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Biomedical subjects

A Coetzee

Publications and source records attributed to A Coetzee.

At least 37 records · Page 2Linked to original sources
PubMed1991

Postsystolic shortening as an index of regional myocardial ischemia in an experimental model.

This study explored the relationship between regional myocardial postsystolic shortening (PSS) and myocardial tissue oxygenation in an open-chested animal model subjected to halothane anesthesia. Regional function was examined with reference to the ventricular pressure-length loop and tissue oxygenation gauged from regional arterial-venous lactate dynamics. Coronary blood flow was decreased in steps by application of an external constriction to the left anterior descending coronary artery. Results indicate that a significant change in PSS (from 7.46% +/- 2.14%, mean +/- SEM to 17.74% +/- 3.31%; P less than 0.00001) was associated with a reduction in coronary blood flow from 81.48 +/- 8.85 to 56.94 +/- 7.12 mL/min/100 g tissue (P less than 0.0012), but lactate extraction across the myocardium did not change (10.54% +/- 3.20% to 12.17% +/- 2.43%). A further reduction in coronary blood flow to 39.84 +/- 5.63 mL/min/100 g resulted in severe PSS (50.62% +/- 6.14%) and lactate production (183.81% +/- 28.80%). The correlation between PSS and lactate production was significant (r = 0.873; SEE = 50.49; P = 0.000001).

Animals↗
PubMed1991

Halothane does have protective properties in the isolated ischemic rat heart.

To determine whether halothane has protective effects on the ischemic heart, the influence of various concentrations (0.5%-1.5%) of halothane on metabolic and functional recovery during reperfusion after 60-min hypothermic (20 degrees C) and 40-min normothermic cardioplegic arrest was determined in the isolated rat heart. Halothane was administered either before and after arrest or intermittently during arrest. Hearts not receiving halothane demonstrated a reduction in adenosine triphosphate (ATP) content from a control value of 20.35 +/- 1.66 mumol/g dry wt (mean +/- SEM) (before arrest) to 9.34 +/- 1.12 mumol/g dry wt at the end of arrest (P less than 0.001). The myocardial ATP content, when measured 20 min after arrest and during reperfusion, remained decreased (9.57 +/- 0.62 mumol/g dry wt). Under these experimental conditions, aortic flow was reduced from 43.62 +/- 2.40 mL/min before arrest to 1.80 +/- 1.80 mL/min 20 min after arrest and during reperfusion (P less than 0.001). The administration of adrenaline after 20 min of reperfusion resulted in partial recovery to 22.01 +/- 8.36 mL/min. Administration of halothane (0.5%) before the cardioplegic period was associated with a reduction of ATP at the end of the normothermic arrest (4.02 +/- 0.38 mumol/g dry wt; P less than 0.01), but the ATP increased significantly (13.45 +/- 0.32 mumol/g dry wt) when measured after the arrest and after 20 min of reperfusion and stimulation with adrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1991

The effect of prostaglandin E1 on acute pulmonary artery hypertension during oleic acid-induced respiratory dysfunction.

This study examined the general effect of intravenous PGE1 on RV Ees and effective PA elastance (EA) during acute pulmonary hypertension associated with oleic acid infusion. In eight pigs, RV end-systolic elastance was quantified with the Ees and Ea was defined with reference to the Windkessel model. Oleic acid infusion increased mean PAP and Ea. Prostaglandin E1 reduced PAP and decreased Ea. Ees did not change throughout the study. Mean arterial pressure was reduced and the pulmonary shunt was increased after PGE1 infusion. The PaO2 was reduced. Data from this study suggest that although PGE1 is effective in reducing PAP, it is not as effective in reducing RV afterload. Furthermore, PGE1 does have significant side effects such as reduction of systemic arterial pressure and an increase in pulmonary shunt.

Acute Disease↗
PubMed1990

[Preoperative special tests and intraoperative arterial oxygen partial pressure during one-lung ventilation].

The value of preoperative lung function tests was examined in 11 patients as a method to predict changes in intraoperative PaO2 (dPaO2) during one-lung ventilation in pulmonary surgery. Ventilation (Kr-81m and Xe-133) and perfusion (Tc-99m microspheres) to the lung to be operated upon significantly predicted the intra-operative decrease in PaO2. The correlation between ventilation percentage to the diseased lung and dPaO2 was 0.87 (SEE = 9.99) and between perfusion and dPaO2 0.84 (SEE = 9.51).

