-
[show abstract]
[hide abstract]
ABSTRACT: This study was designed to examine the effect of volume loading on haemodynamic responses and regional cardiac function in dogs subjected to two infusion rates of propofol. Instrumentation was established to measure aortic and left ventricular pressures, cardiac output and myocardial segmental lengths. Measurements were taken during two successive infusion rates of propofol: 0.2 (P0.2) and 0.4 (P0.4) mg kg-1 min-1. One group (VL +) (n = 6) received volume loading (dextran 40, 10 mL kg-1 h-1), the other group (VL-) (n = 6) received only basal perfusion (Ringer solution, 2 mL kg-1.h-1). Regional blood flows were measured by radio-labelled microspheres. P0.4 induced a decrease in cardiac output and in dP/dtmax. End-diastolic length decreased with propofol without any difference between groups. Regional contractility was not modified by propofol or by volume loading. P0.4 decreased endocardial and epicardial blood flow in the VL-group only. Renal, small intestine and large intestine blood flows decreased in both groups with P0.4. P0.2 did not alter regional blood flows significantly. It was concluded that in this model, propofol infusion at 0.4 mg kg-1 min-1 induced splanchnic, renal and myocardial hypoperfusion in animals not submitted to a mild fluid loading. Fluid loading allowed myocardial perfusion to be maintained but could not prevent a marked decrease in splanchnic and renal perfusion.
European Journal of Anaesthesiology 10/1999; 16(9):615-21. · 2.23 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Previous work showed a twofold increase in stiffness of nonischemic myocardium at the base during ischemia of the left anterior wall. Whether the diastolic response of nonischemic myocardium to remote ischemia depends on the localization of the ischemic or the nonischemic area is unknown.
In dogs with open chests, regional function in ischemic and nonischemic myocardium was assessed (sonomicrometry) before and 5 min after occlusion of the left anterior descending coronary artery (LAD; n = 7) or the left circumflex coronary artery (LCX; n = 7).
In nonischemic myocardium at the base, left anterior descending and left circumflex coronary artery occlusion both resulted in a twofold increase in chamber stiffness, whereas contractility and peak lengthening rate remained unchanged. In nonischemic myocardium of the posterior wall, left anterior descending coronary artery occlusion resulted in a significant (P<0.05 vs. control, P<0.05 vs. base) increase (mean+/-SD) in chamber stiffness (25+/-6%), contractility (17+/-5%), and peak lengthening rate (28+/-6%). In nonischemic myocardium at the apex, left circumflex coronary artery occlusion resulted in a significant (P<0.05 vs. control, P<0.05 vs. base) increase in chamber stiffness (15+/-5%), contractility (16+/-4%), and peak lengthening rate (19+/-6%).
Stiffening of remote nonischemic myocardium occurs regardless of the localization of the ischemic and nonischemic area. The systolic and diastolic responses of nonischemic myocardium are not necessarily homogenous but may vary among different regions.
Anesthesiology 09/1999; 91(3):815-23. · 5.36 Impact Factor
-
BJA British Journal of Anaesthesia 05/1999; 82(4):622-32. · 4.24 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: One hundred and twenty-seven patients undergoing major lower limb joint replacement surgery were studied to determine the incidence of silent myocardial ischemia and to ascertain any link between pre-operative cardiac risk factors, silent myocardial ischaemia and postoperative morbidity. Patients underwent ambulatory ECG monitoring for 4 days (on the pre-operative night and for 3 days postoperatively). Postoperative cardiorespiratory symptomatology and morbidity was assessed by questionnaire at 3 months. Eighty-seven patients had risk factors for silent myocardial ischaemia; 42 patients (30 with risk factors) had peri-operative silent myocardial ischaemia. The median ischaemic loads (range) were 1.04 (0.32-13.31) min.h-1 pre-operatively and 5.53 (0.26-56.39), 6.69 (0.04-42.71) and 1.23 (0.1-53.74) min.h-1 on postoperative days 1-3, respectively. Risk factors did not predict the occurrence of silent myocardial ischaemia or an increased ischaemic load pre-operatively or overall postoperatively. New symptoms (chest pain, palpitations, breathlessness or fatigue) were associated with both silent myocardial ischaemia and ischaemic load (p < 0.05). Thus cardiac risk factors do not predict the occurrence of silent myocardial ischaemia or adverse outcome. Peri-operative silent myocardial ischaemia was associated with increased postoperative fatigue.
