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A Hjalmarson

Publications and source records attributed to A Hjalmarson.

At least 325 records · Page 18Linked to original sources
PubMedDate not supplied

Effects of anti-peptide antibodies against the second extracellular loop of human M2 muscarinic acetylcholine receptors on transmembrane potentials and currents in guinea pig ventricular myocytes.

The effects of anti-peptide antibodies against the second extracellular loop of human M2 muscarinic receptor on transmembrane potentials and currents in guinea pig single ventricular cells were analyzed using whole-cell patch clamp technique. These effects were compared with those of the muscarinic receptor agonists carbachol and acetylcholine. The antibodies shortened the action potential duration in a dose-dependent manner. By using a ramp or step rectangular pulse protocol, it was found that the antibodies increased the outward K+ current and decreased the inward basal ICa significantly. The reversal potential of both carbachol- and antibody-induced extra currents were close to -80 mV, being in proximity to the calculated Ek of -90 mV. A beta-adrenergic receptor agonist, isoprenaline, prolonged the action potential and increased the overshoot which could be inhibited by both antibody and carbachol. Isoprenaline increased inward ICa and outward Ik simultaneously. Both antibody and carbachol could significantly reduce the isoprenaline-stimulated ICa but not the isoprenaline-stimulated Ik. The antibody- or carbachol-induced outward K+ current and the depressant effects of antibody and carbachol on isoprenaline-stimulated ICa were partially antagonized by atropine. These results suggest that the anti-M2 muscarinic receptor antibodies display a stimulatory activity similar to muscarinic receptor agonist on the receptor-mediated electrophysiological events.

Acetylcholine↗
PubMedDate not supplied

Effect of metoprolol on activity of beta-adrenoceptor coupled to guanine nucleotide binding regulatory proteins in adriamycin-induced cardiotoxicity.

Prevention of cardiotoxicity without interfering with the therapeutic efficacy of adriamycin is a very crucial question. We have investigated the activity of beta-adrenoceptor coupled to guanine nucleotide binding regulatory proteins (G-proteins) and Ca(2+)-ATPase activity in experimental adriamycin-induced cardiotoxicity and the influence of metoprolol treatment on these variables. Adriamycin was administered to rats intravenously as a single dose of 6 mg/kg, and metoprol was continuously given by means of implanted osmotic pumps. beta-Adrenoceptor characteristics were measured by radioligand-binding experiments and by basal and stimulated adenylyl cyclase activity. Northern blot and dot blot analysis was used to quantify G-protein mRNA. It was shown that adriamycin did not induce any change in the total beta-adrenoceptor density, nor did the high affinity agonist binding to beta-adrenoceptor change. Adriamycin did not induce any alteration in the amount of mRNA encoding for stimulatory (Gs) or inhibitory (Gi) G-proteins. Also, basal and stimulated adenylyl cyclase activities were identical in the different experimental groups. In contrast, the Ca(2+)-ATPase was shown to increase in adriamycin-treated rats compared to control rats (45 +/- 3.8 versus 23 +/- 1.2 mumol Pi/mg/h, P less than .01). Metoprolol was shown to normalize this increase (29 +/- 2.1 mumol Pi/mg/h). Thus, it may be concluded that in experimental adriamycin-induced cardiotoxicity, despite Ca(2+)-overloading, the beta-adrenoceptor-G protein-adenylyl cyclase system remains intact. Metoprolol seems to prevent Ca(2+)-overloading independently of the beta-adrenoceptors studied here.

Adenylyl Cyclases↗
PubMedDate not supplied

Cardiovascular and psychosomatic symptoms among relatives of patients waiting for possible coronary revascularization.

OBJECTIVE: To examine the consequences for close family members of patients on a waiting list for possible coronary revascularization. BACKGROUND: An increasing number of patients with symptomatic ischemic heart disease require evaluation for possible revascularization. Many of these patients must wait a long time before receiving treatment. The negative consequences of this long wait for patients and their relatives have not been satisfactorily evaluated previously. DESIGN: Cross-sectional descriptive study. SETTING: All hospital in Southwestern Sweden. STUDY POPULATION: One hundred relatives of patients referred for possible revascularization and a sex- and age-matched reference group. The convenience sample consisted of 85% (n = 76) women and 15% (n = 13) men. OUTCOME MEASURES: Frequency of cardiovascular and psychosomatic symptoms. EVALUATION: One hundred relatives and 100 members of the control group were sent a questionnaire to evaluate their clinical condition; working situation; use of tobacco, alcohol and sedatives; and cardiovascular and psychosomatic symptoms. RESULTS: Family members had a significantly higher frequency of anxiety, depression, and irritability compared with the control group. Furthermore, family members reported sleeping disorders, including difficulty waking, tiredness due to lack of sleep, and restless sleep, more frequently than did the control group. CONCLUSION: Close family members of patients waiting for coronary revascularization have particular difficulties, and these difficulties should receive more attention.

