery. Healthy young males, serving as controls, were subjected to the same procedure. Arterial and coronary venous blood was drawn at rest and during atrial pacing to angina (patients) or to a heart rate of 140 beats/min (healthy volunteers) for analysis of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and prostacyclin-like activity (PILA). 6-Keto-PGF1 alpha levels were measured using radioimmunoassay; PILA in the blood was assayed by rapid preparation of platelet-rich plasma followed by determination of the ADP-induced platelet aggregation. Increased arterial levels of PILA and of radioimmunoactive 6-keto-PGF1 alpha (RIA-6-keto-PGF1 alpha) were observed in the patients at rest as well as during pacing. No obvious release of RIA-6-keto-PGF1 alpha occurred at rest, either in the patients or in the controls. However, during pacing, increased amounts of RIA-6-keto-PGF1 alpha appeared in the coronary venous blood of the patients. The results demonstrate that an increased cardiac prostacyclin formation prevails in patients with signs of impaired coronary flow and suggest that ischemic heart disease is characterized by an insufficient vascular response to this vasodilator prostaglandin rather than by its insufficient endogenous production.
6-Ketoprostaglandin F1 alpha↗
Release of adenosine and prostacyclin from ischemic human hearts.
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6-Ketoprostaglandin F1 alpha↗
Cardiac formation of prostacyclin during cardioplegia in man.
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6-Ketoprostaglandin F1 alpha↗
Autonomic regulation of cardiopulmonary functions in sleep apnea syndrome and narcolepsy.
Thirteen patients with sleep apnea syndrome, nine with narcolepsy, and age-matched controls were studied to evaluate possible impairment of autonomic nervous control of cardiovascular and pulmonary function. The sleep apnea group had subnormal increases in heart rate and blood flow in the resting arm upon muscle contraction, although they were higher than seen in the narcolepsy group. Some sleep apnea patients had marked bradycardia in response to a dive reflex test. Other cardiovascular results did not differ from controls. Some sleep apnea patients had low ventilatory response to CO2. One had abnormal spirometry, two had enlarged tonsils, and five were snorers. The narcolepsy group had subnormal heart rate, blood pressure, and forearm blood flow responses to muscle contraction, subnormal respiratory sinus arrhythmia, and subnormal heart rate response to the Valsalva maneuver. Ventilatory function was normal. Thus, narcolepsy is associated with attenuation of some cardiovascular reflexes. The impairment is probably of central origin. The causative factor for the sleep apnea syndrome is probably also in the central nervous system rather than in the pulmonary or upper airway region. Great interindividual variations in the sleep apnea group point to a more multifactorial etiology. Thus, the two conditions of increased sleepiness are associated with autonomic dysfunction, but the differences in autonomic abnormalities reinforce that sleep apnea and narcolepsy, also in this respect, represent different clinical entities.
Adult↗
Diet induced changes in sympatho-adrenal activity during submaximal exercise in relation to substrate utilization in man.
In order to study how the diet may influence sympatho-adrenal activity during exercise, 7 subjects were examined at rest and during submaximal exercise (25 min at 65% of VO2 max) on two occasions. The first occasion was preceded by 5 days on a carbohydrate poor diet (5% carbohydrate, 72% fat and 23% protein) and the second one by 5 days on a carbohydrate rich diet (78% carbohydrate, 8% fat and 14% protein) with the same energy content. Oxygen uptake, respiratory exchange ratio (R), heart rate and arterial plasma concentrations of adrenaline, noradrenaline, dopamine, insulin, glucose, lactate, free fatty acids (FFA), glycerol and beta-hydroxybutyrate were measured at rest and during exercise. Oxygen uptake and heart rate during exercise were higher and R was lower after the carbohydrate poor than after the carbohydrate rich diet. During exercise the arterial plasma concentrations of FFA, glycerol and beta-hydroxybutyrate were higher after the carbohydrate poor than after the carbohydrate rich diet whereas concentrations of insulin and lactate were lower. At rest arterial plasma noradrenaline and adrenaline levels were similar on the two diets (0.70 +/- 0.31 nM noradrenaline and 0.35 +/- 0.32 nM adrenaline one the carbohydrate rich diet, mean values +/- SD). Exercise induced increases in noradrenaline were more pronounced after the carbohydrate poor than after the carbohydrate rich diet (12.42 +/- 3.41 vs. 7.45 +/- 2.68 at 25 min of exercise, p less than 0.001). A similar, although more variable accentuation of exercise induced increases in adrenaline was found. It is concluded that, when compared to a carbohydrate rich diet, a carbohydrate poor diet increases the relative contribution of fat to oxidative metabolism and increases the sympatho-adrenal response to exercise. Stimulation of lipolysis by sympatho-adrenal mechanisms might be of importance for the substrate availability when carbohydrate intake in low.