Anaesthesia 03/1999; 54(3):235-40. · 2.96 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Nonischemic end-systolic performance decreases during ischemia. These changes in performance are likely to be dependent on the size and site of the ischemic zone, as well as the prevailing loading conditions. This study was designed to examine the effect of regional and generalized changes in inotropy on nonischemic end-systolic performance, independent of the ischemic zone size. Twenty dogs were instrumented with sonomicrometers and micromanometer pressure gauges. End-systolic pressure-thickness relationship data were obained during vena-caval balloon inflation. Measurements were obtained before and 90 s after left circumflex (LC) artery occlusion. Then, simultaneous with the occlusion of the LC artery, isoproterenol (0.04 microg/ml) was infused into the left anterior descending artery. After recovery, the same protocol was repeated before and after propranolol (0.5 mg/kg). In a separate set of animals, the same measurements were made following 2.5 and 5 microg/kg/min dobutamine. The effect of ischemia on the nonischemic end-systolic pressure-thickness relationship was expressed as the extent to which the relationship is shifted to the left. Infusion of intracoronary isoproterenol into the perfusion bed of the nonischemic zone produced a significant increase in the slope of the end-systolic pressure-thickness relationship. During ischemia, however, the extent of leftward shift of this relationship was less than that following beta-blockade. Intravenous dobutamine resulted in a dose-dependent increase in the slope of the nonischemic end-systolic pressure thickness relationship, but the extent of leftward displacement of the relationship in response to regional ischemia was less than that following the control occlusion. The nonischemic segment is coupled with the nonfunctioning ischemic zone in such a way that it is required of the nonischemic segment to operate at decreased end-systolic thickness for any end-systolic pressure, the extent of which is to be determined, in part, by the size of the ischemic zone and the contractile state of the nonischemic myocardium. The lower the contractile state prior to coronary occlusion the greater extent of leftward shift of the pressure-thickness relationship.
Cardiology 02/1999; 91(1):14-24. · 1.71 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The protective efficacy of halogenated anaesthetics on myocardial injury has never been compared during early reperfusion and late reperfusion in an in vivo animal model. We compared recovery of left ventricular function under isoflurane (0.5 MAC) and halothane (0.5 MAC) anaesthesia after a brief period of regional ischaemia (15 min) in acutely instrumented rabbits. Rabbits were instrumented for the measurement of regional segment length and left ventricular pressure. Rabbits receiving isoflurane showed greater recovery of systolic shortening fraction (%SS) both during early and late reperfusion compared with halothane anaesthesia. Isoflurane protected the post-ischaemic myocardium to a greater extent than halothane anaesthesia. Early recovery of contractile function may be a predictor of contractile recovery during the later stages of reperfusion.
