Search PubMed⌕ Search

Biomedical subjects

A Coetzee

Publications and source records attributed to A Coetzee.

At least 19 recordsLinked to original sources
PubMed1995

Comparison of sodium nitroprusside- and esmolol-induced controlled hypotension for functional endoscopic sinus surgery.

The purpose of this study was to compare surgical conditions for functional endoscopic sinus surgery (FESS) under general anaesthesia during controlled induced hypotension, using either sodium nitroprusside (SNP) or esmolol. Twenty patients, assigned to receive either of the drugs as the primary hypotensive agent, were studied. The same surgeon, blinded to the hypotensive agent used and the haemodynamic variables, performed all the operations. The surgeon used a category scale (0-5) to assess surgical conditions--a value of 2-3 being ideal. Patients were positioned in 5 degrees reverse Trendelenburg position and the mean arterial blood pressure (MABP) was reduced in steps of 5 mmHg. The anaesthetist prompted category scale estimations by the surgeon following a change in any of the haemodynamic variables. Average category scale (ACS) values were compared between the two groups for four data groups, i.e., MABP > 65 mmHg (mild), 60-64 mmHg, 55-59 mmHg and 50-54 mmHg. Pre-treatment MABP was 79.8 +/- 10.4 mmHg in the SNP group and 76.1 +/- 6.8 mmHg in the esmolol group. At mild SNP-induced hypotension, surgical conditions were poor (ACS = 3.63 +/- 0.22; mean +/- SEM), while in the esmolol group, ideal surgical conditions (ACS = 2.94 +/- 0.34) were recorded at MABP > 65 mmHg. The combined effects of increased venous drainage due to the reverse Trendelenburg position, hypotension as well as capillary vasoconstriction due to unopposed alpha-adrenergic effect on the mucous membrane vasculature in the esmolol group (as opposed to vasodilatation in the SNP group) probably caused the superior surgical conditions.

Adrenergic beta-Antagonists↗
PubMed1993

Effects of beta-blockers and Ca(2+)-antagonists on the response of the isolated working rat heart to adrenergic stimulants after cardioplegic arrest.

During coronary artery bypass graft (CABG) surgery, patients pretreated with the combination of beta-blocking drugs and Ca2+ antagonists for control of myocardial ischemia often respond inadequately to adrenergic stimulants administered after cardioplegic arrest. In this study, the effects of the combination of a beta-blocker (propranolol) and a Ca2+ antagonist (nifedipine) on the spontaneous recovery, as well as the adrenergic response of the isolated, perfused, working rat heart after a period of cardioplegic arrest were evaluated. After pretreatment of the animals with propranolol and/or nifedipine, hearts were removed, perfused in the presence of pretreatment drugs, subjected to 45 minutes of normothermic cardioplegic arrest, reperfused, and finally stimulated with exponentially increasing concentrations of a sympathomimetic drug. Propranolol, and to a lesser extent nifedipine, protected the hearts during cardioplegic arrest, as indicated by the improved recovery and maximum response to adrenergic stimulation after cardioplegia. Isoprenaline, a beta-stimulant, (at a 100 x higher than conventional concentration), elicited an adequate inotropic and chronotropic response. Stimulation by the alpha, beta-stimulant adrenaline or dobutamine improved only the inotropic response of propranolol and combination treated hearts. Cautious extrapolation of the results to human may suggest continuation of drug therapy of patients before CABG surgery.

Adenine Nucleotides↗
PubMed1993

Enflurane and isoflurane reduce reperfusion dysfunction in the isolated rat heart.

