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Biomedical subjects

M W Crawford

Publications and source records attributed to M W Crawford.

8 recordsLinked to original sources
PubMed1996

The neuromuscular effects of mivacurium chloride during propofol anesthesia in children.

Previous studies examined the neuromuscular effects of mivacurium in doses up to, but not exceeding, 2.5 times 95% effective dose (ED95) in children. To determine whether larger doses offer clinical advantages, we compared the onset and duration of neuromuscular block, intubating conditions, and changes in plasma histamine concentration (PHC) after mivacurium (0.2, 0.3, or 0.4 mg/kg) with those after succinylcholine (2.0 mg/kg) during propofol/N2O anesthesia in 48 children aged 3-10 yr. The evoked electromyograph (EMG) of the adductor digiti minimi after supramaximal train-of-four (TOF) stimulation was recorded. When T1 was 10% of control, laryngoscopy and intubation were performed. PHC was measured immediately before and at 2 and 5 min after administration of the relaxant. Venous blood was sampled for determination of plasma cholinesterase activity. Axillary temperature was measured. Increasing the dose of mivacurium from 0.2 to 0.3 mg/kg accelerated the onset of block (time to 90% block, 1.6 +/- 0.2 vs 1.2 +/- 0.2 min) (P < 0.001), but did not significantly prolong recovery (time to 95% recovery, 16.0 +/- 3.8 vs 18.6 +/- 3.6 min). A further increase in dose to 0.4 mg/kg produced no significant decrement in onset time, but did prolong recovery (time to 95% recovery, 23.8 +/- 5.0 min) (P < 0.001). The duration of action of mivacurium 0.3 and 0.4 mg/kg correlated inversely with plasma cholinesterase activity. PHC increased significantly after mivacurium 0.3 and 0.4 mg/kg; however, mean arterial pressure did not change significantly. We conclude that mivacurium 0.3 mg/kg provides a relatively rapid onset and short duration of neuromuscular block in healthy children. Increasing the dose to 0.4 mg/kg does not significantly accelerate the onset of neuromuscular block.

Anesthetics, Intravenous↗
PubMed1994

The effect of adenosine-induced hypotension on systemic and splanchnic hemodynamics during halothane or sevoflurane anesthesia in the rat.

BACKGROUND: It has been suggested that the liver may be at risk for ischemic damage during adenosine-induced hypotension. This notion, however, is somewhat inconsistent with the understanding that adenosine is a powerful vasodilator of the splanchnic circulation. To help clarify the effect of adenosine-induced hypotension on splanchnic hemodynamics, we studied the systemic and splanchnic hemodynamic responses to adenosine, both alone and in the presence of halothane or sevoflurane. METHODS: Systemic and splanchnic hemodynamics were determined during the infusion of adenosine in 36 rats allocated randomly to one of three study groups: (1) awake, (2) halothane anesthesia (1.0 MAC), or (3) sevoflurane anesthesia (1.0 MAC). Adenosine was infused at a rate sufficient to decrease the mean arterial pressure by 35-38% from awake control values. Cardiac output and organ blood flows were measured using the radiolabeled microsphere technique. RESULTS: Adenosine infusion produced stable hypotension of rapid onset due to a reduction in systemic vascular resistance. Stroke volume increased, but cardiac output remained unchanged in the awake and sevoflurane groups because of a decrease in heart rate. Infusion of adenosine during halothane anesthesia increased cardiac output enough to compensate for the decrease in cardiac output due to halothane alone. In the splanchnic circulation, there was an increase in portal tributary (42%, P < 0.01) and hepatic arterial (38%, P < 0.05) blood flows during adenosine infusion in awake rats. This resulted in an overall increase in total liver blood flow (42%, P < 0.01). Halothane anesthesia was associated with a decrease in portal tributary blood flow (28%, P < 0.05). In contrast, sevoflurane anesthesia was associated with an increase in hepatic arterial flow (35%, P < 0.05) but with no change in portal tributary blood flow. During halothane anesthesia, adenosine infusion increased portal tributary (90%, P < 0.01) and hepatic arterial (37%, P < 0.05) blood flows, thereby increasing total liver blood flow to values similar to those in awake adenosine-infused rats. During sevoflurane anesthesia, adenosine infusion increased portal tributary blood flow (48%, P < 0.01), but hepatic arterial blood flow did not increase beyond the values observed during sevoflurane anesthesia alone. CONCLUSIONS: These findings demonstrate that adenosine is a potent vasodilator of portal tributary and hepatic arterial vasculature in the rat and that the splanchnic hemodynamic effects of adenosine predominate over those of halothane and sevoflurane.

Adenosine↗
PubMed1993

Effect of propofol infusion on splanchnic hemodynamics and liver oxygen consumption in the rat. A dose-response study.