BJA British Journal of Anaesthesia 09/1998; 81(2):224-9. · 4.24 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Nicorandil, a new KATP channel opener, is used in clinical practice for anti-anginal therapy. It exhibits vasodilator properties as does the halogenated anaesthetic isoflurane. We have examined the cardiovascular effects of increasing concentrations of isoflurane after administration of nicorandil in 10 adult beagle dogs anaesthetized with thiopental and whose lungs were ventilated mechanically. During surgery, anaesthesia was maintained with 1.0-1.5% isoflurane. A left thoracotomy was performed and the heart suspended in a pericardial cradle. Monitoring included: ECG; aortic, left ventricular, arterial, central venous and pulmonary artery pressures; cardiac output; coronary flow; and segmental length in the apical region. After surgery, isoflurane anaesthesia was set at an end-tidal concentration of 1.05% (1 MAC) and measurements obtained; these were repeated with 1.4%, 1.75%, 2.1% and 1.05% isoflurane concentrations after appropriate stabilization periods. Nicorandil (100 micrograms kg-1 bolus, 25 micrograms kg-1 min-1 infusion) was begun and a second dose-response study of isoflurane was obtained as before. Blood samples were obtained for measurement of concentrations of nicorandil. Systolic ventricular function was assessed by systolic shortening (%SS) and preload recruitable stroke work (PRSW). Increasing isoflurane concentration produced decreases in heart rate, systolic pressure, cardiac output, %SS and PRSW. Nicorandil produced a slight decrease in systolic arterial pressure (10 and 15 mm Hg after 1.05% and 2.05% isoflurane) and a slight increase in heart rate (10 and 5 beat min-1 after 1.05% and 2.05% isoflurane). Preload, assessed by end-diastolic length, decreased. Coronary blood flow increased with infusion of nicorandil. Left ventricular function was not affected by infusion of nicorandil. We conclude that nicorandil has only minor vaso/venodilatory effects in the presence of isoflurane. Ventricular function was not altered by infusion of nicorandil.
BJA British Journal of Anaesthesia 05/1998; 80(4):481-7. · 4.24 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The intravenous anaesthetic propofol has been shown to possess free radical scavenging activity and calcium channel blocking effects in a number of in vitro models. We decided to compare the effects of propofol with those of fentanyl on myocardial contractility during and after ischaemia to determine whether propofol could protect the heart and improve recovery of ventricular contractile function in open-chested dogs.
Twenty adult beagles were acutely instrumented, under halothane anaesthesia, to measure ECG; aortic, left ventricular pressures; cardiac output; coronary flow; and segmental lengths in the regions perfused by the left anterior and left circumflex coronary arteries. After surgery and a stabilisation period halothane anaesthesia was terminated and fentanyl (100 microg x kg[-1] bolus followed by 2 microg x kg[-1] x min[-1] infusion; n=10) or propofol (5 mg x kg[-1] bolus followed by 0.3 mg x kg[-1] x min[-1] infusion; n=10) anaesthesia commenced. After a stabilisation period the LAD coronary artery was occluded for 10 min and then reperfused for 3 h. Measurements were taken throughout the protocol.
We found no significant difference in recovery of contractile function between propofol and fentanyl as assessed by normalised preload recruitable work area (50+/-10 vs 47+/-16%), normalised systolic shortening (36+/-12 vs 48+/-14%) and peak left ventricular dP/dt (1665+/-276 vs 1846+/-151 mmHg x s[-1]) at the end of reperfusion.
We conclude that at the concentration used in this study propofol shows no improvement in contractility during "stunning" when compared to fentanyl.
Acta Anaesthesiologica Scandinavica 02/1998; 42(1):23-31. · 2.19 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: A large epidemiological data set was used to identify 115 patients who died from a cardiovascular cause within 30 days of elective surgery under general anaesthesia. For each patient, a control was identified, matched for age (within 5 yr of the patient), sex, operation and consultant. Patients and controls were compared for cardiovascular risk factors in a matched analysis using conditional logistic regression, and a prognostic model was generated. Three risk factors were included in the final model: previous myocardial infarction (odds ratio 3.18 (95% confidence intervals (CI) 1.22-8.28), P = 0.018), history of hypertension (odds ratio 1.90 (0.99-3.62), P = 0.047) and renal failure (odds ratio 3.56 (1.04-12.10), P = 0.043).
BJA British Journal of Anaesthesia 01/1998; 80(1):14-9. · 4.24 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The effects of changes in preload on paradoxical myocardial wall motion during ischemia have been previously studied. However, the studies have been performed using slow volume changes. It was decided to study the effects of fast changes in preload, which would occur during caval occlusion, on the regional pressure-length loops during ischemia.