We evaluated the possible cardioprotective effects of enflurane (E) and isoflurane (I) in isolated rat hearts subjected to 40 min normothermic arrest. After reperfusion, hearts were stimulated with adrenaline to evaluate their systolic reserves. In hearts not receiving I or E, adenosine triphosphate (ATP) was reduced from 23.0 +/- 0.8 to 9.3 +/- 1.1 mumol/g dry weight (means +/- SEM; P < 0.001) after arrest. This was associated with a significant reduction in ventricular work (Wt) from 13.6 +/- 0.7 to 1.6 +/- 0.7 mW (P < 0.001). Adrenaline partially restored Wt but not the ATP. E and I given only during normothermic arrest (in the cardioplegic solution) resulted in reductions in ATP similar to the hearts not receiving the drugs. However, on reperfusion and subsequent administration of adrenaline, hearts subjected to the anesthetic drugs performed as well as hearts before arrest. For example, in hearts not exposed to I or E, the Wt after the elective arrest was 1.55 +/- 0.05% (mean +/- SEM) of the pre-arrest value. This was significantly less than hearts exposed to either one of the inhalational agents (40.02 +/- 3.49% of the pre-arrest value; P < 0.0001). Adrenaline improved function in hearts which did not receive I or E to 55.02 +/- 12.80% of the pre-arrest value, but this was significantly less than the Wt performed by the hearts exposed to the anesthetic agents (122.67 +/- 7.78% of pre-arrest value; P < 0.001). This beneficial effect of I and E during reperfusion probably is mediated by the effect of the anesthetic agents on Ca2+ slow channels. The effect could not be ascribed to depression of global myocardial contractile function associated with I and E.

Adenosine Triphosphate↗
PubMed1993

Halothane and the reperfusion injury in the intact animal model.

We studied the effect of halothane on regional myocardial function during acute ischemia and reperfusion in an open-chest pig model. Anesthesia was induced with thiopental and fentanyl and maintained with an intravenous (IV) infusion of pentobarbital and fentanyl. Regional myocardial function was studied with microsonometers placed in the subendocardium supplied by the left anterior descending coronary (LAD) and circumflex coronary artery (LX). Systolic function was evaluated with reference to the end-systolic pressure-length relationship (ESPLR) and regional systolic shortening. Diastolic dysfunction was studied with postsystolic shortening (PSS). Ischemia was induced with 15 min of total occlusion of the LAD artery, and thereafter reperfusion was allowed for 120 min. Five groups were studied: one group received only pentobarbital and fentanyl (n = 10); the other groups received halothane 0.2% (n = 5), 0.4% (n = 7), 0.6% (n = 5), and 0.8% (n = 5). The pentobarbital and fentanyl infusion was adjusted in the halothane groups in an effort to maintain arterial blood pressure and heart rate within specified limits (when possible). Results indicate that regional dysfunction during acute ischemia was equal among all the groups. However, on reperfusion, halothane significantly reduced the incidence of ventricular arrhythmias. Halothane (0.6% and 0.8%) was associated with less regional postischemic systolic dysfunction during reperfusion when compared to the other groups. Hearts subjected to 0.6% and 0.8% halothane also were less stiff at the end of systole (i.e., the extrapolated ventricular volume at zero ventricular pressure was less) after 120 min reperfusion compared to animals receiving less halothane. However, diastolic dysfunction was equal among the groups during reperfusion. We conclude that, in this model, administration of halothane is associated with improved recovery of regional systolic function and potentially beneficial pressure-length relations at the end of systole after acute severe myocardial ischemia and reperfusion. Furthermore, administration of halothane was associated with fewer reperfusion arrhythmias compared to animals not receiving halothane.

Animals↗
PubMed1992

The effects of sevoflurane, halothane, enflurane, and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs.

Inhalational anesthetics produce differential effects on hepatic blood flow and oxygenation that may impact hepatocellular function and drug clearance. In this investigation, the effects of sevoflurane on hepatic blood flow and oxygenation were compared with those of enflurane, halothane, and isoflurane in ten chronically instrumented greyhound dogs. Each dog randomly received enflurane, halothane, isoflurane, and sevoflurane, each at 1.0, 1.5, and 2.0 MAC concentrations. Mean arterial blood pressure and cardiac output decreased in a dose-dependent fashion during all four anesthetics studied. Heart rate increased compared to control during enflurane, isoflurane, and sevoflurane anesthesia and did not change during halothane anesthesia. Hepatic arterial blood flow and portal venous blood flow were measured by chronically implanted electromagnetic flow probes. Hepatic O2 delivery and consumption were calculated after hepatic arterial, portal venous, and hepatic venous blood gas analysis. Hepatic arterial blood flow was maintained with sevoflurane and isoflurane. Halothane and enflurane reduced hepatic arterial blood flow during all anesthetic levels compared to control (P less than 0.05), with marked reductions occurring with 1.5 and 2.0 MAC halothane concomitant with an increase in hepatic arterial vascular resistance. Portal venous blood flow was reduced with isoflurane and sevoflurane at 1.5 and 2.0 MAC. A somewhat greater reduction in portal venous blood flow occurred during 2.0 MAC sevoflurane (P less than 0.05 compared to control and 1.0 MAC values for sevoflurane). Enflurane reduced portal venous blood flow at 1.0, 1.5, and 2.0 MAC compared to control. Halothane produced the greatest reduction in portal venous blood flow (P less than 0.05 compared to sevoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1992

Acute colloid administration increases ischemia in the myocardium supplied by a stenotic coronary artery.

