Biomedical subjects

W A Ryder

Publications and source records attributed to W A Ryder.

At least 19 recordsLinked to original sources

PubMed1996

Myocardial ischemia and reperfusion are associated with an increased stiffness of remote nonischemic myocardium.

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.

Animals↗

PubMed1995

The influence of preload on post-systolic shortening in ischaemic myocardium.

Post-systolic shortening is a wall motion abnormality defined as shortening of cardiac muscle after the end of ejection and usually regarded as a manifestation of ischaemia. This study was designed to determine whether changes in preload may alter the magnitude of ischaemia-induced post-systolic shortening. Eleven beagles were anaesthetized (halothane 0.8%) and instrumented for measurement of pressures, flows and dimensions in the apical subendocardium supplied by the left anterior descending coronary artery. Myocardial ischaemia was obtained by tightening a micrometer-controlled snare around the left anterior descending coronary artery. Post-systolic shortening, calculated as end-systolic length minus minimum length divided by end-systolic length, was measured at different levels of preload. Increasing the preload from 4 to 17 mmHg caused a significant reduction in post-systolic shortening (8.9% vs. 12.9%, P < 0.05, Student's paired t-test); post-systolic shortening was negatively correlated with coronary perfusion pressure (r = 0.35, P < 0.01) and positively correlated with systolic bulging. This study demonstrates that the amount of post-systolic shortening depends on the volume status, which therefore has to be taken into account in interpreting regional wall motion abnormalities, such as those detected by echocardiography.

Animals↗

PubMed1994

Post-ischemic diastolic dysfunction.

Though a sustained post-ischemic decrease in contractile function has been clearly established, post-ischemic diastolic function has not been thoroughly investigated. Accordingly, 11 anesthetized (isoflurane 1%) open-chest beagles were instrumented to measure left ventricular pressure and dimensions (circumferential length and wall thickness) in an apicoanterior area supplied by the left anterior descending coronary artery (LAD). Pressure-dimension relations were modified by stepwise infusion and withdrawal of 200 mL of the animals' own blood during baseline, 45 minutes partial occlusion of the LAD (systolic bulging), and 60 minutes after the onset of reperfusion. Stiffness constants were derived from the end-diastolic pressure-length and stress-strain relations, respectively. Myocardial ischemia was associated with significant (P < 0.05) alterations of the following parameters of diastolic function: (1) 47% increase in end-diastolic pressure; (2) 22% decrease in peak negative dP/dt; (3) 9% increase in the time constant of isovolumic relaxation (tau); (4) postcystolic contraction; (5) 6% increase in end-diastolic length and 10% decrease in end-diastolic thickness; (6) 12% increase in unstressed length (creep) and 13% decrease in unstressed thickness; (7) 51% increase in chamber stiffness and a 63% increase in myocardial stiffness; and (8) 40% decrease in the peak lengthening rate. After 60 minutes of reperfusion, only end-diastolic pressure and tau had returned to baseline values whereas systolic shortening fraction, postsystolic contraction, and end-diastolic and unstressed dimensions had only partially recovered. No recovery occurred in peak negative dP/dt, chamber stiffness, myocardial stiffness, and peak lengthening rate. Thus, both myocardial ischemia and reperfusion are associated with complex changes in global and regional left ventricular diastolic function.

Anesthesia, Inhalation↗

PubMed1994

Assessment of cardiorespiratory function using oscillating inert gas forcing signals.

A theoretical model (Hahn et al. J. Appl. Physiol. 75: 1863-1876, 1993) predicts that the amplitudes of the argon and nitrous oxide inspired, end-expired, and mixed expired sinusoids at forcing periods in the range of 2-3 min (frequency 0.3-0.5 min-1) can be used directly to measure airway dead space, lung alveolar volume, and pulmonary blood flow. We tested the ability of this procedure to measure these parameters continuously by feeding monosinusoidal argon and nitrous oxide forcing signals (6 +/- 4% vol/vol) into the inspired airstream of nine anesthetized ventilated dogs. Close agreement was found between single-breath and sinusoid airway dead space measurements (mean difference 15 +/- 6%, 95% confidence limit), N2 washout and sinusoid alveolar volume (mean difference 4 +/- 6%, 95% confidence limit), and thermal dilution and sinusoid pulmonary blood flow (mean difference 12 +/- 11%, 95% confidence limit). The application of 1 kPa positive end-expiratory pressure increased airway dead space by 12% and alveolar volume from 0.8 to 1.1 liters but did not alter pulmonary blood flow, as measured by both the sinusoid and comparator techniques. Our findings show that the noninvasive sinusoid technique can be used to measure cardiorespiratory lung function and allows changes in function to be resolved in 2 min.