Retrospective trial.
Experimental animal laboratory in a university medical center.
Ten anesthetized adult dogs.
In an open chest preparation, regional ischemia was achieved by occluding the left anterior descending coronary artery for 10 minutes, with sudden caval occlusions being performed to assess the influence of preload on wall motion.
Left ventricular pressure and regional segmental lengths were measured. During caval occlusion, beat by beat, percent postsystolic shortening and percent systolic bulging in the ischemic region, percent isovolumetric shortening in the nonischemic region, and percent systolic shortening in both regions were calculated. Caval occlusion significantly decreased the end-diastolic pressure (12.62 +/- 1.02 to 3.39 +/- 0.59 mmHg) and length. In the ischemic area, although systolic shortening became more negative (-1.8 +/- 0.79% to -9.65 +/- 1.08%), postsystolic shortening (9.66 +/- 0.73% to 15.53 +/- 1.2%) and systolic bulging (4.6 +/- 0.49% to 12.67 +/- 1.04%) increased. In the nonischemic area, systolic shortening decreased slightly but significantly (18.01 +/- 3.24% to 14.93 +/- 3.64%) as isovolumetric shortening increased (2.77 +/- 0.68 to 7.37 +/- 1.29%). Caval occlusion increased the rightward shift and accentuated the distortion of the ischemic loop. The nonischemic loop displayed a leftward shift of the systolic isovolumetric component and a slight decrease in percent total length change.
Caval occlusion modifies the shape of the pressure-length loop of the ischemic myocardium. This change in shape may interfere with the assessment of regional systolic indexes obtained by caval occlusion in ischemic hearts.
Journal of Cardiothoracic and Vascular Anesthesia 07/1997; 11(4):445-52. · 1.64 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The effects of anaesthesia on the compromised heart are complex. They depend exquisitely upon the type of any ischaemic threat,
the level of autonomic nervous system activity, and the quality of the endothelium. In the face of acute coronary occlusion,
most anaesthetic agents minimize the extent of ischaemia and limit infarct size. In the face of critical or supracritical
coronary stenosis, anaesthetic agents which decrease pressure cause selectively exaggerated depression of compromised myocardium.
The possibility of exaggerated myocardial depression also exists when agents cause coronary vasodilatation. However, inhalational
anaesthetics appear to protect the stunned myocardium. The overall effect of anaesthetic agents on the myocardium will be
the result of the balance struck between several complex effects. It is probably because of the complexity of the regulation
of the coronary circulation in patients with ischaemic heart disease and the varied effects of anaesthetic agents on the compromised
heart that outcome appears to be little influenced by the choice of the anaesthetic agent. The quality of the control of the
circulation (blood pressure, heart rate) throughout the perioperative period is likely to play a more important role that
the choice of the anaesthetic agent.
Les effets de l’anesthésie sur le coeur malade sont complexes. Ils dépendent particulièrement du type de menace ischémique,
du niveau d’activité du système nerveux autonome et de la qualité de l’endothélium. En face d’une occlusion coronaire aiguë,
la plupart des agents anesthésiques réduisent au minimum l’étendue de l’ischémie et limite la dimension de l’infarctus. Face
à une sténose coronaire critique ou supracritique, les anesthésiques qui abaissent la pression produisent une dépression exagérée
sélective du myocarde compromis. Il est possible que la dépression myocardique soit amplifiée par les anesthésiques qui entraînaient
une vasodilatation coronaire. Cependant, lors du stunning, les anesthésiques volatils semblent protéger le myocarde. L’effet
global des anesthésiques sur le myocarde est le résultat de l’équilibre établi entre plusieurs effets complexes. La complexité
de la régulation de la circulation coronaire dans la coronaropathie et la grandes variété des effets anesthésiques sur le
coeur malade peut expliquer pourquoi le choix de l’agent anesthésique a peu d’influence sur la fréquence des complications
cardiovasculares de l’anesthésie et de la chirurgie. La qualité du contrôle de la circulation (pression artérielle, fréquence
cardiaque) pendant la période périopératoire est susceptible de jouer un rôle plus important que le choix de Panesthésique.