BACKGROUND: Propofol has been used for the maintenance of anesthesia. The effects of propofol infusion on splanchnic hemodynamics and liver oxygen consumption, however, have not been reported. In the current investigation, the authors studied the effects of a continuous infusion of propofol on systemic and splanchnic hemodynamics using a new method to measure liver oxygen consumption in awake control and anesthetized rats. METHODS: Cannulas were inserted into the left ventricle, femoral artery, portal vein, and hepatic vein during ether anesthesia, and the rats were allowed to awaken and recover for 3-4 h before study. Animals were infused for 30 min with either saline (controls) or propofol at a rate of 300, 600, 900, or 1,200 micrograms.kg-1 x min-1. Cardiac output and organ blood flows were measured using radiolabelled microspheres, and blood samples from the femoral artery, portal vein, and hepatic vein were used to determine liver oxygen consumption. RESULTS: Mean arterial pressure decreased in a dose-dependent manner with a 25% reduction at the highest infusion rate. Systemic vascular resistance similarly decreased, whereas cardiac output remained unchanged at all the infusion rates. Hepatic arterial blood flow increased in a dose-dependent fashion over the dose range studied, to a maximum increase of 120%. Portal tributary blood flow increased by 30% at the highest infusion rate. Total liver blood flow increased in a dose-dependent manner to a maximum of 38%. Total oxygen delivery to the liver by the hepatic artery and portal vein increased in a dose-dependent fashion. Liver oxygen consumption increased in a dose-dependent fashion to a maximum increase of 51% at an infusion rate of 1,200 micrograms.kg-1 x min-1. The percent of oxygen extracted by the liver was not altered by propofol infusion, and hepatic venous oxygen saturation did not decrease at any dose studied. Coronary and renal blood flows were not altered. Arterial PaCO2, increased from 31 +/- 2 mmHg in awake control rats to 41 +/- 2 mmHg in spontaneously breathing rats infused with 1,200 micrograms.kg-1 x min-1 propofol. CONCLUSIONS: The maintenance of anesthesia using an infusion of propofol resulted in an increase in liver oxygen consumption that was fully compensated for by an increase in oxygen delivery to the liver. Splanchnic hemodynamics and liver oxygenation are not adversely affected during maintenance of anesthesia with propofol in the normal rat.

Animals↗
PubMed1992

Haemodynamic and organ blood flow responses to sevoflurane during spontaneous ventilation in the rat: a dose-response study.

To determine the systemic haemodynamic and organ blood flow responses to the administration of sevoflurane during spontaneous ventilation, heart rate, cardiac index, mean arterial pressure, arterial blood gases, and blood flows to the brain, spinal cord, heart, kidneys and splanchnic organs were measured awake (control values) and after 30 min of anaesthesia with 0.5, 1.0, 1.2 or 1.5 MAC sevoflurane in rats. Cardiac output and organ blood flows were measured using radiolabelled microspheres. The MAC (mean +/- SEM) of sevoflurane was found to be 2.30 +/- 0.05%. At each concentration, haemodynamic variables were similar to awake values with the exception of a 12% reduction in mean arterial pressure at 1.5 MAC (P less than 0.01). Arterial PCO2 increased in a dose-related fashion. Cerebral and spinal cord blood flows increased at 1.2 and 1.5 MAC whereas coronary and renal blood flows did not change significantly. Portal tributary blood flow and preportal vascular resistance were unaffected. Hepatic arterial flow increased by 63% at 1.5 MAC (P less than 0.05) but total liver blood flow remained unchanged compared with awake values. In conclusion, the administration of sevoflurane during spontaneous ventilation produces a high degree of cardiovascular stability and maintains blood flow to major organs in the rat.

Anesthesia, Inhalation↗
PubMed1992

Hemodynamic and organ blood flow responses to halothane and sevoflurane anesthesia during spontaneous ventilation.

This study compared systemic hemodynamic and organ blood flow responses to equipotent concentrations of halothane and sevoflurane during spontaneous ventilation in the rat. The MAC values for halothane and sevoflurane were determined. Cardiac output and organ blood flows were measured using radiolabeled microspheres. Measurements were obtained in awake rats (control values) and at 1.0 MAC halothane or sevoflurane. The MAC values (mean +/- SEM) for halothane and sevoflurane were 1.10% +/- 0.05% and 2.40% +/- 0.05%, respectively. The PaCO2 increased to a similar extent in both groups compared with control values. During halothane anesthesia, heart rate decreased by 12% (P < 0.01), cardiac index by 26% (P < 0.01), and mean arterial blood pressure by 18% (P < 0.01) compared with control values. Stroke volume index and systemic vascular resistance did not change. During sevoflurane anesthesia, hemodynamic variables remained unchanged compared with control values. Coronary blood flow decreased by 21% (P < 0.01) and renal blood flow by 18% (P < 0.01) at 1.0 MAC halothane, whereas both remained unchanged at 1.0 MAC sevoflurane. Cerebral blood flow increased to a greater extent with halothane (63%; P < 0.01) than with sevoflurane (35%; P < 0.05). During halothane anesthesia, hepatic arterial blood flow increased by 48% (P < 0.01), whereas portal tributary blood flow decreased by 28% (P < 0.01). During sevoflurane anesthesia, hepatic arterial blood flow increased by 70% (P < 0.01) without a concomitant reduction in portal tributary blood flow. Total liver blood flow decreased only with halothane (16%; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