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Biomedical subjects

W A Ryder

Publications and source records attributed to W A Ryder.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1988

Gradual or abrupt nitrous oxide administration in a canine model of critical coronary stenosis induces regional myocardial dysfunction that is worsened by halothane.

The existence of a dose-response relation between nitrous oxide concentration and regional dysfunction in compromised myocardium, and whether or not halothane-induced myocardial depression alleviated this regional dysfunction was examined. Nitrous oxide was administered to eight dogs with experimentally induced left anterior descending coronary artery (LAD) critical stenosis during fentanyl (100 micrograms/kg bolus plus 1.5 micrograms.kg-1.min-1) anesthesia. Two modes of nitrous oxide administration were employed: gradual (in steps of 20% inspired, i.e., 0%, 20%, 40%, and 60% inspired) and abrupt (0-60% inspired). Regional myocardial function was assessed by sonomicrometry. Regional dysfunction in the compromised myocardium, in the form of postsystolic shortening (PSS), increased above baseline levels during 40% (4.2 +/- 2.3% to 12.1 +/- 3.9%, P less than 0.05) and 60% (4.2 +/- 2.3% to 12.5 +/- 3.6%, P less than 0.05) inspired nitrous oxide (gradual administration) and also during abrupt 60% nitrous oxide administration (6.4 +/- 2.6% to 9.9 +/- 3.2%, P less than 0.05). After abrupt 60% inspired nitrous oxide administration, halothane (0.7% inspired) was introduced and caused decreases in mean arterial pressure (106.1 +/- 4.5 mm Hg to 76.2 +/- 5.5 mm Hg, P less than 0.05) and peak LV dP/dt (1700 +/- 150 mm Hg/sec to 1100 +/- 100 mm Hg/sec, P less than 0.05). Halothane caused a marked increase in PSS (9.9 +/- 3.2% to 30.8 +/- 12.6%, P less than 0.05). Thus nitrous oxide administration caused regional dysfunction in myocardium supplied by a critically narrowed LAD whether administered gradually or abruptly and at concentrations as low as 40% inspired.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Differences in ischaemic dysfunction after gradual and abrupt coronary occlusion: effects on isovolumic relaxation.

The effects of both gradual and abrupt coronary occlusion on regional wall function (sonomicrometry) and left ventricular relaxation were studied in the intact dog heart. The ischaemic dysfunction observed in the two interventions as assessed by pressure-length loops showed considerably different patterns. The regional ischaemia after abrupt occlusion of the left anterior descending coronary artery was characterised by a bulge during isovolumic relaxation in contrast to the pattern observed during gradual occlusion, which was characterised chiefly by early systolic lengthening and post-systolic shortening. The effect of regional dysfunction on left ventricular relaxation was evaluated using peak negative dP/dt and tau, the time constant of isovolumic pressure decline. Abrupt occlusion had a more profound effect on relaxation than did gradual occlusion, though there were no significant changes in either pressure or flow derived indices of systolic ventricular function with abrupt occlusion of the left anterior descending artery. Two distinct patterns of regional dysfunction were produced at zero coronary flow depending on the time course of the occlusion. The regional dysfunction observed during abrupt occlusion may in part be explained by the mechanical effect of abrupt cessation of coronary flow, which in turn influences relaxation. With gradual occlusion tau was less affected even though substantial regional dysfunction was observed. This may reflect the development of collateral flow. Thus the patterns of regional dysfunction and ventricular relaxation depend on the time course of ischaemia.

Animals↗
PubMed1987

The association isoflurane-verapamil causes regional left-ventricular dyssynchrony in the dog.

In ten dogs anesthetized with 1% inspired isoflurane, the effect of low-dose verapamil on global and regional myocardial function was studied. The administration of verapamil resulted in no change in heart rate or blood pressure, but left ventricular stroke work, peak power, LV dP/dt max, and aortic blood acceleration were significantly reduced, while coronary blood flow remained unchanged. End-diastolic length increased in territory supplied by both left anterior descending (LAD) and left circumflex (LC) artery, but a significant decrease in systolic shortening occurred in the LAD segment only. Dyssynchrony of wall motion, characterized by post-systolic shortening, accompanied in three animals by a small amount of systolic lengthening, appeared with the administration of verapamil and was more pronounced in the LAD segment. Such patterns of wall motion have usually been attributed to myocardial ischemia. In the absence of significant reduction in coronary blood flow, and in the presence of a delay in onset of shortening and lengthening, these patterns of wall motion are more likely to reflect dyssynchrony of regional function than ischemia.