3-Hydroxybutyric Acid↗
Effect of diet on the utilization of blood-borne and intramuscular substrates during exercise in man.
20 subjects were studied at rest and during a 25 min submaximal exercise (65% of VO2 max) on two occasions, the first preceded by a fat rich diet and the second by a carbohydrate rich diet. Oxygen uptake, respiratory exchange ratio (R) and arterial-femoral venous differences for glucose, lactate, beta-hydroxybutyrate and FFA (based on the fractional extraction of 3H-palmitate) were measured at rest and during exercise. Changes in intramuscular glycogen, triglyceride and lactate concentrations were determined in muscle biopsies taken before and immediately after exercise form m. quadriceps femoris. R was lower after the fat than after the carbohydrate diet and simultaneously the FFA extraction by the exercising leg was higher. The muscle triglycerides did not changes significantly during exercise after either diet. The glucose extraction was insignificantly greater after the fat diet. The glycogen reduction was numerically smaller after the fat diet, but the difference was uncertain and difficult to evaluate due to a large variation after the carbohydrate diet. However, muscle lactate accumulation and release by the exercising leg was smaller after the fat diet, indicating a slower rate of muscle glycogenolysis. It is concluded that a fat rich diet increases the relative contribution of fat to the oxidative metabolism, that this increase, to a great extent, is covered by plasma FFA and that the concomitant decrease in carbohydrate utilization concerns muscle glycogen rather than blood glucose.
Adult↗
Effect of diet on muscle glycogen and blood glucose utilization during a short-term exercise in man.
7 subjects were studied at rest and during a 6 min submaximal exercise (65% of VO2 max) on two occasions, the first preceded by a fat rich diet and the second by a carbohydrate rich diet. Oxygen uptake and respiratory exchange ratio (R) were measured at rest and heart rate both at rest and during exercise. Arterial-femoral venous differences for oxygen, glucose, lactate and beta-hydroxybutyrate and arterial concentrations of free fatty acids were measured at rest and during exercise. Changes in muscle glycogen (in 6 subjects) and lactate concentration were determined by biopsies from m. quadriceps femoris taken before and immediately after exercise. Muscle glycogen decreased less during exercise after the fat than after the carbohydrate diet in 5 of the 6 subjects, whereas blood glucose extraction by the exercising legs did not change with diet. Muscle lactate accumulation and release were smaller after the fat diet. In conclusion, the muscle glycogen utilization during a short-term exercise appeared to be lower after the fat than after the carbohydrate diet, but not the concomitant blood glucose extraction. These differences between diets were similar to those observed after a more prolonged work at the same load.
Adult↗
Normothermic ischaemic arrest in one-vessel coronary artery surgery.
