Takeyasu Yamamura

Blood pressure measurement by arterial tonometry in controlled hypotension

A newly developed arterial tonometer enabled us to measure the blood pressure waveforms in addition to determining systolic and diastolic pressures noninvasively and continuously. Twenty-eight adult patients undergoing orthopedic surgery under controlled hypotension were studied. Systolic blood pressure was reduced to two-thirds of baseline values with an infusion of nitroglycerin during nitrous oxide/enflurane anesthesia. Intraarterial blood pressures were simultaneously measured in either the right or the left radial artery with a cannula and a Gould P23XL calibrated transducer; tonometric monitoring was performed on the contralateral radial artery using a Colin CBM-3000 instrument. The outputs of the two blood pressure measurement instruments were recorded for later data analysis. The shape of the tonometric pressure waveform was nearly identical to the waveform recorded intraarterially even during controlled hypotension. Regression analyses of 2039 paired tonometric and intraarterial blood pressure values during the hypotensive period showed good correlations (r = 0.78 for systolic, r = 0.81 for mean, and r = 0.70 for diastolic pressures). The accuracy of systolic, mean, and diastolic readings was from 4 to 7 mm Hg with negligible bias and did not differ significantly among six systolic, four mean, and four diastolic pressure groups. Our results indicate that arterial tonometry can provide accurate, reliable, and real-time monitoring of blood pressure even during controlled hypotension.

End-tidal CO2 changes under constant cardiac output during cardiopulmonary resuscitation

To evaluate a) whether end-tidal CO2 values change under constant cardiac output during cardiopulmonary resuscitation (CPR), and b) what factors are responsible for the change. Design:A cohort study. Setting:University research laboratory. Subjects:Nine mongrel dogs. Interventions:Ventricular fibrillation was electrically induced. After 2 mins, open-chest cardiac massage was initiated to maintain cardiac output at 0.2 L/min (23% of baseline cardiac output) by the measurement of blood flow with an electromagnetic flow probe on the ascending aorta. The cardiac massage was kept constant until 50 mins after the induction of ventricular fibrillation. Measurements and Main Results:Before and during ventricular fibrillation, end-tidal CO2, minute volume of alveolar ventilation, and CO2 excretion were continuously monitored. Blood gases and oxygen saturation values were also measured in arterial and the mixed venous blood samples. CO2 content was calculated. After induction of ventricular fibrillation, end-tidal CO2 decreased and thereafter continued to increase until the end of the experiment. Two mechanisms may have contributed to the early reduction in end-tidal CO2. One mechanism is a further decrease in CO2 excretion compared with the reduction in alveolar ventilation and the other is an increase in alveolar deadspace (estimated from the increase in the difference between Paco2 and end-tidal CO2). The subsequent increase in end-tidal CO2 was mainly due to a change in CO2 excretion. There are two hypotheses concerning the subsequent increase in CO2 excretion: the increase in pulmonary capillary blood flow (estimated from the change in the arteriovenous C02 content gradient) and the increase in CO2 production itself. Conclusions:End-tidal CO2 changes under constant cardiac output during CPR. When end-tidal CO2 is used to estimate the effectiveness of the cardiac massage, this type of change must be recognized. (Crit Care Med 1993; 21:1572–1576)

The effect of fentanyl and morphine on neurons in the dorsal raphe nucleus in the rat: an in vitro study.

The dorsal raphe (DR) nucleus is a system of nuclei lying in the midline of the lower brainstem constituting the largest collection of serotonin-containing neurons in the brain. The DR nucleus, which is under the influence of various synaptic inputs containing the excitatory amino acids (EAAs), serotonin and noradrenaline (NA), has been reported to be involved in the process of nociception. We studied the effects of fentanyl and morphine on the firing activity of neurons within the DR nucleus in the rat brain slice preparation in vitro using extracellular recording techniques. The decreased activity of DR neurons induced by these opioids was reversed upon application of naloxone. Since almost all neurons were silent, N-methyl-D-aspartate (NMDA) and noradrenaline were used to excite the DR neurons. Serotonin contained in the DR nucleus acts as a neuromodulator to enhance the excitatory effects of NMDA. All DR neurons were excited by NMDA, whereas 72% of the neurons were excited by NA. NA has a long-lasting effect on the firing activity of the neurons, although the firing pattern was less regular than that induced by NMDA. Of the total number of the DR neurons excited by NMDA and/or NA, 71% were inhibited by fentanyl and 73% by morphine. The results support our hypothesis that these opioids inhibit the firing activity of DR neurons and, in turn, might alter nociception directly and/or indirectly by modifying the central serotonergic system.

