The pathophysiology of aortic cross-clamping and unclamping.

Mild intraoperative hypothermia is common. We therefore studied the effects of mild hypothermia on propofol pharmacokinetics, hepatic blood flow, and atracurium duration of action in healthy volunteers. Six young volunteers were studied on two randomly assigned days, at either 34 degrees C or 37 degrees C. Anesthesia was induced with thiopental, 3 mg/kg, and maintained with 70% N2O and 0.6% isoflurane. Core hypothermia was induced by conductive and convective cooling. On the other study day, normothermia was maintained by a Bair Hugger (Augustine Medical, Inc., Eden Prairie, MN) forced-air warmer. Propofol, 1 mg/kg lean body mass (LBM), then was given, followed by a 4-h infusion at 5 mg.kg-1.h-1. After 2 h, atracurium 0.5 mg/kg was administered as an intravenous bolus. Indocyanine green was administered for estimation of hepatic blood flow. Arterial blood was assayed for propofol and indocyanine green concentration. Pharmacokinetic analysis was performed using NONMEM. Results are reported as means +/- SEM. Propofol blood concentrations averaged approximately 28% more at 34 degrees C than at 37 degrees C (P < 0.05). Hepatic blood flow decreased 23% +/- 11% in normothermic volunteers during the propofol infusion, and 33% +/- 11% in hypothermic volunteers (P = not significant). A three-compartment mamillary model fitted the data best. Inclusion of hepatic blood flow change from the prepropofol baseline as a covariate for total body clearance significantly improved the fit. The intercompartmental clearances were decreased in the presence of hypothermia.(ABSTRACT TRUNCATED AT 250 WORDS)

Mild hypothermia alters propofol pharmacokinetics and increases the duration of action of atracurium

Summary SNP remains an effective, reliable, and commonly used drug for the rapid reduction of significant arte- rial hypertension regardless of the etiology, for after- load reduction in the face of low CO when blood volume is normal or increased, and for intraoperative induced hypotension. After establishing indwelling arterial monitoring, an initial infusion rate of 0.3-0.5 pg * kg-’ . min -’ is be f: un with titration as needed up to 2.0 p.g * kg-’ * min- . Higher rates for brief periods of time (10 min) are acceptable. The use of alternative drugs to reduce the dose or shorten the duration of infusion should be considered when the 2.0 pg * kg-’ * mine1 range is exceeded (Table 1). SNP should not be used by individuals unfamiliar with its potency and metabolic pathways, as the many reports of adverse reactions testify. Careful attention to infusion rates, particularly in patients at risk for depleted thiosulfate stores, is mandatory, and the use of other drugs in conjunction with or instead of SNP should always be considered. As with many therapeu- tic interventions, SNP requires careful administration to appropriately selected patients by a clinician who knows its inherent hazards. Despite its toxicity, SNP is popular because it often the most (in some cases, the only) effective drug in some difficult clinical circumstances.

Sodium nitroprusside: twenty years and counting.

Surgical experience in descending thoracic aneurysmectomy with and without adjuncts to avoid ischemia.

Combined use of cerebral spinal fluid drainage and naloxone reduces the risk of paraplegia in thoracoabdominal aneurysm repair

Cardiac output distribution and regional blood flow in 18 dogs during isoflurane and halothane anesthesia were studied in dose-related fashion. Surgical preparation consisted of left thoracotomy and placement of catheters in the left atrium and aorta through a femoral artery. Regional blood flow was studied one week after surgical preparation using a microsphere technique at the three stages: awake, 1 MAC, and 2 MAC of inhalation anesthesia. At each stage of the experiment, two sets of microspheres (15- and 9-micron diameter), labeled with different isotopes, were used simultaneously. Both anesthetics increased cerebral blood flow, decreased blood flow through preportal area, and preserved renal blood flow. Isoflurane increased hepatic artery blood flow at both levels of anesthesia, while halothane preserved the flow during 1 MAC and decreased it at 2 MAC. Apparently, isoflurane provided better oxygenation to the liver than halothane. Myocardial blood flow was increased during isoflurane (despite decrease in blood pressure and cardiac output) and decreased during halothane anesthesia. Isoflurane appears to be a coronary vasodilator with potential beneficial (improvement in myocardial blood supply) as well as hazardous ("steal effect") effects on the heart.

Regional blood flow during isoflurane and halothane anesthesia.