Cardiac metabolism following normothermic ischaemic arrest was studied in 14 patients undergoing coronary bypass surgery for single vessel coronary artery disease. Simultaneous blood samples were taken from the radial artery and from the coronary sinus before and during the first 60 min after aortic crossclamping. O2-saturation and content, potassium, lactate and the isoenzyme MB of the creatine kinase (CK-MB) were assessed. In addition, CK-MB was followed in peripheral venous blood for 8 hours after operation. Analysis of the results revealed decreased oxygen extraction by the heart immediately after the release of the aortic crossclamping and marked lactate and potassium release with delayed metabolic recovery of the myocardium despite the very short aortic occlusion time. Increased postoperative CK-MB serum activity was also seen. We concluded that the use of normothermic ischaemic arrest is hazardous even in such surgical procedures requiring aortic occlusion times as short as 15 min and should be avoided at least by the less experienced surgeon.
Coronary Artery Bypass↗
Pulmonary formation of prostacyclin in man.
The pulmonary formation of prostacyclin (PGI2), as reflected by the difference in concentration of pulmonary and systemic arterial radioimmunoassayed 6-keto-PGF1 alpha, was determined in six healthy waking subjects. The systemic arterial 6-keto-PGF1 alpha levels were low (less than or equal to 50 pg/ml), and no evidence of pulmonary formation and release of the compound was noted. In other experiments systemic arterial 6-keto-PGF1 alpha levels were determined in patients prior to and during artificial ventilation, as well as during and after occlusion of the pulmonary circulation (extra-corporeal circulation, ECC). The arterial 6-keto-PGF1 alpha concentration prior to artificial ventilation was 17 +/- 4 pg/ml, i.e. within the range observed in the healthy subjects. During artificial ventilation the arterial levels of 6-keto-PGF1 alpha increased to 191 +/- 21 pg/ml, suggesting that pulmonary formation of PGI2 was stimulated. In the patients subjected to ECC with occluded pulmonary circulation the arterial content of 6-keto-PGF1 alpha was stabilised at an elevated level (120-170 pg/ml). Following re-establishment of the pulmonary circulation the arterial concentrations of 6-keto-PGF1 alpha increased markedly, to 284 +/- 50 pg/ml. It is suggested that the basal pulmonary formation of PGI2 in man is low or non-existent, and that enhanced formation of the compound in the lungs is a consequence of intervention with normal pulmonary ventilation of perfusion.
6-Ketoprostaglandin F1 alpha↗
Early exercise tests after uncomplicated acute myocardial infarction before early discharge from hospital.
As part of an early mobilization and early discharge scheme, 76 consecutive low-risk patients were selected from a population of 298 acute myocardial infarction (AMI) patients, to undergo an exercise test. The test was done on the 7th day after an AMI. The patients were 57 men and 19 women of mean age 57 and 68 years, respectively. Twelve patients were unable to complete the test, but no serious complications were observed. Average heart rate during the highest exercise load (50 W) was 106 beats/min. The following risk indices (RI) were considered abnormal and were looked for during or after exercise: 1) heart rate greater than 125 (n = 12), 2) major ventricular arrhythmias (n = 3), 3) angina pectoris (n = 9), 4) ST deviation of more than 1 mm (n = 11). Two RIs were found in 9 patients during the exercise test which led to prolonged hospitalization. One RI was found in 26 patients (34%). Eighty-eight per cent (n = 36) of the patients with normal exercise test had an uneventful recovery during the six-month observation period, in contrast to 35% (n = 9) of patients with heart rate greater than 125 recovered normally, a significantly lower number (p less than 0.05) than among patients with a normal exercise test. Reinfarction occurred in one patient with normal exercise test and in six (23%) of those with one RI (p less than 0.01) and two of those with two RIs (N.S.). We conclude that a submaximal bicycle exercise test seven days after an AMI is a safe and useful selection instrument for early discharge from hospital as well as a useful predicting instrument of future complications.
Adult↗
Digital pulse volume in the evaluation of haemodynamic effects of cardiac pacing.
