Effects of isoflurane on oxygenation during one-lung ventilation in pulmonary emphysema patients.

BACKGROUND: Hypoxic pulmonary vasoconstriction has an important role in human one-lung ventilation (OLV) in the lateral decubitus position under general anesthesia. During OLV, inhalational anesthesia may inhibit hypoxic pulmonary vasoconstriction and the decrease in arterial oxygenation. We studied the effect of isoflurane administration on arterial oxygen tension in chronic obstructive pulmonary disease patients. METHODS: Ten patients who had thoracoscopic laser ablation of bullous emphysema were studied. Patients received 2% isoflurane in oxygen from induction until the first 20 min of OLV in the lateral decubitus position, then were switched to 1% isoflurane lasting 20 min and next were switched to 0.5% isoflurane lasting 20 min. After each 20-min inhalation, pulmonary and hemodynamic parameters were measured. The given concentrations for isoflurane were merely vapor meter concentrations. RESULTS: PaO2/FIO2, Qs/Qt respiratory rate peak inspiratory pressure and PaCO2 showed no significant changes at each point of isoflurane. Expiratory tidal volume significantly decreased (P < 0.05) with 0.5% isoflurane compared to that with 2% isoflurane. Cardiac output, mean arterial pressure, mean pulmonary arterial pressure, systemic vascular resistance and pulmonary vascular resistance showed no significant changes at each point of isoflurane. CONCLUSIONS: In patients with pulmonary emphysema, arterial oxygenation is not affected by low isoflurane concentration during OLV in the lateral decubitus position.

[Assessment of left ventricular contractility during intravenous induction of anesthesia by echocardiographic automated border detection].

A recently developed echocardiographic imaging system provides real-time automated border detection (ABD), which enables the measurement of cyclic changes in cavity area, and thus the calculation of changes in intracavity volumes. Eight patients (ASA 1-2) for non-cardiac surgery received thiopental (6 mg.kg-1) and succinylcholine (1 mg.kg-1) intravenously, and the trachea was intubated. The transthoracic echocardiography (TTE) was performed before induction. after induction, and after orotracheal intubation. Left ventricular end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV) and ejection fraction (EF) were measured with ABD in apical four-chamber view. Mean arterial pressure (MAP) was measured simultaneously. MAP/ESV and MAP/SV were calculated as parameters of left ventricular contractility and left ventricular afterload, respectively. EF decreased significantly (P < 0.05) after induction (50.3 +/- 8.6%) compared with the value before induction (57.9 +/- 8.7%), and decreased further after intubation (41.7 +/- 10.6%). MAP/ESV also decreased significantly (P < 0.05) after induction (2.75 +/- 1.12 mmHg.ml-1) compared with the pre-induction value (3.81 +/- 1.73 mmHg.ml-1), and then returned to the pre-induction level after intubation (3.25 +/- 1.22 mmHg.ml-1). MAP/ SV showed no significant change during induction, and increased significantly (P < 0.05) after intubation (4.60 +/- 1.66 mmHg.ml-1) compared with pre-induction value (2.60 +/- 0.46 mmHg.ml-1). These findings suggest that the significant reduction in EF after induction of anesthesia was due to depression of cardiac contractility by thiopental, and that the further decrease after intubation was due to increase in afterload caused by the stimuli during intubation.

Simultaneous demonstration of infecting fungi and DNA-synthesizing epithelial cells in the skin.

An excellent staining method to demonstrate in vivo dermatophytes and DNA-synthesizing cells in the skin is described. Deparaffinized sections of guinea pig skin, infected with dermatophytes and given bromodeoxyuridine (BrdU) by intraperitoneal injection, were used. Periodic acid-Schiff (PAS) stain in combination with an immunohistochemical stain using anti-BrdU monoclonal antibody allowed simultaneous visualization of fungi and DNA-synthesizing epithelial cells in the skin. Many epithelial cells near the infecting fungi in follicles and interfollicular skin were labelled with BrdU. Only a few BrdU-positive cells were observed in the skin of uninfected animals.

[Use of omeprazole for premedication].

Omeprazole, a proton pump inhibitor was used for premedication for general anesthesia, and its effects on gastric secretion and serum gastrin level were investigated in 60 patients. The patients were divided into the following 4 groups and each group received one of the following medications; (I) a tablet of omeprazole 20 mg before sleep at the night before the surgery, (II) a tablet 2 hours before the induction of anesthesia, (III) one on the night before and another tablet 2 hours before the induction, or (0) no tablet. In the patients who received any dose of the drug, the volume of gastric juice at the beginning of the surgery was significantly less than that in those who received no drug (P less than 0.05). Gastric pH showed a tendency to increase depending on the dose of omeprazole (0 less than I less than II less than III), but it was not significant. No significant change in serum gastrin level was observed in this study. A 20 mg omeprazole tablet may not be adequate as the premedication for general anesthesia.

Interaction between CO2 concentration and flow rate on peripheral airway resistance.