Animals↗

PubMed1994

Effect of critical coronary stenosis on regional function of a segment remote from the acute ischemic bed.

BACKGROUND: Limited information is available about the earliest manifestations of ischemia in an area of myocardium supplied by a critically constricted vessel following abrupt occlusion of another vessel. The aim of this study was to describe quantitatively the mechanical behavior of different non-ischemic zones, with and without critical stenosis of the supplying artery. METHODS: Regional myocardial function was measured in 14 open-chest anesthetized dogs, with piezoelectric length and thickness crystals placed within the perfusion beds of the proximal left anterior descending and left circumflex arteries. After baseline recordings, the left circumflex artery was critically constricted and the left anterior descending artery was abruptly occluded for 60 s. The same procedure was repeated after 30 min without stenosis of the artery. After 45 min of recovery, the same protocol was repeated for a narrowed left anterior descending artery. RESULTS: Regional performance was assessed by analyzing the phases of segmental contraction. In the non-ischemic zone, isovolumic shortening and thickening and systolic shortening increased following left anterior descending artery occlusion, whereas, in the presence of critical constriction of the circumflex artery, isovolumic and systolic shortening and thickening did not increase. Occlusion of the left circumflex artery resulted in a significant increase in isovolumic shortening and thickening, ejection shortening, systolic shortening and thickening, whereas, with critical constriction of the left anterior descending artery, the same segment did not exhibit hyperkinesis. CONCLUSIONS: The compensatory potential of the non-ischemic zone seems to be dependent on whether there is restriction to its vascular supply.

Animals↗

PubMed1993

Graded myocardial ischemia is associated with a decrease in diastolic distensibility of the remote nonischemic myocardium in the anesthetized dog.

OBJECTIVES: This study was designed to investigate the changes in regional distensibility of the ischemic segment and of a remote nonischemic segment brought about by graded myocardial ischemia. BACKGROUND: Ventricular distensibility is a major determinant of left ventricular end-diastolic pressure. The effects of graded myocardial ischemia on the regional distensibility of the ischemic area have not been studied. Moreover, there are few data on the effects of myocardial ischemia on the regional distensibility of the nonischemic myocardium. METHODS: Nine anesthetized open chest mongrel dogs were fitted with instruments to measure left ventricular pressure and circumferential length (sonomicrometry) in the ischemic segment and in a nonischemic segment. The pressure-length relation was modified by stepwise infusion and withdrawal of 200 ml of each dog's own blood over 30 min in five consecutive stages of regional ischemia. Unstressed dimensions were obtained by repeated inferior vena cava occlusions. In both segments, regional distensibility was assessed at end-diastole by means of the constants of the pressure-length (chamber stiffness), the pressure-strain and the force-strain (myocardial stiffness) relations. RESULTS: In the ischemic segment, partial and complete coronary occlusions were associated with a twofold increase in the chamber stiffness constant, the pressure-strain constant and the myocardial stiffness constant, whereas in the nonischemic segment the chamber stiffness constant, the pressure-strain constant and the myocardial stiffness constant increased by 50%. CONCLUSIONS: Regional myocardial ischemia is associated with a decrease in distensibility of both the ischemic and the remote nonischemic myocardium.

Analysis of Variance↗

PubMed1993

Regional distensibility, chamber stiffness, and elastic stiffness constant in halothane and propofol anesthesia.

Nine mongrel dogs were acutely instrumented in order to investigate cardiac stiffness at end-diastole while left ventricular circumferential lengths were measured at two different sites (near-apical region and near-basal region). Two hundred mL of autologous blood were infused and then withdrawn to create different volume loading conditions. Four different anesthetic settings were tested: two concentrations (0.7% and 1.7%) of halothane, and two infusion rates (0.2 mg/min/kg, and 0.4 mg/min/kg) of propofol. Three parameters of cardiac stiffness were calculated: distensibility, chamber stiffness (Kp), and elastic stiffness constant (k). Chamber stiffness and elastic stiffness constant were smaller in the apical region than the basal region under halothane anesthesia at both the 0.7% and 1.7% concentrations. There were no regional differences in elastic stiffness constant (k) under propofol anesthesia at either infusion rate. However, Kp was smaller in the apical region at the low propofol infusion rate. There were no significant differences in Kp and k between the anesthetic agents, or with the increase in concentration of either agent. However, when both agent and concentration were taken into consideration, an increase in stiffness was observed with deepening halothane, but not propofol anesthesia. These results show that assessment of diastolic function must take into consideration both regional differences and the anesthetic agent, because the latter may alter such differences and, thus, alter diastolic function.