Anesthesia, Inhalation↗
PubMed1986

Hysteresis of left ventricular end ejection pressure-dimension relations after acute pressure loading in the intact canine heart.

The left ventricular end systolic pressure-volume relation of the isolated canine heart is linear and independent of the loading conditions. The effects of acute pressure loading on the left ventricular end ejection pressure-length relations were studied in the intact canine heart. The lengths of two wall segments of the left ventricle parallel to the minor axis were measured with pairs of miniature piezoelectric crystals. At two levels of filling pressure, with and without control of heart rate, acute increases in left ventricular afterload were produced for six successive beats by occluding the thoracic aorta. After abrupt release of this occlusion, at left ventricular end diastolic pressure less than 10 mmHg, end ejection lengths were longer than before the occlusion for both segments despite the same or lower end ejection pressures. When heart rate was not controlled the mean(SD) difference in end ejection length was 0.46(0.21) mm (n = 100). When heart rate was controlled by atrial pacing after autonomic blockade the difference was 0.37(0.11) mm (n = 80). In contrast, at left ventricular end diastolic pressure greater than 10 mmHg there was no significant difference between end ejection lengths before and after release of the aortic occlusion. Gradual release of the aortic occlusion over 4-5 beats produced clockwise hysteresis of the left ventricular end ejection pressure-length relation when left ventricular end diastolic pressure was less than 10 mmHg. No hysteresis occurred when left ventricular end diastolic pressure was greater than 10 mmHg. Hysteresis of the end systolic pressure-dimension relation was also seen when major and minor axis dimensions of the left ventricular were measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Regional and global myocardial function in the dog when nitrous oxide is added to halothane in the presence of critical coronary artery constriction.

The effect of substituting 66% nitrous oxide for nitrogen on global and regional myocardial function before and after critical constriction of the left anterior descending coronary artery (LAD) was studied in six open-chested dogs anesthetized with 1% halothane (inspired). Regional myocardial function was measured in the region of the LAD and in the region of the left circumflex artery using sonomicrometry, and LAD blood flow was measured. Administration of nitrous oxide produced moderate depression of global performance. Regional shortening in both myocardial segments was reduced, and dysfunction also appeared in the LAD segment. This dysfunction was observed in the presence of both normal coronary blood flow, and after critical constriction. The appearance of dysfunction when coronary blood flow was unimpaired suggests that ischemia may not be the only cause of regional myocardial dysfunction.

Animals↗
PubMed1985

Postsystolic shortening of canine left ventricle supplied by a stenotic coronary artery when nitrous oxide is added in the presence of narcotics.

The effects of fentanyl and sufentanil with and without N2O on left ventricular myocardium supplied by a critically narrowed and a normal coronary artery were studied in 16 dogs. Regional ventricular function was measured by recording ventricular segment length with the use of ultrasonic length detectors in the left anterior descending (LAD) and the left circumflex (LC) coronary artery territories before and during critical stenosis of the LAD. Critical stenosis was documented by the absence of a hyperemic response following a 10-s total occlusion of the LAD. Hemodynamic variables (aortic flow and pressure, left ventricular pressure, heart rate, and coronary blood flow) were measured and the first derivative of left ventricular pressure (LVdP/dt) and coronary perfusion pressure derived. Eight dogs received fentanyl 100 micrograms X kg-1 followed by an infusion of 1 microgram X kg-1 X min-1 while ventilated with O2:N2 (1:2), and eight dogs received sufentanil 30 micrograms X kg-1 with an infusion of 0.3 micrograms X kg-1 X min-1. Replacement of N2 with N2O produced evidence of mild systolic myocardial depression but no dysfunction in either group. After application of the critical constriction, the addition of N2O rapidly produced evidence of dysfunction with significant postsystolic shortening only in the LAD territory. This was not accompanied by hypotension or a decrease in coronary flow and was not always reversible. Higher infusion rates of either narcotic (fentanyl 2 micrograms X kg-1 X min-1, 4 micrograms X kg-1 X min-1; sufentanil 0.6 micrograms X kg-1 X min-1, 1.2 micrograms X kg-1 X min-1) in the absence of N2O did not produce dysfunction but had no protective effect when N2O was added.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1985

Effects of dopamine and dobutamine on the distribution of pulmonary blood flow during lobar ventilation hypoxia and lobar collapse in dogs.