The effect of acute colloid administration was evaluated in the pig heart in which an external coronary artery stenosis was applied. Seven pigs received thiopentone and halothane anesthesia. Ultrasonic crystals were inserted in the myocardium supplied by the left anterior descending (LAD) and circumflex coronary arteries. Left ventricular pressure was measured and regional myocardial function was quantified with the pressure-length loop and the end-systolic pressure-length ratio. A significant stenosis was applied to the LAD artery, after which the animal received fixed colloids to increase the left ventricular end-diastolic pressure. Regional myocardial ischemia was defined with reference to postsystolic shortening and lactate production from the region supplied by the LAD artery. The application of the stenosis caused an increase in postsystolic shortening from 9.62% +/- 4.24% to 26.12% +/- 5.81% (mean +/- SEM; P less than 0.05), and lactate extraction changed from 15.88% +/- 2.38% to -9.56% +/- 5.32% (P less than 0.05). Acute colloid administration increased the left ventricular end-diastolic pressure from 9.71 +/- 1.77 to 15.93 +/- 2.07 mm Hg (P less than 0.05), and lactate extraction further decreased to -76.63% +/- 19.19% (P less than 0.05). Postsystolic shortening increased to 36.22% +/- 5.10% (P less than 0.05). The oxygen tension in the venous blood draining the LAD region decreased from 36.74 +/- 9.37 to 17.34 +/- 1.23 mm Hg (P less than 0.05). We conclude that in the acute pig model, augmentation of the preload worsens regional myocardial ischemia in an area supplied by a stenotic coronary artery.

Animals↗
PubMed1992

Peri-operative mortality in the anaesthetic service at Tygerberg Hospital.

This study reports on the process of peer review of peri-operative mortality at Tygerberg Hospital. The peri-operative mortality rate for the past 3.5 years was 11.9/10,000. The departmental evaluation committee thought that 3.4/10,000 of these deaths were anaesthetic-related. In 2.3/10,000, the anaesthetic contributed to the death of the patient and in 10 cases (total case load = 94,945; i.e. 1.1/10,000) anaesthesia was responsible for the death of the patient. The majority of the peri-operative deaths (8.5/10,000) were caused by a combination of trauma and haemorrhagic shock.

Anesthesia↗
PubMed1991

Oxygenation of cardioplegic solutions: a note of caution.

The merits of oxygenated crystalloid cardioplegic solutions have been well established in experimental animals. The positive effects of oxygenation of Plasmalyte B (Sabax Ltd) and St. Thomas Hospital solution (Plegisol) were achieved by gassing with 95% O2/5% CO2 and 100% O2, respectively. In view of the marked pH differences induced by these gas mixtures, we evaluated the effect of mode of oxygenation on myocardial recovery during reperfusion after hypothermic cardioplegic arrest. Oxygenation with 100% O2 of Plasmalyte B containing high K+ levels caused marked deterioration in myocardial recovery, whereas the mode of oxygenation did not affect recovery after arrest with St. Thomas Hospital solution. Because the major differences between these solutions reside in their respective K+, Mg2+, and HCO3- contents, the effects of variations in the levels of these ions were investigated. The results showed that oxygenation with 100% O2 was deleterious only in the presence of high K+ (29 mmol/L), low Mg2+ (3 mmol/L), and high NaHCO3 (28 mmol/L) levels. The marked decline in mechanical recovery during reperfusion was associated with significant changes in myocardial adenosine triphosphate and intracellular Ca2+ levels. Although an explanation for these findings is not readily available, it is suggested that complex ionic interactions and possibly oxygen free radical generation may lead to intracellular Ca2+ overload, depression in mitochondrial adenosine triphosphate generation, and, hence, deterioration in mechanical recovery.

Acid-Base Equilibrium↗
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↗