Thoracic epidural anaesthesia combined with enflurane anaesthesia reduces atrioventricular conduction in dogs

Cardiac electrophysiological variables during thoracic epidural lidocaine (TEL) were compared with those during continuous intravenous lidocaine (IVL) infusion in 14 mongrel dogs anaesthetized with enflurane in order to investigate the combined effects of thoracic epidural anaesthesia (TEA) and enflurane anaesthesia on intracardiac conduction. Thoracic epidural lidocaine suppressed intracardiac conduction. Sinus cycle length (SCL) and Atrium-His (AH) interval increased by 9 and 11 per cent respectively (P < 0.05), 30 min after TEL. Intravenous lidocaine did not increase either SCL or AH. The functional refractory period of the atrioventricular node increased five per cent above the control value 15 min after TEL (P < 0.05), while it was unchanged in the IVL group. The mean plasma concentrations of lidocaine ranged from 0.48 ± 0.07 to 1.00 ± 0.14 μg · ml−1 in the TEL group and from 0.98 ± 0.13) to 1.21 ± 0.15 μg · ml−1 in the IVL group. There were no significant differences in plasma concentrations of lidocaine in both groups during the observation period. Therefore, it is concluded that the depressant effects of TEA on intracardiac conduction were caused by blocking of the sympathetic efferent activity. Caution may be advised in administering TEA when cardiac conduction is already compromised.RésuméLes variables electrophysiologiques cardiaques lors d’une anesthésie thoracique épidurale avec la lidocaïne (TEL) ont été comparées avec celles obtenues lors d’une perfusion intraveineuse de lidocaine (IVL) chez 14 chiens bâtards anesthésiés avec l’enflurane afin d’investiguer les effets combinés de l’anesthésie épidurale thoracique (TEA) et l’anesthésie à l’enflurane sur la conduction intracardiaque. La lidocaine administrée par voie épidurale thoracique a supprimé la conduction intracardiaque. La longueur du cycle sinusal (SCL) et l’intervalle de His auriculaire (AH) ont augmenté de 9 et 11 pour cent, respectivement (P < 0,05), 30 minutes après TEL. La perfusion intraveineuse de lidocaïne n’a augmenté ni le SCL ni le AH. La période réfractaire fonctionnelle du nœud atrioventriculaire augmenta de cinq pour cent de la valeur de contrôle 15 minutes après TEL (P < 0,05) alors qu’elle fut inchangée dans le groupe IVL. Les concentrations plasmatiques moyennes de lidocaïne variaient entre 0,48 ± 0,07 à 1,00 ± 0,14 μg · ml−1 pour le groupe TEL et de 0,98 ± 0,13 à 1,21 ± 0,15 μg · ml−1 pour le groupe IVL. Il n’y avail aucune différence significative dans les concentrations plasmatiques de lidocaïne dans les deux groupes pendant la période de surveillance. Ainsi on conclut que les effets dépresseurs de la TEA sur la conduction intracardiaque sont causés par le blocage de l’activité efférente sympathique. La prudence est conseillée lors de l’administration de la TEA quand la conduction cardiaque est déjà compromise.

Influence of hypoxic and hypercapnic acidosis on brain water content after forebrain ischemia in the rat

Objective.To determine whether hypoxia or hypercapnia superimposed on ischemia affects brain water content after ischemia. Design.Prospective, randomized, controlled trial. Subjects.Thirty-one male Wistar rats. Interventions.The rats were assigned randomly into one of six groups: a) control; b) ischemia; c) ischemia combined with hypoxia; d) ischemia combined with hypercapnia; e) hypoxia; f) hypercapnia. Forebrain ischemia was induced for 5 mins by clamping both carotid arteries and inducing exsanguination. Either hypoxia or hypercapnia was induced until the arterial pH decreased to 7.0. The rats were decapitated after the protocol. Measurements and Main Results.After the decapitation, the specific gravities of the neocortex, caudatoputamen, hippocampus, cerebellum, and midbrain were measured using a variable-density bromobenzene-kerosene column technique as an index of brain swelling. The specific gravities of the hippocampus and the neocortex were significantly lower in the ische-mic group than in the control group. Specific gravities of the caudatoputamen and neocortex in the ischemia plus hypercapnia group, and specific gravities of the caudatoputamen, neocortex, and hippocampus in the ischemia plus hypercapnia group, were significantly lower than in the ischemia group. Conclusions.Cerebral water content increases more when ischemia is accompanied by hypoxia or hypercapnia than after ischemia alone. Hypoxic and/or hypercapnic acidosis during the periresuscitation period may be one of the causes of brain swelling after the resuscitation of patients after an anoxic-ischemic insult. (Crit Care Med 1993; 21:907–913)