Some artificially paced patients experience symptoms referrable to competition between spontaneous and pacemaker-induced heart activity. Haemodynamic studies are necessary to establish a relationship. Non-invasive techniques are desirable. Because of the considerable variations in haemodynamic variables from one beat to another it seems necessary to do beat-to-beat analysis. In the present study a comparison has been made between digital arterial pulse amplitude (DAPA) and central haemodynamic parameters in six patients at different pacing modes. A good correlation was found between DAPA and arterial pulse pressure (r = 0.83-0.99). The mean difference in cardiac output between atrio-ventricular pacing and ventricular pacing with atrial activation in early systole was 1.11 /min (P less than 0.01). A mean increase of 70% in DAPA was found at optimal PR-time as compared to simultaneous atrial and ventricular activation; wide individual variations were, however, seen. The results presented indicate that peripheral pulse volume registrations may be helpful in evaluating the consequences of atrial contractions for haemodynamic variables and to find those paced who may benefit from atrial or bifocal heart stimulation.
Aged↗
Cardiovascular response to spinal anaesthesia in elderly men: effects of head-up tilt and dihydroergotamine administration.
In nine elderly (mean age 60, rang 42-74 years) cardiovascular pressures and cardiac output have been measured by catheterization of the pulmonary and brachial artery during spinal anaesthesia without and with dihydroergotamine (DHE) and during an added slight head-up (10-15 degrees). Spinal anaesthesia lowered arterial pressure and also stroke volume. After DHE arterial pressures as well as stroke volume were normalized. Tilting before spinal anaesthesia lowered stroke volume but arterial pressures were maintained. During spinal anaesthesia, tilting lowered arterial pressures as well as filling pressures of the heart. After administration of DHE during spinal anaesthesia the pressures were unaffected by tilting. It is concluded that in elderly men, unlike the young men previously studied, spinal anaesthesia decreases arterial blood pressures by a combination of reduced peripheral resistance and decreased stroke volume. The decreases in stroke volume and cardiac output were most pronounced in those patients with a reduced blood volume. DHE also prevents arterial pressure fall with head-up tilt during spinal anaesthesia.
Adult↗
Conversion of exogenous arachidonic acid to prostaglandins in the pulmonary circulation in vivo. A human and animal study.
The capacity of human lungs to synthetize prostaglandins (PGs) from exogenous arachidonic acid (AA) was investigated in healthy male volunteers. 14C-labelled AA was infused at a constant rate into the right atrium under simultaneous sampling of blood from the ascending aorta. The arterial content of 14C-AA metabolites was extracted, separated with thin-layer chromatography and quantified using fractionated liquid scintillation spectrometry. Conversion of exogenous AA to prostacyclin (PGI2) was also studied in the lungs of anaesthetized cats. In these experiments different doses of unlabelled AA were administered intravenously. Simultaneously PGI2-activity in the arterial blood was assayed using a technique for continuous measurement of platelet aggregation on blood superfused collagen strip. Radiochromatograms of the human arterial plasma revealed no clearly defined peaks corresponding to any of the unlabelled standards of PGD2, PGE2, 6-keto-PGF1 alpha, PGF2 alpha or TxB2. The 14C-activity in the chromatograms materialized only in one (apart from AA) prominent peak in parallel to 13,14-dihydro-15-keto-PGE2. Neither in cats did significant amounts of PGI2 appear in the arterial blood after administration of AA in moderate doses. Only very high AA doses caused a slight increase in arterial PGI2-activity. The results demonstrate that human lungs do not convert exogenous AA to PGs under physiological conditions. In cats the reluctance of the lungs to utilize exogenous precursor can only be overcome with high, non-physiological AA doses. The data may suggest the existence of special regulatory mechanisms which control release of PGs from the lungs and promote utilization of endogenous precursor.
Adult↗
Myocardial protection during aortic valve replacement. effects of mannitol in the cardioplegic solution on cardiac metabolism and enzyme release.