Hypoxic pulmonary vasoconstriction was induced in the left lower lobe of fifteen dogs by ventilating the lobe with 7% O2 or by absorption collapse, and the distribution of flow between the lobe and the remainder of the lung was measured with electromagnetic flow probes. The lobar to total blood flow ratio was reduced by lobar ventilation hypoxia and decreased further during lobar collapse. In seven dogs, an infusion of 20 micrograms kg-1 min-1 of dopamine produced an increase in total blood flow, an increase in pulmonary artery pressure (P less than 0.01), and an increase in lobar to total flow ratio (P less than 0.05) during both hypoxic states. There was a significant fall in arterial PO2 (P less than 0.01) during ventilation hypoxia. Similar changes in total and lobar to total flow ratio (P less than 0.01) were observed in eight dogs given 20 micrograms kg-1 min-1 of dobutamine, but there were no changes in pulmonary artery pressure. The greater increase in total flow (+ 111%) resulted in a marked increase in mixed venous PO2 and no significant changes in arterial PO2 in this group of dogs. It is concluded that both drugs produce an increase in lobar to total blood flow ratio and shunt fraction, but that the mechanisms causing the redistribution of flow may differ.

Animals↗
PubMed1981

Interactions of adrenergic beta-receptor blockade (oxprenolol) and PCO2 in the anaesthetized dog: influence of intrinsic beta-sympathomimetic activity.

Effects of change in PaCO2 on systemic and coronary haemodynamics and on coronary sinus blood-gases have been studied in 10 open-chested dogs in which the lungs were ventilated with 0.8% halothane in oxygen, before and after administration of oxprenolol 0.3 mg kg-1 i.v. The hyperdynamic response of the circulation to hypercapnia was only marginally reduced after oxprenolol (cardiac output increased by 10% as opposed to 16% before oxprenolol). Before and after oxprenolol, hypocapnia caused large reductions of coronary blood flow (--24% and --20% respectively), while hypercapnia caused large increases of coronary blood flow (+ 59% and + 34% respectively). Oxprenolol does not appear to modify significantly the circulatory response to arterial carbon tension.

Anesthesia, General↗
PubMed1981

Regional ischemic ventricular dysfunction in myocardium supplied by a narrowed coronary artery with increasing halothane concentration in the dog.

The effects of increasing inspired halothane concentration (0.5, 1.0, 1.5, 2.0 per cent) upon left ventricular myocardium supplied by a critically narrowed coronary artery and a normal coronary artery were studied in 11 open-chested dogs. Regional ventricular function was measured by continuous recording of ventricular segment length using pairs of implanted miniature ultrasonic length detectors in the left anterior descending coronary artery (LAD) and left circumflex coronary artery (LC) territories before and during critical stenosis of the LAD by a micrometer-controlled snare. Critical narrowing was documented by ischemic regional ventricular function (i.e., post-systolic shortening; systolic lengthening) limited to the LAD territory when FIO2 = 0 for 90 seconds. Hemodynamic variables (aortic, left atrial and left ventricular pressure, and heart rate) were measured, ECG lead II was recorded, and the first derivative of left ventricular pressure (LV dP/dt) and coronary perfusion pressure derived for each halothane concentration before and during LAD narrowing. Increasing halothane was associated with equivalent progressive depression of global ventricular function before and during LAD constriction. Prior to LAD constriction, no ischemic changes in regional function occurred. Regional ventricular function was normal during 0.5 percent halothane in the presence of LAD constriction. With increasing halothane during LAD constriction, ischemic regional ventricular function was observed in the LAD territory in eight of eleven hearts, whereas regional ventricular function remained normal in the LC territory. The epicardial ECG was recorded in three dogs and was insensitive as an indicator of ischemia, becoming abnormal only after severe ischemic changes were established. In these studies, in which heart rate remained constant, arterial blood pressure and LV dP/dt decreased, and left ventricular end-diastolic pressure increased, decrease in blood flow and oxygen delivery due to a lower perfusion pressure distal to the coronary artery narrowing appears to be primarily responsible for the observations. The authors hypothesize that clinically unapparent episodes of regional myocardial ischemia distal to narrowed coronary arteries may be an important cause of perioperative myocardial infarction.