Canadian Journal of Anaesthesia 06/1997; 44(5 Pt 2):R67-76. · 2.35 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: This study sought to explore the separate and combined effects of changes in preload, afterload and contractility on the dynamics of systolic bulging.
The extent of ischemic systolic bulging has been shown to be mechanically disadvantageous to left ventricular pump performance. The factors that determine ischemic segmental wall motion have not been systematically studied.
Fourteen beagles were instrumented with sonomicrometers, micromanometer pressure gauges and a balloon in the inferior vena cava. Regional function was evaluated before and after 90 s of proximal left circumflex coronary artery occlusion. Occlusions were repeated after increasing systolic pressure by 5 to 10 (afterload I) and 15 to 20 mm Hg (afterload II) with graded aortic occlusion during inotropic stimulation with dobutamine (2.5 and 5 micrograms/kg body weight per min intravenously), with simultaneous 5 micrograms/kg per min dobutamine infusion and afterload II and during 2.5% halothane (negative inotrope) concentration. A 20-min recovery period was allowed between each stage of the experiment so that regional function returned to its preocclusion level. Ischemic wall motion was characterized by percent systolic bulging and its peak positive systolic lengthening rate (+dL/dt).
Because bulging is markedly influenced by regional preload, systolic bulging was characterized over a wide range of end-diastolic lengths of the ischemic segment during caval balloon occlusion. During each intervention, a decrease in regional preload increased the extent of percent systolic bulging. This preload dependency was more pronounced with dobutamine infusions. An increase in afterload was not associated with increased percent systolic bulging at any given preload. At a predetermined preload, bulging was not appreciably altered when an increase in left ventricular systolic pressure was not associated with a change in peak positive first derivative of left ventricular pressure (+dP/dt) but was significantly worse when peak +dP/dt increased. Dobutamine caused a dose-dependent increase in percent systolic bulging and peak +dL/dt that was positively correlated with peak +dP/dt.
By using different loading and inotropic interventions and analyzing the regional wall motion behavior over a range of regional preloads, we can conclude that preload and rate of pressure (tension) development are the principal determinants of systolic bulging. Increases in left ventricular pressure alone had a minimal effect on systolic bulging.
Journal of the American College of Cardiology 04/1997; 29(4):846-55. · 14.16 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: One hundred and eighty-three patients were studied to examine the role of a number of risk factors in the development of silent ischaemia after general anaesthesia for general and vascular surgery. We collected evidence of cardiovascular risk factors using a binary questionnaire. The patients were monitored pre- and postoperatively using a Holter ECG monitor. Usable data were collected on 140 patients. Pre-operative silent myocardial ischaemia was found to be strongly associated with postoperative silent myocardial ischaemia (odds ratio: 10.8, 95% confidence intervals: 3.8-30.7). A history of hypertension, indicated by treatment with antihypertensive drugs, was associated with increased risk (odds ratio: 2.58, 95% confidence intervals: 1.12-5.96). A linear trend was found for risk associated with increasing admission systolic blood pressure (odds ratio: 1.20 for each 10-mmHg increase in systolic pressure, 95% confidence intervals: 1.01-1.42). An association between vascular surgery and postoperative silent myocardial ischaemia was also confirmed (odds ratio: 2.36, 95% confidence intervals: 1.1-5.1).
