PubMed Health⌕ Search

Biomedical subjects

Jan Aldershvile

Publications and source records attributed to Jan Aldershvile.

11 recordsLinked to original sources
PubMed2005

Effects of high thoracic epidural analgesia on myocardial blood flow in patients with ischemic heart disease.

BACKGROUND: In patients with ischemic heart disease, high thoracic epidural analgesia (TEA) has been proposed to improve abnormalities of coronary function by inhibiting cardiac sympathetic tone. We evaluated the effect of TEA on myocardial blood flow in patients with ischemic heart disease. METHODS AND RESULTS: Twenty male patients with multivessel ischemic heart disease were studied. An epidural catheter was inserted between the second and third thoracic vertebral interspace (Th2 to Th3). Analgesia was induced by epidural injection of bupivacaine 0.5%, and a sensory block from the sixth cervical (C6 to C7) to Th10 (Th8 to Th11) vertebral interspace was achieved. Myocardial blood flow was measured with dynamic 13N-ammonia PET with and without TEA at rest, during pharmacological vasodilation with dipyridamole, and during sympathetic stimulation with the cold pressor test. Myocardial blood flow during dipyridamole increased similarly, regardless of TEA, in all regions except in myocardium subtended by collateral arteries in which blood flow increased more with than without TEA (P<0.05). Without TEA, myocardial blood flow during the cold pressor test remained unchanged compared with myocardial blood flow at rest. In contrast, with TEA, myocardial blood flow increased in all vascular territories. Coronary vascular resistance increased during the cold pressor test without TEA, whereas with TEA, coronary resistance decreased in myocardium subtended by nonstenotic and stenotic coronary vessels and remained unchanged in myocardium subtended by occluded vessels. CONCLUSIONS: In patients with multivessel ischemic heart disease, TEA partly normalizes the myocardial blood flow response to sympathetic stimulation.

Aged↗
PubMed2005

The effect of thoracic epidural analgesia on the occurrence of late postoperative hypoxemia in patients undergoing elective coronary bypass surgery: a randomized controlled trial.

STUDY OBJECTIVES: To evaluate the effect of perioperative thoracic epidural analgesia followed by postoperative epidural analgesia compared with conventional IV anesthesia on the occurrence of late postoperative hypoxemia in patients undergoing elective coronary bypass graft (CABG) surgery. DESIGN: Randomized controlled trial. SETTING: Cardiac surgery unit at a university hospital. PATIENTS: A total of 50 patients undergoing elective CABG surgery. INTERVENTION: Patients were randomly assigned to receive either conventional IV anesthesia (CON) or general anesthesia combined with thoracic epidural anesthesia followed by postoperative epidural analgesia (TEA) with bupivacaine. Postoperatively, the patients were monitored in the surgical ward with a pulse oximeter for a total of two postoperative nights (the second and third postoperative nights). MEASUREMENTS AND RESULTS: The overall incidence of episodic hypoxemia was 56% (28 of 50 patients) on the second postoperative night and 89% (41 of 46 patients) on the third postoperative night. More than 30 episodes of hypoxemia developed on the second night in 22% of patients (11 of 50 patients), and on the third night in 30% of patients (14 of 46 patients). Despite oxygen therapy, 7% of patients (3 of 46 patients) experienced constant hypoxemia on the third night. In general, hypoxemia seemed to be slightly worse on the third postoperative night compared with the second postoperative night. Significantly more patients in the TEA group (25 of 25 patients) experienced episodic hypoxemia on the third postoperative night compared with the CON group (16 of 21 patients; p < 0.05). Otherwise, there were no significant differences between the two regimens. CONCLUSIONS: Both episodic and constant hypoxemia were common in the late postoperative period in patients on the ward after CABG surgery with no clinically significant intergroup differences. Thus, perioperative epidural anesthesia/analgesia combined with postoperative epidural anesthesia/analgesia was not protective against hypoxemia, and therapy with opioids did not seem to be of importance for the occurrence of late postoperative hypoxemia on nights 2 and 3 after CABG surgery.

Aged↗
PubMed2004

Pro-brain natriuretic peptide as marker of cardiovascular or pulmonary causes of dyspnea in patients with terminal parenchymal lung disease.