Hepatic arterial blood flow (HABF) and portal blood flow (PBF) were measured in 18 dogs while awake and during isoflurane and halothane anesthesia. Surgical preparation 1 week before the measurements consisted of a left thoracotomy, placement of a left atrial catheter, and insertion of another catheter into the distal aorta via the left femoral artery. Cardiac output and liver blood flow were determined using microspheres at three stages: stage 1-awake state; stage 2-after 45 min of 1 MAC of isoflurane (eight dogs) or halothane (10 dogs) anesthesia; and stage 3-after 45 min of 2 MAC of inhalation anesthesia. Half-life and fractional clearance for indocyanine green (ICG) were determined 1 day before the experiment (awake state), and at the end of stages 2 and 3. Mean arterial pressure (MAP) and cardiac index (CI), as well as PBF, decreased during isoflurane and halothane anesthesia. HABF increased significantly during isoflurane anesthesia, remained unchanged during 1 MAC of halothane anesthesia, and significantly decreased during 2 MAC of halothane anesthesia. Apparently, hepatic oxygen supply was maintained much better during isoflurane than during halothane anesthesia. PBF correlated with CI during halothane (r = 0.97) and, to a certain extent, with MAP during isoflurane (r = 0.66). HABF correlated with CI and MAP during halothane (r = 0.74 and 0.71, respectively) but did not correlate with systemic hemodynamic variables during isoflurane. ICG half-life significantly increased during 1 and 2 MAC of halothane anesthesia. The degree of increase did not correlate with the level of anesthesia or the decrease in total hepatic blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Liver Circulation and Function during Isoflurane and Halothane Anesthesia

Regional blood flow during cross-clamping of the thoracic aorta and infusion of sodium nitroprusside.

This study was designed to evaluate the influence of inhalational agents on the intestinal circulation in an isolated loop preparation. Sixty dogs were studied, using three intestinal segments from each dog. Selected intestinal segments were pumped with aortic blood at a constant pressure of 100 mmHg. A mixture of /sub 86/Rb and 9-microns spheres labeled with /sup 141/Ce was injected into the arterial cannula supplying the intestinal loop, while mesenteric venous blood was collected for activity counting. A very strong and significant correlation was found between rubidium clearance and microsphere entrapment (r = 0.97, P less than 0.0001). Nitrous oxide anesthesia was accompanied by a higher vascular resistance (VR), lower flow (F), rubidium clearance (Cl-Rb), and microspheres entrapment (Cl-Sph) than pentobarbital anesthesia, indicating that the vascular bed in the intestinal segment was constricted and flow (total and nutritive) decreased. Halothane, enflurane, and isoflurane anesthesia were accompanied by a much lower arteriovenous oxygen content difference (AVDO/sub 2/) and oxygen uptake than pentobarbital or nitrous oxide. Compared with pentobarbital, enflurane anesthesia was not accompanied by marked differences in VR, F, Cl-Rb, and Cl-Sph; halothane at 2 MAC decreased VR and increased F and Cl-Rb while isoflurane increased VR and decreased F. alpha-Adrenoceptormore » blockade with phentolamine (1 mg . kg-1) abolished isoflurane-induced vasoconstriction, suggesting that the increase in VR was mediated via circulating catecholamines.« less

Intestinal Circulation during Inhalation Anesthesia

This study evaluated the role of ventilatory and circulatory depression in anesthesia-induced hepatotoxicity in rats. Male Sprague-Dawley rats (181 animals) were pretreated with phenobarbital and exposed to hypoxia (FIO2 = 0.14) for 2 hr. The animals were divided into four groups: group 1 received 1% inspired halothane in the hypoxic gas mixture; group 2 received 1.4% inspired isoflurane and hypoxia; group 3 had 25-30% of their blood volume removed 2 hr before exposure to hypoxia; and group 4 served as a control with no treatment other than hypoxia. Hepatic blood flow was studied using microspheres; oxygen availability to the liver was calculated using values of hepatic blood flow and oxygen content of arterial and portal venous blood; and liver injury was quantitatively evaluated. Ventilation was depressed in rats that received halothane and, to a lesser extent, isoflurane. The lowest portal blood flow was observed in groups 1 and 3. Hepatic arterial blood flow was lowest in group 1 and highest in group 3. There was an inverse relationship between hepatic oxygen availability and severity of histologic lesions. The most severe lesions and lowest oxygen availability was associated with halothane. Hemorrhage and isoflurane were associated with less diminution of oxygen availability and less severe hepatic lesions. The least decrease in oxygen availability and the least severe histologic changes occurred in control rats subjected to hypoxia only.

Kathryn C. Fowler

Papers

Regional blood flow during isoflurane and halothane anesthesia.

Liver Circulation and Function during Isoflurane and Halothane Anesthesia

Regional blood flow during cross-clamping of the thoracic aorta and infusion of sodium nitroprusside.

Intestinal Circulation during Inhalation Anesthesia

The effect of halothane, isoflurane, and blood loss on hepatotoxicity and hepatic oxygen availability in phenobarbital-pretreated hypoxic rats.