Anaesthesia 03/1997; 52(2):107-11. · 2.96 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The effects of nitrous oxide on left ventricular diastolic function and its potential interactions with ischemia-induced diastolic dysfunction have not been described. Accordingly, we investigated the effects of nitrous oxide in ischemic and remote nonischemic myocardium during baseline, 90 min severe low-flow myocardial ischemia (systolic bulge), and reperfusion in 11 open-chest dogs. Anesthesia was maintained with fentanyl infusion (2 micrograms.kg-1.min-1), animals were ventilated with 60% nitrogen in oxygen, and hemodynamic variables were recorded prior to and after the replacement of nitrogen by 60% nitrous oxide. During baseline, nitrous oxide moderately increased chamber stiffness (+ 10%), myocardial stiffness (+33%), and unstressed length (+4%) and decreased the peak lengthening rate (-10%). Moreover, nitrous oxide decreased regional contractility during baseline (-12% at apex, -8% at base) as well as in nonischemic myocardium during myocardial ischemia (-9%) and reperfusion (-8%). However, nitrous oxide did not modify ischemia-induced systolic or diastolic dysfunction in ischemic myocardium during ischemia and reperfusion. Myocardial ischemia (+45%) and reperfusion (+57%) were associated with an increase in myocardial stiffness of nonischemic myocardium regardless of the anesthetic technique used. This study is the first to demonstrate that in addition to its well established negative inotropic effect, nitrous oxide affects regional diastolic function.
Anesthesia & Analgesia 02/1997; 84(1):39-45. · 3.29 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Nonischemic segmental performance, assessed by end-systolic measures of shortening and thickening, decreases during ischemia. These changes in performance are likely to be dependent on the size, and, possibly, the site of the ischemic zone. This study was designed to examine the effect of preload, independently from ischemic zone size, on nonischemic end-systolic performance.
Twelve beagles were instrumented with sonomicrometers and micromanometer pressure gauges. End-systolic pressure length and thickness relationship data were obtained during vena caval balloon inflation. Control data were obtained both in left anterior descending and in left circumflex regions at left ventricular end-diastolic pressures of 5, 10 and 15 mmHg. The left circumflex artery was occluded for 90 s and nonischemic end-systolic pressure length and thickness data were obtained at each diastolic pressure. A 20 min recovery period was allowed between coronary occlusions.
The isovolumic bulge in the ischemic area was more pronounced at an end-diastolic pressure of 5 mmHg than it was at an end-diastolic pressure of 15 mmHg. The slope of the nonischemic end-systolic pressure length and thickness relationships decreased at an end-diastolic pressure of 5 mmHg, whereas at 10 and 15 mmHg the slope of these relationships did not change significantly. The shift in the nonischemic end-systolic pressure-length relationship to the right was more pronounced at a low end-diastolic pressure (5 mmHg) than it was at a high end-diastolic pressure (15 mmHg). Similarly, the extent of the shift in the end-systolic pressure-thickness relationship to the left was more marked at a low end-diastolic pressure than it was at the higher end-diastolic pressure.
Regional ischemia decreases the end-systolic performance of the nonischemic region. The extent of the shift and the degree to which the slopes of the nonischemic end-systolic relations decrease are influenced by loading conditions.
Coronary Artery Disease 12/1996; 7(11):797-806. · 1.24 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We performed a retrospective case-control study to investigate hypertension and admission blood pressure as risk factors for postoperative cardiovascular death. We identified records of 76 patients who had died of a cardiovascular cause within 30 days of anaesthesia and elective surgery and 76 matched controls. From the records of each patient (case and control) we recorded the admission blood pressure and details of any history of hypertension. A pre-operative history of hypertension was strongly associated with perioperative cardiovascular death (p < 0.001 with one degree of freedom: odds ratio 4.14, 95% confidence intervals 1.63-11.69). There was no association between systolic or diastolic pressure at admission for operation and perioperative cardiovascular death. The mean admission systolic pressure of the cases was 145.5 mmHg (range 90-250 mmHg) and that of the controls was 146.5 mmHg (range 100-200 mmHg). The mean admission diastolic pressure of the cases was 83.2 mmHg (range 60-130 mmHg), and that of the controls was 84.5 mmHg (range 60-110 mmHg).