Anesthesia, Inhalation↗

PubMed1993

Nitrous oxide causes myocardial ischemia when added to propofol in the compromised canine myocardium.

We sought to determine the influence of nitrous oxide on the compromised heart during propofol anesthesia. This study investigated the cardiovascular effects of the combination propofol and nitrous oxide (N2O). Seven beagles were monitored to measure global and regional left ventricular function. Recordings both before and after critical constriction (CC) of the left anterior descending coronary artery (LAD) were performed after propofol, 300 micrograms.kg-1.min-1, and 10 min after exposure to and discontinuation of 67% N2O. Data were analyzed with ANOVA for repeated measures at 95% confidence level. In the absence of CC, N2O caused moderate, reversible hemodynamic depression (LVdP/dtmax, -13.8%; cardiac output, -17.2%; LAD coronary blood flow, -10.9%) and no regional dysfunction. After CC global hemodynamic depression was of similar magnitude (LVdP/dtmax, -19.9%; cardiac output, -9.2%; stroke volume, -9.2%) but did not recover completely. Systolic shortening in the compromised area decreased (-30.3%) and postsystolic shortening developed to represent 20.3% of total shortening. Despite only moderate hemodynamic depression, 67% N2O causes substantial regional dysfunction in compromised myocardium when added to propofol.

Anesthesia, Intravenous↗

PubMed1993

Effect of isoflurane and halothane on regional cardiac stiffness.

To investigate the possibility of regional differences in cardiac stiffness which may relate to the known regional differences in systolic left ventricular function, seven mongrel dogs were acutely instrumented and regional cardiac stiffness was measured at both apical and basal region under two different concentrations of isoflurane (1.08% and 1.9%) as well as equipotent concentrations of halothane (0.9% and 1.58%). Cardiac stiffness was determined in terms of distensibility, chamber stiffness (derived from pressure-length relationships), and an elastic stiffness constant (derived from stress-strain relationships). Regional differences in cardiac stiffness were observed for all three indices and for each anaesthetic setting except for the elastic stiffness constant under 1.9% of isoflurane. The data indicate that regional differences in cardiac stiffness exist between the apex and the base of the heart. These regional differences do not depend on the anaesthetic agent or its concentration and may contribute to the differences in systolic function.

Anesthesia, Inhalation↗

PubMed1992

Effect of graded infusion rates of propofol on regional and global left ventricular function in the dog.

We have studied the effects of graded infusion rates of propofol (0.2-0.5 mg kg-1 min-1) on left ventricular global and regional function, in eight acutely instrumented dogs. Global function was assessed by measurement of aortic and left ventricular pressure, LV dP/dtmax, aortic blood acceleration and stroke volume. Regional function was assessed by measurement of systolic shortening and the end-systolic pressure-length relationship. The response of the coronary circulation to short periods of occlusion was also assessed. Administration of propofol significantly reduced left ventricular preload, as indicated by reductions in end-diastolic pressure and length; contractility was depressed, the depression being greater in the apex than in the base of the left ventricle. High infusion rates impaired relaxation. Regulation of coronary blood flow was not disrupted. Reductions in preload and contractility contributed to the propofol-induced hypotension. After 60 min, recovery from the greatest infusion rate was incomplete.

Animals↗

PubMed1992

Effects of progressive myocardial ischaemia on systolic function, diastolic dysfunction, and load dependent relaxation.

OBJECTIVE: The aims were to determine (1) the relationship between changes in contractile function (systolic shortening) and the appearance of diastolic dysfunction (postsystolic shortening) during progressive regional left ventricular ischaemia; (2) the effects of increased afterload (acute constriction of the descending thoracic aorta) on ischaemic contractile dysfunction; and (3) the effects of loading during ischaemia on load dependent relaxation. METHODS: Regional myocardial function, using sonomicrometry, was measured in the short and long axes of the apex of the left ventricle of eight open chest anaesthetised dogs (16-20 kg). Progressive apical ischaemia was induced by graded reductions in left anterior descending coronary artery flow (critical constriction, ischaemia 1, ischaemia 2, total coronary occlusion, and postocclusive maximum reactive hyperaemia). Acute afterloading was induced by a snare placed around the descending aorta. RESULTS: Consistent decreases in systolic shortening and increases in postsystolic shortening relative to the total segmental shortening in the short axis of the apical region were seen with worsening ischaemia. Aortic constriction increased the magnitude of apical postsystolic shortening and decreased apical systolic shortening in the short axis during critical constriction, ischaemia 1, and ischaemia 2. Long axis function changed in a qualitatively similar but quantitatively different manner. There was a significant decrease in the load dependency of relaxation with total coronary occlusion. CONCLUSIONS: (1) Changes in systolic and diastolic function occurred concomitantly as mild regional myocardial ischaemia developed and intensified; (2) afterloading significantly worsened regional systolic and diastolic dysfunction during mild ischaemia; and (3) progression of regional ischaemia resulted in loss of load dependent relaxation.