Adult↗
PubMedDate not supplied

Effects of nifedipine on arterial concentration and myocardial extraction of catecholamines during pacing-induced angina pectoris.

We studied nine patients with arteriosclerotic coronary heart disease (Group I) and 10 patients with normal coronary arteries (Group II) to elucidate mechanisms by which nifedipine affects catecholamine arterial levels and myocardial extraction at rest and during pacing. Nifedipine induced signs of general and coronary vasodilatation and improved myocardial lactate metabolism during pacing. Noradrenaline arterial concentration increased significantly after nifedipine in both groups (p less than 0.01). In Group I, the values were 40-50% higher compared with Group II. The net myocardial extraction of noradrenaline was not significantly affected by nifedipine, except during pacing in Group II, in which an increase in myocardial release was seen (p less than 0.05). In Group I, there was no correlation between arterial concentration of noradrenaline and myocardial release, while there was a significant negative correlation in Group II (p less than 0.0001). Adrenaline arterial concentration and myocardial extraction were not altered by nifedipine, but there was a positive significant correlation in Group I between arterial concentration and myocardial extraction of adrenaline (p less than 0.001). In conclusion, nifedipine increased noradrenaline levels in both groups of patients, probably reflecting a rise in sympathetic activity. Because myocardial lactate production turned into extraction in patients with coronary artery disease, the increased sympathetic tone evidently did not outweigh the beneficial antianginal effects of nifedipine.

Adult↗
PubMedDate not supplied

Effects of felodipine on pacing-induced angina pectoris.

We determined hemodynamics and myocardial lactate extraction in 11 patients with severe coronary disease after 0.010 (D1), 0.015 (D2), and 0.025 nmol/min (D3) of the arteriolar dilator felodipine during pacing-induced angina pectoris. Plasma concentrations of felodipine after the 3 doses were 12 (5), 25 (6) and 43 (8) nmol/ L, respectively. At corresponding pacing rates, mean blood pressure fell from 126 (24) to 90 (15) mm Hg at D3 (p less than 0.01) and pulmonary capillary wedge pressure was reduced from 14 (10) to 9 (8) mm Hg (p less than 0.05). Cardiac output increased at all three doses (p less than 0.01). The reduction of systemic vascular resistance at D3 was 49% (p less than 0.01) and of coronary vascular resistance 35% (p less than 0.05). At D1, there was no change in lactate extraction, while 8/10 lactate producers improved at D2 and D3. ST depression was diminished at all three doses (p less than 0.05) at the control pacing rate. During maximal pacing rate at D3, the myocardial oxygen consumption was 14% above control level (N.S.). Thus, felodipine was beneficial in most patients at higher dosage. Ventricular unloading and improved coronary perfusion might explain some of these positive effects.

Aged↗
PubMedDate not supplied

Diabetes-induced changes in the Gi-modulated muscarinic receptor-adenylyl cyclase system in rat myocardium.

The inhibitory guanine nucleotide binding regulatory protein (Gi)-mediated muscarinic receptor-adenylyl cyclase system was studied in myocardium from adult male Wistar rats with 10 weeks of diabetes induced by a single intravenous injection of streptozotocin (60 mg/kg). Neither the messenger ribonucleic acid level nor the amount of Gi was changed in the streptozotocin diabetic group as compared to the control group. The activity of the adenylyl cyclase stimulated by guanyliminodiphosphate was decreased by 48% in the streptozotocin diabetic group whereas stimulated activities of adenylyl cyclase by sodium fluoride and forskolin remained unchanged. The inhibition of forskolin-stimulated adenylyl cyclase activity by carbachol was more potent in membranes from the streptozotocin diabetic group than that in membranes from the control group. The competition binding curve between (3H)- quinuclidinyl benzilate and carbachol obtained from the streptozotocin diabetic group was shifted to the left as compared to the control group. These results suggest that the myocardium of streptozotocin-induced diabetic rats exhibited an increase in Gi function as demonstrated by the increased inhibition of guanyliminodiphosphate-mediated adenylyl cyclase and the superhigh affinity for carbachol of the muscarinic receptors. As there were signs, similar to those seen in clinical heart failure, in the streptozotocin diabetic group, these results demonstrate that functional alteration of Gi might underlie, at least in part, the cardiac dysfunction that is associated with diabetes.

Adenylyl Cyclases↗