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Biomedical subjects

C D Mazer

Publications and source records attributed to C D Mazer.

12 recordsLinked to original sources
PubMed1992

Effect of warm heart surgery on perioperative management of patients undergoing urgent cardiac surgery.

The anesthetic management and outcome data were examined in a retrospective case-controlled study that compared a conventional hypothermic cardioplegic technique with the recently described method of warm heart surgery, in patients undergoing urgent cardiac surgery. Hypothermic continuous oxygenated blood crystalloid cardioplegia with systemic hypothermia was used for 37 patients who underwent cardiac surgery by the same surgeon over a 16-month period from July 1986 (group 1), whereas normothermic continuous oxygenated blood crystalloid cardioplegia with systemic normothermia was used on 56 patients over the following 16-month period until March 1990 (group 2). The groups were similar in terms of age, sex, ASA status, NYHA classification, and preoperative left ventricular function. Defibrillation following cardiopulmonary bypass was required in only 3.6% of the warm heart surgery patients (group 2) compared with 83.8% in group 1 (P less than 0.0001), and use of warm heart surgery (group 2) eliminated the need for rewarming. There was a trend towards a reduced incidence of myocardial infarction (19% in group 1 vs 9% in group 2), low cardiac output syndrome (40% vs 29%), and use of the intraaortic balloon pump (16% vs 9%) in warm heart surgery patients, but these differences did not reach statistical significance. There were no differences between the two groups in terms of anesthetic drug usage, total heparin or protamine doses, blood loss, transfusion requirements, or duration of ICU stay.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1991

Evaluation of a "do not resuscitate" policy in intensive care.

The decision to withhold cardiopulmonary resuscitation from a patient within an intensive care unit (ICU) may be a difficult but appropriate one for which there are few guidelines. We describe the formulation of a Do Not Resuscitate (DNR) policy in our multidisciplinary ICU. To evaluate the effect of implementation of the DNR policy on physician practice and on communication among physicians, nurses, patients and their families, we interviewed physicians and nurses caring for patients designated DNR before (n = 8) and after (n = 17) implementation of the DNR policy. We found that DNR orders in the ICU were not infrequent (2-3 per week). All patients designated DNR were either irreversibly ill or not responsive to maximal therapy, and 22 of 25 were not competent. The DNR order was not accompanied by withdrawal of other therapy in 50% of cases and one patient recovered and was discharged from hospital. The implementation of the DNR policy encouraged greater physician consultation with other physicians, patients and their families. Although there were differences in perception of communication between physicians and nurses, we believe that the DNR policy influenced physician practice and enhanced overall communication in the ICU.

Age Factors↗
PubMed1991

Effects of nitrous oxide on coronary pressure and regional contractile function in experimental myocardial ischemia.

To determine whether nitrous oxide (N2O) worsens myocardial ischemia by diminishing coronary pressure, we performed two sets of experiments using an acutely instrumented swine model of regional coronary ischemia. In constant pressure experiments (n = 11), coronary pressure and heart rate were kept constant as N2O (77%-79%) was substituted for N2 in the inspired gas. Nitrous oxide decreased systolic shortening, measured by sonomicrometry, from 68.0% to 63.6% (P less than 0.05) of preischemic control values in the ischemic zone and from 116.2% to 103.2% (P less than 0.05) of control values in the adjacent normal myocardium. There was no disproportionate effect of N2O on ischemic myocardium, and the N2O-induced depression of contractile function was fully reversible. In a series of constant external stenosis experiments (n = 13), the effects of N2O on heart rate, mean arterial pressure, and the coronary stenosis itself were not controlled. In these experiments, substitution of N2O for N2 induced deterioration in both the ischemic zone (systolic shortening decreased from 68.7% to 58.4% of preischemic control values, P less than 0.05) and in the adjacent normal myocardium (systolic shortening decreased from 113% to 102.9% of preischemic control, P less than 0.05). Nitrous-oxide-induced ischemic zone contractile dysfunction was often not reversible. The pressure gradient across the coronary stenosis did not increase and peripheral coronary pressure did not decrease because of N2O. Diffusion hypoxia was also excluded. This study confirms that N2O has a significant but mild depressant effect on the performance of both normal and ischemic myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Myocardial metabolism during hypoxia: maintained lactate oxidation during increased glycolysis.