BACKGROUND: Increased plasma concentrations of pro-atrial natriuretic peptide (proANP) and pro-brain natriuretic peptide (proBNP) are features of left ventricular impairment. However, concentrations of proANP and proBNP in patients with isolated terminal parenchymal lung disease are not known. Therefore, we measured the plasma concentrations of natriuretic precursor peptides in patients with terminal parenchymal lung disease who had normal left ventricular function and who were referred for evaluation for lung transplantation. METHODS: We measured plasma N-terminal proANP and proBNP in patients undergoing right heart catheterization (n = 50) and related results to hemodynamic variables obtained during catheterization. RESULTS: Plasma proBNP concentrations were unaffected in patients with terminal parenchymal lung disease and normal left ventricular function (median, 2.5 pmol/liter; range, 0-22; upper reference limit, 15 pmol/liter). In contrast, patients with primary pulmonary hypertension displayed more than a 40-fold increase in plasma proBNP concentrations (median, 107 pmol/liter vs 2.5 pmol/liter, p < 0.0001). Plasma N-terminal proANP increased moderately (median, 664 pmol/liter; range, 36-1620; upper reference limit, 600 pmol/liter) but correlated to plasma proBNP concentrations (r = 0.47, p < 0.0001). Finally, regional vascular proBNP concentrations revealed the heart as the secretory site. CONCLUSIONS: Our findings strongly support the contention that natriuretic peptide measurements are efficient markers for cardiovascular causes of dyspnea. Moreover, our results eliminate natriuretic peptides as markers of moderate pulmonary hypertension in patients with terminal parenchymal lung disease.

Adult↗
PubMed2004

Effects of amiodarone and thoracic epidural analgesia on atrial fibrillation after coronary artery bypass grafting.

OBJECTIVE: This study was designed to assess the effects of a perioperative dosing regimen of amiodarone administration, high thoracic epidural anesthesia (TEA), or a combination of the 2 regimens on atrial fibrillation (AF) after coronary artery bypass grafting (CABG). DESIGN AND SETTING: The study was prospective, controlled, and randomized and was performed in a tertiary health care center associated with a university. PARTICIPANTS: One hundred sixty-three patients scheduled for coronary artery bypass graft surgery. INTERVENTIONS: In this 2 x 2 factorial-designed study the patients were randomized to 1 of 4 regimens in which group E had perioperative TEA, group E+A had TEA and amiodarone, group A had amiodarone, and group C served as control. The epidural catheter was inserted at T1-3 the day before surgery. TEA groups received TEA for 96 hours. The amiodarone regimen consisted of a single loading dose of 1,800 mg of amiodarone orally. Intravenous infusion of amiodarone was started after induction of anesthesia and was administered at 900 mg over 24 hours for the subsequent 3 days. MEASUREMENTS AND MAIN RESULTS: AF was documented using Holter monitoring. In group E 22 of 44 (50%), in group E+A 10 of 35 (28.6%), in group A 10 of 36 (27.8%), and in the control group 20 of 48 (41.7%) patients developed AF (odds ratio amiodarone/nonamiodarone 0.47 [0.24-0.90]; P = 0.02). CONCLUSIONS: The perioperative amiodarone regimen used in this study was effective in reducing the incidence of AF after CABG while TEA was not.

Aged↗
PubMed2002

Effects of large conductance Ca(2+)-activated K(+) channels on nitroglycerin-mediated vasorelaxation in humans.

Nitric oxide (NO)-induced vasorelaxation and the regulation of endothelial superoxide anion levels is partly mediated by vascular large conductance Ca(2+)-activated K(+) (BK(Ca)) channels. Nitroglycerin acts through the release of NO and its effect is modulated by changes in endothelial superoxide levels. This study examines the effect of BK(Ca) channel blockade on nitroglycerin-induced vasorelaxation in human arterial and venous vascular segments and whether responses to BK(Ca) channel blockade are influenced by the development of venous nitroglycerin tolerance. Dose-relaxation curves to nitroglycerin (10(-10)-10(-4) M) were obtained in segments of the saphenous vein and the left mammary artery. Studies were performed with and without pre-incubation with the BK(Ca) channel blocker iberiotoxin (10(-7) M) and venous tolerance to nitroglycerin were induced by a 24-h i.v. infusion (0.5 microg/kg/min). Iberiotoxin reduced the vasorelaxant effect of nitroglycerin (E(max)) by 60% in endothelium-intact arteries and 13% in endothelium-denuded arteries (P<0.05). Development of nitroglycerin tolerance did not affect the response to iberiotoxin in the venous vascular segments (P>0.05) and (compared to arterial segments) veins were less sensitive to BK(Ca) channel blockade (30% reduction in E(max)) or endothelial removal. The results suggest that primarily arterial effects of nitroglycerin are significantly inhibited by changes in the activity of the endothelial BK(Ca) channels. Although endothelial BK(Ca) are likely regulators of mechanisms underlying arterial tolerance development to nitroglycerin, they do not appear to play a role in human venous nitroglycerin tolerance development.