Animals↗

PubMed1992

Regional interaction and its effect on patterns of myocardial segmental shortening and lengthening during different models of asynchronous contraction in the dog.

OBJECTIVE: The aim was to examine the effect of asynchrony and regional myocardial interaction on the pattern of segmental contraction and relaxation. METHODS: Three models of asynchrony were produced. Firstly the left anterior descending artery was abruptly occluded for 60 s. Secondly, the same artery was gradually occluded to produce four degrees of ischaemia based on the severity of the mechanical dysfunction. Finally, asynchrony was created by infusing isoprenaline (0.04 microgram.ml-1) into the left circumflex artery. Twelve anaesthetised beagles, weighing 16-21 kg, were used for the study. RESULTS: The patterns of contraction and relaxation were characterised by analysing the phases of shortening and lengthening, the peak lengthening rate (dL/dt), and the timing from the onset of systole to minimum systolic length. A consistent pattern of shortening and lengthening was evident during all three models of asynchrony. There were reciprocal relations between the extent of isovolumetric shortening in the normal segment and in the abnormal segment, and on occasion between the extent of isovolumetric shortening in the normal segment and the extent of isovolumetric lengthening in the same segment. Normal segments that showed minimal shortening or even some lengthening during isovolumetric systole tended to shorten beyond ejection, while segments that shortened significantly during isovolumetric contraction, lengthened earlier. Despite no change in isovolumetric shortening, segments also shortened after ejection when the opposite segment lengthened in late systole and early diastole. CONCLUSIONS: The pattern of shortening and lengthening depends on the path of contraction or on its entire loading pattern throughout systole. It is also possible that during early isovolumetric systole a segment can either be unloaded or preloaded by an opposing segment.

Animals↗

PubMed1992

Femoral arteriovenous extracorporeal carbon dioxide elimination using low blood flow.

BACKGROUND AND METHODS: Conventional extracorporeal CO2 removal systems require blood flow rates of 1 to 2.5 L/min in the extracorporeal circuit. We hypothesized that standard hemofiltration equipment can be combined with a high-performance extracorporeal lung to achieve high rates of CO2 removal at lower blood flow rates. To test this hypothesis, we performed experiments on nine sheep to examine the extent to which CO2 elimination can be achieved at blood flow rates less than 600 mL/min using a 5-m2 hollow fiber membrane lung with countercurrent gas flow, combined with a hemofiltration blood pump, and connected to femoral arterial and venous hemodialysis catheters. RESULTS: CO2 eliminations of 130 to 180 mL/min at standard temperature and pressure were achieved with blood flow rates in the range 470 to 600 mL/min. With a pumpless artery-to-vein shunt, up to 90 mL/min of CO2 at standard temperature and pressure was eliminated. However, in this mode, the resistance of the access catheters and tubing was the main factor limiting CO2 elimination. CONCLUSIONS: Standard hemofiltration equipment may be combined with a hollow fiber membrane lung to remove the equivalent of a high proportion of the basal metabolic CO2 production of an adult human at low blood flow rates. Use of this technology would bring extracorporeal CO2 removal within the budget and capability of more ICUs.

Animals↗

PubMed1991

Dose-related effects of isoflurane associated with low plasma concentrations of verapamil on global and regional function in normal and compromised canine myocardium.

Global and regional myocardial functions were studied in seven open-chest dogs with constant low plasma concentrations of verapamil as increasing concentrations of isoflurane (0.75, 1, 1.5 MAC) were administered in the presence of normal myocardial perfusion and after application of critical constriction of the left anterior descending coronary artery. In the presence of verapamil, increases in isoflurane concentrations caused dose-dependent myocardial depression both before and after critical coronary constriction. The systemic and coronary vasodilatation associated with high concentrations of isoflurane did not occur in the presence of verapamil. The association of verapamil with isoflurane caused regional myocardial dysfunction that worsened at high isoflurane concentrations. This regional dysfunction could not be antagonized in two dogs. The effects of isoflurane on regional function were not modified by application of a critical coronary constriction.