Myocardial substrate metabolism and enzyme release following hypothermic potassium cardioplegia with and without the addition of mannitol in the cardioplegic solution were studied in two series of patients undergoing isolated aortic valve replacement. Measurements were made of PO2. O2-saturation and content, PCO2, pH, glucose, lactate, pyruvate, potassium, myoglobin, creatine kinase (CK), its isoenzyme MB and aspartate aminotransferase (ASAT) simultaneously in arterial and coronary sinus blood before cardioplegia and during the first 60 min after the release of aortic cross-clamping. In addition, myoglobin and enzymes were followed in peripheral venous blood for 72 hours after cardioplegia. Analysis of the results revealed no striking difference between the groups. Nevertheless, with the addition of mannitol, there was a slightly lower release of lactate and myoglobin probably indicating a more rapid metabolic recovery of the myocardium.
Aortic Valve↗
Myocardial protection during aortic valve replacement. Comparison between sanguineous and Asanguineous Cardioplegic Solutions.
Myocardial substrate metabolism and enzyme release following hypothermic potassium cardioplegia were studied in two series of patients undergoing isolated aortic valve replacement. In 15 patients blood was used as cardioplegia vehicle (blood cardioplegia group) and a plain electrolyte solution was used in a control group of 17 patients. Simultaneous blood samples were drawn from arterial and coronary sinus blood before and during the first 60 min after release of aortic cross-clamping. Blood samples were analyzed for PO2. O2-saturation and content, PCO2, pH, lactate, pyruvate, glucose, potassium, myoglobin, creatine kinase (CK), its isoenzyme MB and aspartate aminotransferase (ASAT). In addition, myoglobin and enzymes were followed in peripheral venous blood for 48 hours. The pattern of metabolic changes after cardioplegia was similar in both groups, but some differences were encountered in the degree of the changes in potassium, myoglobin and CK-MB between the groups. The differences were nevertheless small and cell damage was probably of reversible nature in all patients, but the myocardial protection afforded by single dose blood cardioplegia was not unquestionably better than that of the control group.
Aortic Valve↗
Myocardial protection during aortic valve replacement. Cardiac metabolism and enzyme release following continuous blood cardioplegia.
Cardiac metabolism following hypothermic potassium cardioplegia with blood as cardioplegia vehicle was studied in two groups of patients undergoing aortic valve replacement. In 15 patients, blood was given as single dose infusion (single dose group) and in 18 patients the same initial bolus was followed by a continuous perfusion (25-30 ml/min) with modified blood from the heart-lung machine (continuous blood group). Simultaneous samples were drawn from arterial and coronary sinus blood before and during the first 60 min after cardioplegia. In the continuous blood group, samples were also drawn during the period of cardioplegic perfusion. The samples were analyzed for PO 2, O2-saturation and content, PCO2, pH, lactate, pyruvate, glucose, potassium, myoglobin, creatine kinase (CK), its isoenzyme MB, and aspartate aminotransferase (ASAT). In addition myoglobin and enzymes were followed in peripheral venous blood for 24 hours. Myocardial biopsies were taken from the left ventricle at the beginning and end of cardioplegia and analyzed for adenosine triphosphate (ATP), creatine (C) and creatinephosphate (CP). The pattern of metabolic changes after cardioplegia was similar in both groups with decreased myocardial oxygen extraction, marked lactate and potassium release, increased glucose uptake and significant enzyme and myoglobin release. However, the degree of changes was significantly smaller in the continuous blood group. The myocardial biopsies also showed significantly less ATP and CP decrease in the continuous blood group, suggesting, together with the other metabolic results, that the myocardial protection afforded by continuous blood cardioplegia was superior to that of the single dose group. Furthermore, continuous perfusion permitted easy control of myocardial temperature during the period of aortic cross-clamping.
Aortic Valve↗
Myocardial protection during aortic valve replacement. Comparison of different methods by intrtaoperative coronary sinus blood sampling and postoperative serial serum enzyme determinations.
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Aortic Valve↗