In the intact animal, myocardial lactate utilization and oxidation during hypoxia are not well understood. Nine dogs were chronically instrumented with flow probes on the left anterior descending coronary artery and with a coronary sinus sampling catheter. [14C]lactate and [13C]glucose tracers, or [13C]lactate and [14C]glucose were administered to quantitate lactate and glucose oxidation, lactate conversion to glucose, and simultaneous lactate extraction and release. The animals were anesthetized and exposed to 90 minutes of severe hypoxia (PO2 = 25 +/- 4 torr). Hypoxia resulted in significant increases in heart rate, cardiac output and myocardial blood flow, but no significant change in myocardial oxygen consumption. The arterial/coronary sinus differences for glucose and lactate did not change from normoxia to hypoxia; however, the rate of glucose uptake increased significantly due to the increase in myocardial blood flow. Tracer-measured lactate extraction did not decrease with hypoxia, despite a 250% increase in lactate release. During hypoxia, 90% +/- 4% of the extracted 14C-lactate was accounted for by the appearance of 14CO2 in the coronary sinus, compared with 88% +/- 4% during normoxia. Thus, in addition to the expected increase in glucose uptake and lactate production, we observed an increase in lactate oxidation during hypoxia.

Acetates↗
PubMed1990

Increased lactate appearance and reduced clearance during hypoxia in dogs.

In order to assess the effects of severe hypoxia on whole body glucose and lactate kinetics, nine experiments were performed on anesthetized, ventilated mongrel dogs. [U-13C]glucose and [1-14C]lactate (n = 5), or [6-14C]glucose and [U-13C]lactate (n = 4) were infused using the primed-continuous infusion method. Cardiac output was measured by thermodilution. After a control period with 21% O2, inspired O2 was reduced for 90 minutes. Three of the experiments resulted in unstable hemodynamics and lactate levels, and are excluded from the mean data. Arterial PO2 fell from a control level of 106.8 +/- 11.9 to 24.2 +/- 3.5 mmHg during the last 45 minutes of hypoxia, and O2 transport fell to 52% of normoxic values. Arterial lactate concentration and the rate of appearance increased by 428% and 182%, respectively, from control to hypoxia. The metabolic clearance rate for lactate fell by 34%. Arterial glucose levels did not change significantly with hypoxia, but the rate of glucose disappearance rose by 70%, and the rate of glucose conversion to lactate increased 3-fold. It is concluded that acute severe hypoxia in anesthetized dogs causes 1) a large increase in arterial lactate levels, but no significant change in glycemia, 2) a large increase in the rate of lactate disappearance and only a small increase in the rate of glucose disappearance and 3) a fall in the metabolic clearance rate of lactate.

Animals↗
PubMed1990

Effect of halothane and isoflurane on postischemic "stunned" myocardium in the dog.