Anaesthesia 11/1996; 51(11):1000-4. · 2.96 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Ninety four patients undergoing transurethral resection of the prostate underwent Holter electrocardiographic monitoring pre- and postoperatively. There was no difference in silent myocardial ischaemia incidence or load between the spinal (n = 60) and the general anaesthesia (n = 34) groups. Ischaemic heart disease and a higher Detsky score both significantly increased the incidence of silent myocardial ischaemia but not the ischaemic load of those patients that actually demonstrated ischaemia. In this specific surgical population, not undergoing cardiac or vascular surgery, both ischaemic heart disease and cardiac risk scores are poor predictors of ischaemic load. Merely the presence of short duration silent myocardial ischaemia probably has little predictive value for postoperative adverse outcome.
Anaesthesia 09/1996; 51(8):728-32. · 2.96 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We have determined the effects of alterations in preload on ischaemia-induced diastolic dysfunction in anaesthetized beagles instrumented to measure left ventricular pressure and regional dimensions. Low-flow regional ischaemia decreased peak lengthening rates in ischaemic (mean -26 (SEM 6) mm s-1, P < 0.01) and non-ischaemic (-8.6 (3.4) mm s-1, P < 0.05) myocardium. Peak lengthening rates and the time constant of iso-volumic relaxation (tau) were not affected by alterations in preload. Absolute values of tau failed to distinguish between ischaemia and control. The ischaemia-induced decrease in peak negative dP/dt was preload dependent and caused mainly by a concomitant decrease in peak left ventricular pressure. We conclude that indices derived from segmental lengthening are sensitive to ischaemia and insensitive to preload, in contrast with indices derived from left ventricular pressure. It remains to be determined if monitoring of early segmental lengthening will improve detection and assessment of perioperative myocardial ischaemia.
BJA British Journal of Anaesthesia 04/1996; 76(3):419-27. · 4.24 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: During and after an ischemic injury, maintenance and recovery of cardiac function may critically depend on remote nonischemic myocardium. Graded myocardial ischemia is associated with an approximately 50% increase in stiffness of nonischemic myocardium. We determined whether this increase in stiffness is unique to the ischemic period or persists during reperfusion. Ten anesthetized (isoflurane 1.0% vol/vol) open-chest dogs were instrumented to measure left ventricular pressure and dimensions (sonomicrometry) in ischemic and nonischemic myocardium. Regional chamber stiffness and myocardial stiffness were assessed using the end-diastolic pressure-length relationship which was modified by stepwise infusion and withdrawal of 200 mL of the animals' own blood during baseline, 45 min low flow ischemia (systolic bulge), and 60 min after the onset of reperfusion. In remote nonischemic myocardium, regional myocardial ischemia was associated with a significant (P < 0.05) increase in chamber stiffness (+44%) and myocardial stiffness (+48%). Sixty minutes after the onset of reperfusion, chamber stiffness (+54%, P < 0.05 versus baseline) and myocardial stiffness (+55%, P < 0.05 versus baseline) remained increased. Thus, the ischemia-induced increase in stiffness of remote nonischemic myocardium persists for at least 60 min after reperfusion.
Anesthesia & Analgesia 04/1996; 82(4):695-701. · 3.29 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Platelet-activating factor might be responsible for the alterations of diastolic function observed in different disease states and these potential effects have not been studied. The effect of incremental concentrations of platelet-activating factor (to a maximum of 200 nM) was therefore examined in isolated perfused rat heart. Platelet-activating factor decreased coronary flow rate and contractility in a dose-dependent manner. Although high-dose platelet-activating factor decreased peak -dP/dt compared to baseline, this was not significant when compared to vehicle-administered control. There were no changes in the time constant of left ventricular relaxation and the chamber stiffness constant. These results do not support a major direct role of platelet-activating factor in diastolic dysfunction.
Cardiovascular Research 01/1996; 30(6):1028-32. · 6.06 Impact Factor