Adult↗
PubMed1990

Preservation of myocardial function and biochemistry after blood and oxygenated crystalloid cardioplegia during cardiac arrest.

We compared the ability of blood cardioplegia and oxygenated crystalloid cardioplegic solutions to maintain regional left ventricle contractility and adenosine triphosphate levels after cardiopulmonary bypass. Ten baboons were subjected to 90-minute cardiopulmonary bypass conducted at 28 degrees C. Hemodynamic measurements were made before and after the bypass procedure, and biopsies for high-energy phosphate determinations were performed at different time intervals during and after bypass. The results showed improved maintenance of myocardial contractility (measured with the regional end-systolic pressure-length relationship) with the oxygenated crystalloid solution. Expressed as a percentage of values before bypass, contractility after bypass averaged 81.69% +/- 4.81% and 80.47% +/- 10.05%, respectively, after 10 and 20 minutes using the oxygenated crystalloid cardioplegia. For blood cardioplegia, the corresponding values were 71.9% +/- 8.73% and 64.99% +/- 8.60% (mean +/- standard error of the mean). The 10- and 20-minute postbypass values between the two groups differed significantly (t test, Welch modification: p = 0.0464 and p = 0.0342). Myocardial adenosine triphosphate level was higher immediately after induction of cardiac arrest when blood cardioplegia was used (blood cardioplegia, 6.82 mol.g wet wt-1; crystalloid cardioplegia, 4.95 mol.g wet wt-1; p = 0.0314), but values subsequently equalized.

Adenosine Triphosphate↗
PubMed1990

Regional myocardial function in the presence of coronary artery stenosis and inotropic intervention: a case for myocardial hibernation?

The aim of this study was to examine the effect of an inotropic intervention on regional myocardial function in the presence of a significant stenosis in a coronary artery. During 0.5% halothane anesthesia, intravenous dobutamine (2.5 and 5 micrograms.kg-1.min-1) was administered to eight pigs. A critical constriction was applied to the left anterior descending (LAD) coronary artery and regional myocardial function was determined with the end-systolic pressure-length relationship in the area of distribution of the LAD and left circumflex coronary artery. Infusion of dobutamine was associated with an increase in the end-systolic pressure-length relationship in the left circumflex coronary artery region from 31.81 +/- 7.87 to 81.03 +/- 21.43 mm Hg.mm-1 (X +/- SEM, P = 0.005), whereas function in the LAD coronary artery region did not change significantly (21.78 +/- 3.97 to 21.97 +/- 6.91 mm Hg.mm-1, P = 0.124). Regional stroke work in the left circumflex coronary artery distribution area increased from 124.38 +/- 24.04 to 222.00 +/- 37.83 mm Hg.mm during the administration of 5 micrograms.kg-1.min-1 dobutamine (P = 0.0125). In the LAD coronary artery area, regional stroke work remained at baseline values. Once the constriction was released, the end-systolic pressure-length relationship in the LAD artery segment increased from 21.97 +/- 2.45 to 35.36 +/- 4.55 mm Hg.mm-1 (P = 0.121). These results suggest that hibernation develops in the myocardial segment supplied by a stenotic coronary artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The oxyhemoglobin dissociation curve before, during and after cardiac surgery.

The oxyhemoglobin dissociation curve was quantified in 15 patients subjected to hypothermic cardiopulmonary bypass under opiate-benzodiazepine anesthesia using the alpha-stat approach to control blood acid-base status. The P50 was calculated from a single measurement of oxygen tension and hemoglobin saturation in blood obtained from the pulmonary artery or the venous line from the cardiopulmonary bypass circuit. In addition, the P50 was directly determined at the registered patient temperature. The P50 decreased from 3.87(+/- 0.15) kPa (mean, SEM) before anesthesia to 1.55(+/- 0.16) kPa during hypothermic (25.43 +/- 1.99 degrees C) cardiopulmonary bypass (p less than 0.001). On rewarming, the P50 increased to 4.89 +/- 0.27 kPa (at 36.14 +/- 0.14 degrees C, p less than 0.001 compared to the preinduction and hypothermic values). Eight hours after cardiopulmonary bypass the P50 returned to the preinduction value (3.72 +/- 0.22 kPa). The relationship between temperature and P50 is described by the regression equation: P50 = 0.22(+/- 0.02).Temperature--3.78(+/- 0.62). The correlation was 0.78 (p less than 0.001). It is concluded that (1) the leftward shift of the oxyhemoglobin dissociation curve during hypothermia may be detrimental to oxygen delivery and (2) the oxygen saturation of the venous blood should not be used indiscriminately to evaluate cellular oxygen status.