Calcium↗
PubMed2002

Temporal changes in myocardial endothelial nitric oxide synthase expression following human heart transplantation.

BACKGROUND: The incidence of cardiac allograft vasculopathy increases with time after heart transplantation. Allograft vasculopathy is associated with endothelial dysfunction and reduced endothelium-dependent nitric oxide-mediated vascular effects. In this study, temporal changes in endothelial nitric oxide synthase (NOS3) expression in human myocardial biopsies were investigated during the first 3 years after heart transplantation. METHODS: In each patient (n = 7), the immunohistochemical presence of NOS3 and inducible nitric oxide synthase were examined in serial biopsies taken at 1, 4, and 26 weeks and at 1, 2, and 3 years after transplantation. RESULTS: Endothelial nitric oxide synthase was present in vascular endothelial cells in all biopsies at the time of transplantation. A rapid fall within the first months in the number of NOS3-positive biopsies was observed, with a possible difference in the rate of disappearance among the capillaries, the arterial endothelium, and the venous endothelium. After 2 years, very little NOS3 could be detected. Inducible nitric oxide synthase was present in vascular smooth muscle cells throughout the study period and did not change. CONCLUSION: Endothelial nitric oxide synthase immunoreactivity is gradually lost after heart transplantation. These changes may be responsible for the coronary endothelial dysfunction often seen after human cardiac transplantation.

Adult↗
PubMed2002

Nitroglycerin tolerance: different mechanisms in vascular segments with or without intact endothelial function.

In vivo tolerance to nitroglycerin seems to be induced by an increase in vascular superoxide anion levels. In rabbits with normal endothelial function, in vivo induced tolerance is functionally reversed by ex vivo removal of the endothelium, probably due to a reduction in superoxide anion levels. However, the impact of in vivo endothelial dysfunction on tolerance development has not been examined. This study investigated how in vivo endothelium denudation affects the development of in vivo nitroglycerin tolerance. The effect of in vivo endothelium denudation was examined ex vivo (myograph experiments) after prolonged continuous nitroglycerin infusion in a conscious rat model. The vascular reactivity to nitroglycerin was studied in vivo in endothelium-denuded and corresponding endothelium-intact arteries. The results show that in vivo endothelium denudation does not affect the degree of tolerance development but significantly alters the effect of interventions targeted to inhibit tolerance development. In endothelium-intact vessels, superoxide dismutase and the angiotensin II receptor blocker losartan significantly inhibited tolerance-inducing properties of the prolonged nitroglycerin infusion (E[max, nitroglycerin] response in % of normal controls: nitroglycerin tolerant 70%, superoxide dismutase 93%, losartan 99%). This effect was absent in in vivo endothelium-denuded segments (nitroglycerin tolerant 57%, superoxide dismutase 72%, losartan 60%). These findings suggest that interventions against in vivo tolerance development, within the same animal, may elicit different results depending on the presence or absence of an in vivo dysfunctional endothelium.

Acetylcholine↗
PubMedDate not supplied

Simultaneous cardiac output and regional myocardial perfusion determination with PET and nitrogen 13 ammonia.

BACKGROUND: The purpose of this study was to evaluate the possibility of measuring cardiac output during positron emission tomography (PET) examination of myocardial perfusion with nitrogen 13 ammonia. METHODS AND RESULTS: In 7 patients undergoing right-sided cardiac catheterization for evaluation of heart failure and 6 patients who had undergone heart transplantation, a thermodilution catheter for continuous measurement of cardiac output was inserted. An N-13 ammonia scan of the heart was subsequently performed, and with use of factor analysis, the time-activity curve from the right ventricle was derived from the dynamic image sequence. The PET-derived cardiac output was subsequently obtained according to the Stewart-Hamilton principle as the amount of injected tracer divided by the area under the time-activity curve. PET-acquired cardiac output measurements correlated closely with the invasively determined values for a wide range of cardiac output values (P < .0001). The mean difference was 0.12 L/min, with an SD of 0.74 L/min. The interobserver variation was low, with a mean difference of 0.06 L/min and an SD of 0.46 L/min. CONCLUSIONS: Cardiac output determination with N-13 ammonia and PET appears to be both accurate and precise and can be performed simultaneously with measurement of myocardial perfusion.

Adult↗