Hiroshi Hasuo

Comparative analysis of systemic and coronary hemodynamics during sevoflurane- and isoflurane-induced hypotension in dogs.

We studied the effects of sevoflurane on myocardial contractility and systemic and coronary hemodynamics, as compared with the effects of isoflurane in dogs under the same cardiac work conditions. Sixteen mongrel dogs were anesthetized with alpha-chloralose. Heart was paced at 100 beats/min after producing a complete atrioventricular (A-V) block. Controlled hypotension to a mean arterial pressure (MAP) of 60 mm Hg was induced and maintained by inhalation of either anesthetic, lasting for 60 min. Measurements were made at baseline, 15 min (T1), and 60 min (T2) after starting hypotension, and 30 min after discontinuing equihypotension (T3). Although left ventricular systolic segment shortening (%SS) decreased approximately 20% in both groups, cardiac output (CO) decreased only in sevoflurane during equihypotension (-27.6% at T2). Sevoflurane decreased the coronary blood flow (CBF; -34.8% at T2) with no significant change of coronary vascular resistance (CVR), whereas isoflurane produced a significant decrease in CVR resulting in no change of CBF despite of decreased coronary perfusion pressure (-37.4% at T2). These systemic and coronary vascular effects were continued even at T3. In conclusion, myocardial depressant effects were comparable between sevoflurane and isoflurane. Both systemic and coronary vasodilatory effects of isoflurane are greater than those of sevoflurane.

Anticholinesterase drugs stimulate phosphatidylinositol response in rat tracheal slices

Some anticholinesterase (anti-ChE) drugs induce airway smooth muscle contraction. Whether anti-ChE drugs stimulate muscarinic receptors in airway smooth muscle as well as nicotinic receptors in neuromuscular junction is unknown. Since there is a direct relationship between phosphatidylinositol (PI) response and airway smooth muscle contraction induced by muscarinic agonists, we examined the effects of neostigmine, physostigmine, pyridostigmine, and edrophonium on PI response in the airway smooth muscle. The rat tracheal slices were incubated in Krebs-Henseleit solution containing LiCl and [(3) H]myo-inositol in the presence of carbachol, anti-ChE, or none of them. [(3) H]inositol monophosphate (IP1), which is a degradation product of PI response, was counted with a liquid scintillation counter. Inositol monophosphate accumulation was stimulated by neostigmine, physostigmine, and pyridostigmine in a dose-dependent manner, but was not affected by edrophonium. These increases were completely inhibited by atropine. The results suggest that neostigmine, physostigmine, and pyridostigmine stimulate PI response in the airway smooth muscle, which would cause bronchoconstriction, while edrophonium does not affect PI response. (Anesth Analg 1996;82:1211-4)

Effects of sevoflurane compared with those of isoflurane on arterial oxygenation and hemodynamics during one-lung ventilation

AbstractPurpose. This study was designed to compare the effects of sevoflurane and isoflurane on Pao2 and hemodynamic variables during one-lung ventilation (OLV) in surgical patients. Methods. Twelve patients undergoing an esophageal procedure with thoracotomy for which a long period of OLV was required were studied using a randomized crossover design. Group 1 received 1.2% isoflurane from the induction of anesthesia until 30 min after starting OLV, and then received 1.7% sevoflurane during the remaining period. In group 2, the order of the anesthetics was reversed. All experimental procedures were performed in the left lateral decubitus position with the chest opened. Arterial and mixed venous blood gases and cardiac outputs were analyzed immediately before OLV, during OLV, and after resumption of two-lung ventilation (TLV). Results. OLV produced lower Pao2 and higher venous admixture (Qs/Qt) values than TLV. However, there was no significant difference between sevoflurane and isoflurane in Pao2 or Qs/Qt during OLV. Other hemodynamic variables except for Pv¯o2 showed no significant differences between the anesthetics. Conclusion. The effects of sevoflurane on Pao2 and the hemodynamic variables were similar to those of isoflurane during TLV and OLV in the lateral decubitus position.

Effect of ONO-1101, a novel short-acting β-blocker on hemodynamic responses to isoflurane inhalation and tracheal intubation

PurposeWe investigated the effect of a new ultrashort-acting β-blocker, ONO-1101, on hemodynamic responses to isoflurane inhalation and tracheal intubation.MethodsFifty-four ASA PS 1 or 2 patients were randomly allocated to receive either ONO-1101, 0.04 mg·kg−1·min−1, or saline prior to tracheal intubation. Anesthesia was induced with thiamylal, 4 mg·kg−1, and vecuronium, 0.15 mg·kg−1. Tracheal intubation was carried out after 3 min controlled mask ventilation with 66% N2O and 3% inspired isoflurane in oxygen. Heart rate and blood pressure were continuously recorded from the start of induction until 5 min after intubation. Plasma concentrations of catecholamines were measured before induction, 3 min after initiating inhalation of isoflurane, and 1 min after tracheal intubation.ResultsSignificant increases in heart rate occurred in both groups in response to isoflurane inhalation and tracheal intubation, but the magnitude of the increase was significantly less in the ONO-1101 group. Blood pressure increased after tracheal intubation in the saline group but remained unchanged in the ONO-1101 group. Plasma concentrations of norepinephrine increased after induction and intubation in both groups, with no significant difference between the groups.ConclusionONO-1101 infusion is effective for the attenuation of hemodynamic responses to isoflurane inhalation and tracheal intubation.

Induced Hypothermia in Cardiovascular and Brain Surgery

Clinical application of induced hypothermia for brain protection has expanded in recent years. There are many developments in laboratory and clinical investigations relevant to the relationship between neuronal death and brain temperature. Decreases in metabolic rate, tissue oxygen consumption, and energy demand most likely play less important roles in brain protection from ischemia, whereas more important possible mechanisms for brain protection include effects on excitatory neurotransmissions, intracellular calcium flux, membrane lipid peroxidation, free radical reactions, and permeability of the blood-brain barrier. Induced hypothermia has been applied to cardiovascular surgery and cerebral aneurysm surgery. In the intensive care unit, induced hypothermia has been applied to patients with traumatic brain injury, cerebral infarction, and subarachnoidal hemorrhage and after cardiopulmonary resuscitation. As hypothermia is not a physiological state, adverse effects would appear in cardiovascular, respiratory, coagulatory, immunological, metabolic, and other functions. Adequate indication, exact monitoring, temperature control, sufficient care, and an educated team are mandatory to maintain patient condition in a stable fashion and to avoid the complications associated with hypothermia.