Adult↗
PubMed1989

Effect of N2O on segmental left ventricular function and effective arterial elastance in pigs when added to a halothane-fentanyl-pancuronium anesthetic technique.

The interaction of various concentrations of N2O and a stable halothane-fentanyl-pancuronium anesthetic technique was examined in nine pigs. Segmental myocardial contractility was measured with the end-systolic pressure-length relationship (Ees), and the effective arterial elastance (Ea) was quantified based on the Windkessel model. The addition of 30, 50, and 70% N2O did not change myocardial contractility or the effective arterial elastance. During the 30 and 70% N2O challenge, however, arterial capacitance decreased significantly from a mean (+/- SEM) 0.86 +/- 0.15 to 0.71 +/- 0.0.11 mL/mm Hg with 30% N2O (P less than 0.05) and from 0.90 +/- 0.09 to 0.71 +/- 0.07 mL/mm Hg (P less than 0.05) with 70% N2O. A dose-response relationship for the effect on the arterial capacitance could not be demonstrated. We concluded that in the presence of halothane, fentanyl, and pancuronium, N2O does not depress the normal myocardium or change left ventricular afterload. The decrease in arterial capacitance that occurred when 30 and 70% N2O were given was not sufficient to change the effective afterload and appears to be of no importance to normal left ventricular function.

Animals↗
PubMed1989

Effect of various propofol plasma concentrations on regional myocardial contractility and left ventricular afterload.

The cardiovascular effects of propofol infusions, designed to maintain constant plasma concentrations, were examined in an open-chested pig model. Regional myocardial contractility was measured with the end-systolic pressure-length relationship (Ees) and left ventricular afterload quantified by the effective arterial elastance (Ea). The propofol plasma concentrations in this study varied between 0 and 7.73 (SEM 0.96) micrograms/mL. A significant correlation for the increasing propofol plasma concentration and a decrease in myocardial contractility (P = 0.0056) was demonstrated, and the Ea remained constant. This gave rise to a reduction in stroke volume (P = 0.002) and, combined with a decrease in the heart rate (P = 0.0001), led to a reduction in the cardiac output (P = 0.0001). When the propofol infusion was stopped, myocardial contractility did not recover in parallel with the decrease in plasma propofol concentration.

Anesthetics↗
PubMed1988

Oxygen requirements of the isolated rat heart during hypothermic cardioplegia. Effect of oxygenation on metabolic and functional recovery after five hours of arrest.

Previous studies from this laboratory demonstrated that the use of an oxygenated cardioplegic solution in the hypothermic arrested rat heart resulted in improved preservation of high-energy phosphate stores (adenosine triphosphate and creatine phosphate), mechanical recovery during reperfusion, and preservation of myocardial ultrastructure. In the current study the effect of cardioplegic solutions oxygenated with 30%, 60%, and 95% oxygen was evaluated in the isolated rat heart with reference to the maintenance of adenosine triphosphate, creatine phosphate, oxygen consumption, functional recovery, and mitochondrial oxidative phosphorylation in vitro. Results indicate that the hearts receiving cardioplegic solutions supplemented with 95% oxygen and 5% carbon dioxide maintained adenosine triphosphate and creatine phosphate at control values for at least 5 hours. The oxygen consumption during elective cardiac arrest, mechanical performance during reperfusion, and in vitro mitochondrial oxygen uptake and phosphorylation rate were highest in the hearts receiving cardioplegic solutions supplemented with 95% oxygen when compared to solutions with 30% and 60% oxygen. Addition of glucose and insulin to the cardioplegic solution (95% oxygen) increased the adenosine triphosphate levels but failed to improve function after reperfusion. Although myocardial adenosine triphosphate and creatine phosphate were well preserved by the oxygenated cardioplegic solution, there was a discrepancy between the adenosine triphosphate levels at the end of the arrest period, which represents the potential for mechanical function, and the actual function of the hearts after 5 hours.

Adenosine Triphosphate↗
PubMed1987

[The effect of 30% N2O on the general hemodynamics of patients with heart valve lesions].

