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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Halothane was given to dogs which had been bled to an arterial mean blood pressure of 60 mmHg, and the circulatory effects were studied with the aid of the radioactive microsphere technique. The cardiac output and coronary blood flow were well maintained, whereas the arterial mean blood pressure was slightly, and the stroke volume markedly increased, indicating an improved heart function. The blood flows to the brain, lungs, liver and kidneys were well preserved throughout the anesthesia. The effect of retransfusing the withdrawn blood was also studied, and it resulted in an increased cardiac output, arterial mean blood pressure and increased blood flows to the heart, lungs, spleen, bowel and liver.
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PMID:The effect of halothane on the distribution of cardiac output and organ blood flows in the hemorrhagic, hypotensive dog. 65 51

This study, in open-chested dogs, sought to explore the relationship between whole-body oxygen delivery and oxygen consumption during anaesthesia, using increasing concentrations of halothane, enflurane and isoflurane. Results indicate that the cardiac index and oxygen delivery became critical at less than 1 MAC (minimal alveolar concentration of anaesthetic) for the three commonly used vapours. Halothane caused the least depression of contractility, but the stroke volume was reduced by the well-maintained afterload at 1 MAC. Enflurane and isoflurane were associated with more depression of contractility, but the cardiac output was maintained by an increase in heart rate in the case of isoflurane and reduced mean arterial pressure during the use of enflurane.
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PMID:The effect of halothane, enflurane and isoflurane on the circulation. 279 92

By combining surgical and anesthetic techniques that minimize blood loss with the use of autotransfusion, it should now be possible to complete a routine posterior spinal fusion without using allogeneic blood transfusions. Surgical efforts should include careful preoperative planning, positioning with the abdomen hanging free, use of topical hemostatic agents, and decortication late in the procedure. Preoperatively donated autogeneic blood or reclaimed red cells from suction can take the place of allogeneic transfusions. Blood loss during scoliosis surgery correlates closely with left ventricular stroke work index (LVSWI), a measure of blood flow calculated from systemic vascular resistance, cardiac output, and heart rate. All of these parameters are under the anesthesiologist's control, making him the primary determinant of blood loss in scoliosis surgery. Induced hypotensive anesthesia may be ineffective in controlling blood loss if the cardiac output or heart rate is high. Halothane, a commonly used hypotensive agent, is not very useful for scoliosis surgery because spinal cord monitoring and wake-up testing are not possible. Rebound hypertension has been noted with the use of sodium nitroprusside. Trimethaphan works well clinically but experimentally it reduces spinal cord blood flow, which may increase the risk of spinal cord injury.
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PMID:Control of blood loss during scoliosis surgery. 328 Feb 5

The combination of two-dimensional and pulsed Doppler echocardiography was used to measure determinants of cardiac function in 20 ASA physical status I infants and small children (9 days-32 months of age) during equipotent halothane (n = 10) or isoflurane (n = 10) anesthesia in oxygen. Five sets of cardiovascular data were recorded in each patient. In the awake, unmedicated state prior to induction, at three different anesthetic levels, 0.75, 1.0, and 1.25 MAC (corrected for age) and a final measurement repeated at 1.25 MAC after the intravenous infusion of 15 ml X kg-1 of Lactated Ringers solution. The study was completed prior to intubation and surgery. Results are expressed as mean +/- SEM. Isoflurane and halothane decreased mean blood pressure from the awake level (isoflurane 76.6 +/- 2.3 to 60.6 +/- 3.1 mm, halothane 72.2 +/- 3.9 to 60.6 +/- 3.1 mm at 1.25 MAC). Isoflurane increased heart rate at all anesthetic levels (128.7 +/- 4.2 to 142.5 +/- 6.0 beats/min at 0.75 MAC). Halothane decreased heart rate at 1.25 MAC (124.6 +/- 4.6 to 119.4 +/- 3.5 beats/min). Isoflurane and halothane decreased cardiac index at 1.25 MAC. Stroke volume index decreased at 1.0 and 1.25 MAC with both isoflurane (36.9 +/- 3.8 to 30.2 +/- 3.5 ml/m2) and halothane (32.7 +/- 2.5 to 28.9 +/- 2.5 ml/m2). Ejection fractions also decreased significantly at 1.0 and 1.25 MAC in both groups of patients (22 +/- 6% at 1.25 MAC halothane and 28 +/- 8% at 1.25 MAC isoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulsed Doppler and two-dimensional echocardiography: comparison of halothane and isoflurane on cardiac function in infants and small children. 360 47

During normovolemia, nitrous oxide causes mild sympathetic stimulation and direct myocardial depression; these effects offset each other, resulting in only minimal cardiovascular changes. To test the hypothesis that during hypovolemia this balance would change and depression predominate, 10 swine were made hypovolemic (30% blood loss) and then were given 70% N2O (0.25 MAC in swine) or an equipotent concentration of halothane, an agent that does not cause sympathetic stimulation. The alternate anesthetic was given to the same hypovolemic swine on another day. Five minutes after induction of anesthesia during hypovolemia, both N2O and halothane caused significant, physiologically important deterioration of compensation for hemorrhage. Halothane decreased systemic vascular resistance (SVR); N2O was more variable in its action, and SVR did not decrease significantly. Both agents caused similar decreases in cardiac output, mean aortic blood pressure, stroke volume, oxygen consumption, and left ventricular minute work, despite increases in plasma epinephrine concentration and plasma renin activity. No differences were found between groups for any of these variables (P greater than 0.05). Plasma norepinephrine concentration increased only in the N2O group and was greater in that group than in the halothane group. The deterioration of cardiovascular compensation for hemorrhage was expressed metabolically by similar decreases in the two groups in partial pressure of oxygen of mixed venous blood and by increases in blood lactate concentration. Thirty minutes after induction of anesthesia, with stable end-tidal anesthetic concentrations, both groups had some cardiovascular, but no metabolic, recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular actions of nitrous oxide or halothane in hypovolemic swine. 390 22