Short periods of coronary artery occlusion are known to produce prolonged periods of ventricular dysfunction. The effects of halothane or isoflurane on contractility and metabolism in postischemic "stunned" myocardium were studied in an open-chest canine model in which the left anterior descending artery (LAD) was occluded for 15 min and then reperfused. Regional function in the LAD and circumflex artery (CIRC) areas were measured with sonomicrometry, and metabolic data were determined from simultaneous arterial and venous measurements of oxygen and lactate. Halothane and isoflurane produced equivalent decreases in systolic shortening in both normal (CIRC) and stunned (LAD) areas of the heart. Furthermore, the amount of depression was similar with either halothane or isoflurane. Halothane 0.75 MAC significantly decreased systolic shortening in both the LAD region (from 38.8 +/- 25.9% to 11.0 +/- 21.8%) and in the CIRC region (from 116.7 +/- 24.7% to 87.5 +/- 23.3%). At equivalent MAC concentrations of isoflurane, the values were 42.5 +/- 45.7 to -7.0 +/- 49.9% in the LAD region and 91.5 +/- 11.9% to 66.9 +/- 23.9% in the CIRC area. At 1.5-MAC halothane, systolic shortening in the LAD region decreased from 47.9 +/- 47.2% to -0.6 +/- 20.3% and in the CIRC area from 114.6 +/- 16.8% to 76.0 +/- 18.7%. Isoflurane at 1.5 MAC produced significant decreases, from 23.4 +/- 54.5% to -15.6 +/- 27.1% in the LAD region and from 94.4 +/- 33.2% to 61.3 +/- 28.2 in the CIRC area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Myocardial lactate release during ischemia in swine. Relation to regional blood flow.

To determine the relation between regional myocardial blood flow, contractile function, and myocardial lactate release during mild-to-moderate regional myocardial ischemia, nine open-chest swine were instrumented for measurement of regional myocardial blood flow (microsphere method), contractile function (sonomicrometry), and hemodynamics. L-[1-14C]Lactate or L-[U-13C]lactate was infused intravenously using a primed continuous infusion technique to quantify regional myocardial lactate release. D-[U-13C]glucose or D-[6-14C]glucose was simultaneously infused to determine the contribution of exogenous glucose to lactate release. Graded coronary ischemia (two to three levels) was created in the left anterior descending coronary arterial distribution by mechanically constricting the artery in five animals or by decreasing flow through a cannulated left anterior descending artery in four animals. In all nine animals, subendocardial blood flow was 0.99 +/- 0.21 (ml/min)/g during control and 0.34 +/- 0.14 (ml/min)/g during the most severe grade of underperfusion (p less than 0.001) in the left anterior descending coronary arterial distribution. Regional myocardial lactate release was 0.15 +/- 0.09 and 1.19 +/- 0.75 mumols/ml, respectively (p less than 0.003). A highly significant inverse correlation was observed between subendocardial blood flow and myocardial lactate release during the graded reductions in blood flow (r = -0.71, p less than 0.001). Results from sonomicrometry showed a significant reduction in contractile ventricular function in the anterior wall during the graded reductions in blood flow. The regional arterial-venous glucose difference increased significantly with underperfusion in the left anterior descending coronary arterial distribution, from 0.14 +/- 0.15 to 0.56 +/- 0.37 mumols/ml (p less than 0.003). The contribution of exogenous glucose to lactate release also increased significantly; 0.04 +/- 0.03 mumols/ml of the lactate came from exogenous glucose during control compared with 0.64 +/- 0.59 mumols/ml during the most severe underperfusion (p less than 0.02). A significant positive correlation exists between lactate release and lactate from exogenous glucose during graded underperfusion (r = 0.96, p less than 0.001). In summary, these data demonstrate a close inverse relation between regional myocardial lactate release and regional subendocardial blood flow during graded ischemia.

Animals↗
PubMed1986

Influence of mannitol and dopamine on renal function during elective infrarenal aortic clamping in man.

The impact of elective infrarenal aortic clamping on parameters of renal function was evaluated in 27 extracellular fluid volume expanded patients. Significant transient decreases (p less than 0.05) in glomerular filtration rate were observed in all three groups either in the early or late post-clamp release period, despite maintenance of hemodynamic stability. This study documents transient decreases in glomerular filtration rate which occurred following release of the infrarenal aortic cross-clamp. No clinically important benefit from the use of mannitol and dopamine over extracellular fluid volume expansion with saline alone was demonstrated in the prevention of the changes in renal function associated with aortic cross-clamping.

Adult↗