Animals↗

PubMed1989

Effects of halothane on left ventricular relaxation and early diastolic coronary blood flow in the dog.

The effects of graded concentrations of halothane on left ventricular relaxation and phasic coronary blood flow (CBF) were studied in six open-chest, anesthetized dogs. Global and regional left ventricular function were measured. Besides the expected dose-dependent depression of contractility, regional shortening, and cardiac output, halothane caused significant increases in the time constant of relaxation (Trelax), and decreased and delayed the nadir of peak negative left ventricular dP/dt. Dose-dependent reductions of CBF were noted. Percentage CBF during isovolumic relaxation was significantly reduced and showed a strong inverse correlation with Trelax. Halothane appears to interfere with the inactivation process of the heart; this in turn may impede the early rise in CBF during isovolumic relaxation.

Animals↗

PubMed1988

Effects of lignocaine and bupivacaine on regional myocardial function and coronary blood flow in anaesthetized dogs.

Empirical i.v. doses of lignocaine or bupivacaine of equal local anaesthetic potency were administered to halothane-anaesthetized dogs. Both local anaesthetics caused the expected depression of global haemodynamic function. Regional myocardial systolic shortening was depressed similarly by both agents. Regional myocardial dysfunction, seen as post-systolic shortening, occurred to a similar extent with both lignocaine and bupivacaine. Coronary blood flow and coronary perfusion pressure were significantly correlated during the administration of lignocaine; bupivacaine had erratic effects on coronary blood flow and no correlation between coronary blood flow and coronary perfusion pressure was seen. These results suggest that regional myocardial dysfunction occurs with both local anaesthetics and does not account for the apparent increased cardiotoxicity of bupivacaine. Bupivacaine did, however, cause wider individual variations compared with lignocaine with respect to coronary blood flow.

Anesthesia, General↗

PubMed1988

Isoflurane and large coronary artery haemodynamics. A study in dogs.

In the dog, stepped increases in isoflurane concentration (up to 1.5 MAC) caused peripheral and coronary vasodilatation. In the presence of significant decreases in arterial pressure (-35%), contractility (-46%), cardiac output (-17%) and coronary perfusion pressure (-40%), coronary blood flow remained unchanged, while the effective coronary vascular resistance was halved. The coronary reserve, estimated by the hyperaemic response to short periods (10 s) of coronary occlusion was reduced by the stepped increases in isoflurane concentration. Linear relationships were observed between peak hyperaemic flow, volume repayment, repayment: deficit ratio and coronary perfusion pressure. The vasodilation induced by isoflurane was of such magnitude that, at 1.5 MAC, the repayment: deficit ratio was close to unity, indicating that the vasodilatory reserve was almost exhausted.

Anesthesia, Inhalation↗

PubMed1988

Intravenous diltiazem worsens regional function in compromised myocardium.

The effect of intravenous diltiazem on regional myocardial function was assessed in a canine model of critical constriction of the left anterior descending coronary artery (LAD). Maintenance anesthesia with fentanyl (1.5 micrograms.kg-1.min-1), 60% inspired nitrous oxide, and 0.7% inspired halothane resulted in regional dysfunction, measured as postsystolic shortening (20.6 +/- 10.7%), which was significantly worsened after 0.1 mg/kg (48.7 +/- 12.5%, P less than 0.05) and after 0.2 mg/kg (68.8 +/- 11.7%, P less than 0.05) intravenous diltiazem. Systolic shortening in the compromised LAD territory was substantially depressed after 0.1 mg/kg diltiazem (8.2 +/- 0.6% to 5.3 +/- 1.3%, P less than 0.05) and was essentially abolished after 0.2 mg/kg diltiazem (8.2 +/- 0.6% to 0.7 +/- 2.3%, P less than 0.05). At the higher dose of diltiazem, cardiac output was substantially decreased (1.37 +/- 0.23 L/min to 0.88 +/- 0.30 L/min, P less than 0.05) and LV dP/dtmax significantly depressed (1090 +/- 90 mm Hg/sec to 744 +/- 80 mm Hg/sec, P less than 0.05). These results demonstrate significant depression of regional systolic shortening and substantial worsening of regional dysfunction in myocardium with a compromised blood supply, in association with significant depression of left ventricular performance, with intravenous diltiazem administration during anesthesia.

Anesthesia, Inhalation↗