Circulatory and respiratory effects of intravenously administered acetylpromazine (0.033 and 0.067 mg/kg) and xylazine (0.5 and 1.0 mg/kg) were studied in drug cross-over fashion in eight laterally recumbent horses anesthetized only with halothane (1.06%, end-tidal) in O2. Both doses of acetylpromazine caused a significant and sustained elevation in cardiac output via a rise in stroke volume. Xylazine produced an initial significant fall in cardiac output followed by a return to control levels. Halothane anesthesia did not prevent xylazine-related atrioventricular conduction block. All treatments caused a similar significant fall in arterial blood pressure (acetylpromazine, total peripheral resistance-related; xylazine, cardiac output-related). PaCO2 significantly increased after all treatments. PaCO2 decreased significantly only following xylazine treatment. One horse (not included in the tabulation) developed ventricular fibrillation and died 15 min after receiving its first injection (0.5 mg/kg) of xylazine.
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PMID:Cardiovascular and respiratory effects of acetylpromazine and xylazine on halothane-anesthetized horses. 393 74

The effects of halothane on intracellular membrane potential (Em) and force development in cat MCA were studied. Halothane (0.07-0.14 mM/1) relaxed isolated MCA which had developed myogenic tone. Measurement of Em showed that halothane depolarized this preparation in a dose-dependent fashion in the face of vessel relaxation, demonstrating uncoupling of electrical and mechanical activity. Halothane markedly inhibited the contractile effects of histamine and serotonin suggesting that, apart from its direct action on cerebral arterial tone, it also blunts the action of vasoactive agents. When this preparation is partially depolarized from -62 to -50 mV with excess K+, halothane, while having only a small (1.2 mV) additional depolarizing effect, consistently elicits contraction rather than relaxation. Thus, the action of this particular volatile anesthetic on cerebral arteries can depend upon the resting level of Em. These studies indicate that halothane relaxes myogenic tone in cat MCA by an intracellular mechanism, but that the direction of its effect (i.e., relaxation vs. contraction) may depend upon the prior level of Em and muscle cell activation.
Stroke
PMID:Cellular actions of halothane on cat cerebral arterial muscle. 402 80

The effects of halothane on myocardial blood flow and myocardial oxygen balance were studied in seven male patients with stable angina and normal left ventricular function. Patients were receiving maintenance doses of beta-receptor antagonists and underwent coronary artery bypass surgery. Anaesthesia consisted of halothane and 50% nitrous oxide in oxygen. Halothane decreased myocardial blood flow and myocardial oxygen consumption by 29% and 32%, respectively, after induction of anaesthesia, and during sternotomy. Myocardial lactate production was not observed at any time. Cardiac index, stroke volume index, mean arterial pressure and mean diastolic arterial pressure were decreased significantly after induction of anaesthesia and during sternotomy. Heart rate remained unchanged. The global myocardial oxygen supply and demand relationship was maintained. The results suggest that halothane is a safe anaesthetic for coronary revascularization in patients with unimpaired left ventricular function.
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PMID:Myocardial blood flow and oxygen consumption during halothane-nitrous oxide anaesthesia for coronary revascularization. 660 56

The effects of ouabain infusion were tested in six lambs before and after depression of myocardial function by halothane anesthesia. Halothane reduced the left ventricular rate of pressure rise (dp/dt), stroke work, and stroke volume; the ratio of preejection period to left ventricular ejection time rose. Heart rate and systemic vascular resistance did not change. Before halothane, ouabain infusion did not alter the hemodynamic variables measured. After myocardial depression, ouabain infusion returned dp/dt, stroke work, stroke volume and the ratio of preejection period to left ventricular ejection time to control levels. Pacing studies showed a biphasic relationship between left ventricular dp/dt and heart rate. Maximal dp/dt occurred at a heart rate 42 beats/min higher than the resting rate. These studies suggest resting myocardial performance in the healthy, newborn lamb is at near maximal level.
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PMID:The effects of ouabain in lambs with depressed myocardial function. 709 54

Halothane was administered at an end-tidal concentration of 1% to 10 patients with stable ischaemic heart disease and clinical and haemodymanic signs of moderate heart failure. Measurements of central haemodynamic variables, coronary sinus blood flow and oxygen, lactate and hypoxanthine balances over the myocardium were done before and at steady state during halothane anaesthesia. Halothane induced marked haemodynamic changes with decreases in mean arterial pressure (-43%), mean pulmonary arteriolar occlusion pressure (-42%), systemic vascular resistance (-31%), cardiac index (-20%) stoke volume index (-31%) and left and right stroke work indices (-62% and -55%, respectively). Heart rate and pulmonary vascular resistance did not change. Coronary sinus blood flow decreased in parallel with perfusion pressure, and myocardial oxygen consumption decreased (-40%), as did myocardial oxygen extraction. Rate pressure product and triple product correlated better with changes in myocardial oxygen consumption in the present subset of patients than in healthy volunteers during halothane anaesthesia. The findings suggest that halothane, through its systemic vasodilatory effect, unloads the failing left ventricle and that this peripheral action predominates over the direct cardiodepressant action of the agent. The combined findings of unchanged coronary vascular resistance, decreased myocardial oxygen extraction and absence of increasing or pathological levels of lactate and hypoxanthine in coronary sinus blood imply a direct dilatory effect of halothane on the coronary vasculature.
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PMID:Effects of halothane on coronary haemodynamics and myocardial metabolism in patients with ischaemic heart disease and heart failure. 710 35


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