In the present study, we investigated the interaction between CO2 concentration and rate of delivered flow on peripheral airway resistance (Rp) in the intact canine lung. Dogs were anesthetized, intubated, paralyzed, and mechanically ventilated with room air to maintain end-tidal CO2 between 4.8 and 5.2%. Using a wedged bronchoscope technique, we measured Rp at functional residual capacity. The relationship between CO2 concentration and Rp was measured at flow rates of 100 and 400 ml/min with 5, 3, 2, 1, and 0% CO2 in air. Measurements were made at the end of a 3-min exposure to each gas. At low flow rates (100 ml/min) responses to hypocapnia were small, whereas at high flow rates (400 ml/min) responses were large. The PC50 (defined as the CO2 concentration required to produce a 50% increase in Rp above baseline Rp established on 5% CO2) at 400 ml/min (1.73%) was significantly larger than that at 100 ml/min (0.38%). We also directly measured the relationship between Rp and flow rate with 5% CO2 (normocapnia) or 1% CO2 (hypocapnia) delivered into the wedged segment. Increases in normocapnic flow caused small but significant decreases in Rp. In contrast, increases in hypocapnic flow from 100 to 400 ml/min caused a 108% increase in Rp. Thus the response to hypocapnia is augmented by increasing flow rate. This interaction can be explained by a simple model that considers the effect of local ventilation-perfusion ratio and gas mixing on the local CO2 concentration at the site of peripheral airway contraction.

Succinylcholine potentiates responses to intravenous acetylcholine in the canine lung periphery.

Using the wedged bronchoscope technique to measure collateral resistance (Rcs), we evaluated the effect of succinylcholine (SCh) on the response to acetylcholine (ACh) and methacholine (MCh) in the lung periphery in six mongrel dogs. Dogs were anesthetized, intubated, and mechanically ventilated. After a stable baseline Rcs was obtained, responses to intravenous ACh (25-200 micrograms), intravenous MCh (3-30 micrograms), and aerosolized ACh (30-100 micrograms/ml for 15 s) were measured. We compared the Rcs responses with 1) ACh alone, 2) ACh 2 min after SCh (0.5 mg/kg), 3) ACh 2 min after SCh and during hexamethonium infusion (5 mg/kg + 10 mg.kg-1.h-1), 4) MCh 2 min after SCh, and 5) ACh aerosol 2 min after SCh. SCh did not significantly alter baseline airway tone. SCh increased the Rcs response to ACh by 48 +/- 17% (SE) (P less than 0.01). SCh in the presence of hexamethonium increased the Rcs response by 10 +/- 3% (P less than 0.05), while hexamethonium itself increased the response to ACh by 69 +/- 27%. Because SCh did not increase the Rcs response to intravenous MCh or to aerosolized ACh, SCh probably enhances airway reactivity to intravenous ACh by competing for pseudocholinesterase in plasma. We conclude that the level of muscle relaxant must be taken into account in interpreting studies of airway reactivity when intravenous ACh is employed.

[Apnea and oxygen desaturation following nitrous oxide inhalation].

Apnea and desaturation following nitrous oxide inhalation were studied in seven adult volunteers breathing spontaneously. Arterial oxygen saturation (SpO2), end-tidal CO2 concentration in the nasal cavity and respiratory patterns were measured in volunteers breathing air after N2O (50% or 67%) + O2. SpO2 was measured with Biox 3700 and end-tidal CO2 concentration was measured with Normocap, and respiratory patterns were recorded with RESPIGRAPH. After breathing N2O, two volunteers had frequent apnea (greater than 20 sec) accompanied by desaturation (SpO2 less than 90%). The lowest value of SpO2 was 82%. When the apnea occurred, the airway seemed to be open and end-tidal CO2 concentration values were lower than those before N2O inhalation. The authors considered that this kind of apnea was due to several factors, such as hypocapnia caused by hyperventilation during N2O anesthesia, dilution of alveolar O2 and CO2 during N2O excretion, loss of consciousness by N2O, and depression of CO2 ventilatory response by N2O. Inhalation of O2 at high concentrations for five minutes could improve the hypocapnia and prevent the apnea.

Cardiovascular interaction between sevoflurane and nicardipine in open chest dogs.

Cardiovascular interaction between nicardipine and sevoflurane was examined in dogs and compared with nicardipine-thiopental interaction and nicardipine-halothane interaction. The bolus intravenous injection of nicardipine at dosages of 15 micro g/kg and 30 micro g/kg under sevoflurane anesthesia produced transient decreases in blood pressure, systemic vascular resistance, left ventricular pressure, left ventricular (dp)/(dt) and -(dp)/(dt), and a slight increase in cardiac output. The degrees of these changes were almost identical to those under thiopental or halothane anesthesia. Left and right atrial pressure, pulmonary arterial pressure, pulmonary vascular resistance were not changed by nicardipine under any of the three anesthetics. These results suggest that the cardiovascular interaction of nicardipine and sevoflurane is additive and similar to that of nicardipine and halothane and that the cardiovascular changes induced by nicardipine are not modified by the presence of anesthetics.