The effect of 50% N2O on the general haemodynamics of patients with heart valve lesions was evaluated. The addition of N2O to oxygen before cardiopulmonary bypass was associated with a decrease in the cardiac output from 3.60 +/- 0.23 to 3.04 +/- 0.17 l.min-1/m2 (P less than 0.001) although the filling pressure of the left ventricle remained constant and right ventricle preload was increased from 8.18 +/- 0.99 to 9.85 +/- 1.14 mmHg (P less than 0.05). Because the systemic blood pressure fell after N2O was added, the decrease in cardiac output is interpreted as representing a decrease in myocardial contractility. The changes in the inverse relationship between arterial blood pressure and stroke volume also support the concept that N2O suppresses myocardial contractility.

Adolescent↗
PubMed1987

Effect of halothane, enflurane and isoflurane on the end-systolic pressure-length relationship.

Myocardial contractility was measured using the end-systolic pressure-length (ESPL) relationship in dogs subjected to increasing concentrations of halothane (0.5-2 per cent), enflurane (0.77-2.6 per cent) or isoflurane (0.70-2.13 per cent), combined with an infusion 7 micrograms X kg-1 X min-1 of fentanyl, after induction of anaesthesia with 15 mg X kg-1 thiopentone. The relationship between the concentrations of the different drugs and contractility (ESPL) can best be described by ESPL = a + b/(MAC fraction) where "a" is a constant and "b" is the slope of the curve relating ESPL to MAC. At 1.0 MAC values, the ESPL for halothane (69.04 +/- 25.83 mmHg X mm-1) did not differ from that of isoflurane (63.19 +/- 17.36 mmHg X mm-1). However, the myocardial contractility during 1.0 MAC halothane and isoflurane anaesthesia was better preserved than that of enflurane (38.66 +/- 9.73 mmHg X mm-1: p less than 0.01, p less than 0.05 respectively).

Anesthesia, General↗
PubMed1987

Response of the heart to acute hypertension during halothane, enflurane, and isoflurane anesthesia.

In the open chest dog model, the response of the left ventricle exposed to acute mechanical hypertension was evaluated while the animals were receiving various concentrations of halothane, enflurane, and isoflurane. Myocardial contractility was quantified by the end-systolic pressure-length relation (ESPL). When the mean aortic pressure was increased by 40% above the control value for a given concentration of inhalation agent, the end-diastolic volume increased and thereby maintained stroke work. However, as the end-tidal concentrations of the anesthetics increased, this compensatory mechanism became progressively more ineffective as a result of myocardial depression caused by the anesthetics. No evidence could be found of an improvement in myocardial contractility as the aortic pressure was increased. Mild depression of myocardial contractility could be demonstrated for 1.1 MAC halothane, 0.6 MAC enflurane, and 1.0 MAC isoflurane. Severe depression of contractility occurred at 2.3 MAC halothane, 1.2 MAC enflurane, and 1.5 MAC isoflurane.

Acute Disease↗
PubMed1986

Effect of oxygenated crystalloid cardioplegia on the functional and metabolic recovery of the isolated perfused rat heart.

The use of an oxygenated crystalloid cardioplegic solution to improve myocardial preservation during elective cardiac arrest was evaluated with the isolated perfused rat heart used as a model. Experiments were conducted at 4 degrees C and 20 degrees C. The oxygen tension of the nonoxygenated and oxygenated cardioplegic solutions averaged 117 and 440 mm Hg, respectively. At 4 degrees C, the adenosine triphosphate content of hearts subjected to 120 minutes of oxygenated cardioplegia was significantly higher than that of the nonoxygenated cardioplegia group. However, functional recovery during reperfusion was similar for both groups. At 20 degrees C, the myocardial adenosine triphosphate concentration decreased at a significantly faster rate during ischemia in the group receiving nonoxygenated cardioplegia compared with the oxygenated cardioplegia group. Hearts subjected to 180 minutes of ischemia with oxygenated cardioplegia had a normal ultrastructural appearance whereas hearts subjected to 120 minutes of nonoxygenated cardioplegia showed severe ischemic damage. Myocardial functional recovery in the group receiving oxygenated cardioplegia exceeded that of the group receiving nonoxygenated cardioplegia. The use of myocardial adenosine triphosphate concentration at the end of the ischemic period to predict subsequent cardiac output, peak systolic pressure, and total myocardial work showed significant positive correlations.

Adenosine Triphosphate↗