Animals↗
PubMed1980

A comparison of carbon dioxide titration curves of arterial mixed venous and coronary sinus blood.

Two types of titration curve (log PCO2 vs. pH and whole blood [HCO3-] vs. pH) were obtained in anaesthetized dogs by altering FICO2. Both plots reveal a significant progressive decrease in slope from arterial(a) to mixed venous (v) to coronary sinus (cs) blood. Lines drawn between corresponding points on the arterial and mixed venous or coronary sinus curves have slopes determined by the Respiratory Exchange Ratio (R) and are called R lines. Differences in slope between arterial and venous (v or cs) curves may be due to changes in blood flow or of delivery of CO2 to the blood. The former is indicated by constant R values at different CO2 tensions whilst the latter is a reflection of changing R values due to fluctuations in CO2 stores. The myocardium is not an important store for CO2 but CO2 has a profound effect on coronary blood flow and it is this that causes the difference in a-cs slopes. The reverse is true for skeletal muscle where the charging and discharging of CO2 stores brings about the difference in a-v slopes.

Acid-Base Equilibrium↗
PubMed1979

Continuous measurement of blood gases in vivo by mass spectrometry.

Continuous analysis of oxygen and carbon dioxide tension in the blood phase, over periods of 4-5 h, was carried out in the pulmonary artery (93 determinations in six anesthetized dogs) and in the aorta (29 determinations in four anaesthetized dogs). Silastic-covered stainless steel catheters attached to a mass spectrometer were used. The mass spectrometer signals were linearly related to the blood-gas tensions measured by conventional analysis. The mass spectrometer signals were calibrated in vivo by exposing the animals to high and low oxygen and carbon dioxide tension. With such in vivo calibration the slopes of the straight line regressions for mass spectrometer PO2 or PCO2 on PO2 or PCO2 by conventional analysis were comprised between 0.944 and 1.031 while the standard error of the slopes were between 0.019 and 0.031. Deliberate reductions of cardiac output had little effect on the mass spectrometer readings.

Animals↗
PubMed1976

Interaction of anesthesia, beta-receptor blockade, and blood loss in dogs with induced myocardial infarction.

The cardiovascular effects of halothane-nitrous oxide anesthesia, and beta-receptor blockade with either propranolol or practolol, were studied in 15 dogs in which severe myocardial infarction had been induced ten days earlier. The hemodynamic responses to blood loss amounting to 25 per cent of estimated blood volume, and its subsequent replacement, were studied before and after induction of beta-receptor blockade. In terms of cardiac output and aortic blood flow acceleration, cardiac performance in the absence of beta-blockade was markedly impaired during steady-state anesthesia, compared with corresponding values in normal dogs. Practolol (2.0 mg/kg) administered during anesthesia induced no significant circulatory change other than a 14 per cent decrease in heart rate and a 25 per cent increase in strode volum. Propranolol (0.3 mg/kg) caused a comparable reduction of heart rate, but significantly reduced cardiac output (-27 per cent), aortic blood flow acceleration (-26 per cent), and peak LV power (-19 per cent), and increased systemic vascular resistance (+49 per cent). The two drugs caused comparable shifts of the isoproterenol dose-response curve during anesthesia. Graduated blood loss during anesthesia, to a total of 25 per cent of blood volume, caused consistent circulatory changes (decreased mean arterial pressure cardiac output, peak LV power, LV minute work) that were essentially similar before and after beta-receptor blockade with either propranolol or practolol. The positive inotropic effect of calcium gluconate during halothane anesthesia was significantly reduced following either propranolol or practolol, but the hemodynamic responses to changes of systemic vascular resistance induced with acetylcholine or phenylephrine were not modified by beta-receptor blockade.

Acetylcholine↗