Effect of preanesthetic intramuscular ranitidine on gastric acidity and volume in children

STUDY OBJECTIVE To evaluate the effects of preanesthetic administration of intramuscular (IM) ranitidine on pH and volume of gastric contents in children. DESIGN Three randomized treatment groups. SETTING Central operating rooms at a university hospital. PATIENTS Forty children age 1 to 10 years undergoing a variety of elective surgical procedures requiring general anesthesia with endotracheal intubation. INTERVENTIONS IM ranitidine 1 mg/kg (n = 15) or 2 mg/kg (n = 15) was administered 2 hours prior to induction of anesthesia. Ten patients without ranitidine served as the control group. An orogastric tube was inserted into each patient. MEASUREMENTS AND MAIN RESULTS Gastric fluid pH and volume were measured every hour in the three groups. Plasma ranitidine concentrations were measured in ten patients of the ranitidine-treated groups. The mean volume of gastric fluid at induction of anesthesia was significantly lower in the ranitidine-treated patients (2.4 ml for ranitidine 1 mg/kg, 3.2 ml for ranitidine 2 mg/kg) than in the controls (8.6 ml; p less than 0.05). The mean pH values at induction of anesthesia were significantly higher in the ranitidine-treated patients (4.6 for 1 mg/kg, 6.7 for 2 mg/kg) than in the controls (2.1; p less than 0.05). Dose-dependent plasma ranitidine concentrations were obtained. CONCLUSIONS Preanesthetic IM ranitidine 1 to 2 mg/kg resulted in a higher pH and lower volume of gastric fluid at the time of induction and in a higher pH during 3 hours of anesthesia. This therapy may be a useful adjunct to premedication for children who have a greater than normal risk of pulmonary aspiration during anesthesia.

A single-unit device for differential lung ventilation with only one anesthesia machine.

One-lung ventilation during thoracic surgery in the lateral decubitus position occasionally produces hypoxemia, and there has been great interest in methods for maximizing arterial oxygenation (1-3) under such circumstances. Differential lung ventdation is one such method that improves ventilation to the dependent lung and also facilitates surgical manipulation of the nondependent lung. However, differential lung ventilation as generally described requires the simultaneous use of two anesthesia machines and two ventilators. Such complexity severely limits its acceptance into common anesthetic practice (4). In an attempt to settle these problems, we have developed a single-unit device that allows differential lung ventilation with only one anesthesia machine. The present report describes the technical performance of such a device.

Effects of biogenic amines and intravenous anesthetics on the activity of rat locus coeruleus neurons in vitro

To examine the effects of biogenic amines and clinically relevant concentrations of intravenous anesthetics on neuronal activities, the authors analyzed both spontaneous and evoked activities of neurons in the nucleus locus coeruleus (LC)in vitro using a single unit recording technique. Spontaneous firing was observed in 37% (14/38) of LC neurons, andN-methyl-d-aspartate (NMDA, 50 μM), glutamate (250 μM), and carbachol (1–2 mM) elicited firing in 100% (38/38), 63% (12/19), and 58% (7/12) of silent LC neurons respectively. Noradrenaline (50 μM) and serotonin (5-HT) (1–5 μM) suppressed spontaneous and drug-induced activities in 47% (15/32) and 23% (8/35) of LC neurons, respectively. Pentobarbital (100 μM) inhibited 50% (5/10) of LC neurons. All neurons activated by NMDA (n=8) and glutamate (n−3) were suppressed by ketamine (40 μM), but fentanyl (1 μM) only suppressed 60% (3/5) of spontaneously active and 75% (3/4) of glutamate-activated neurons. Identical LC neurons were inhibited by various combinations of noradrenaline, 5-HT, pentobarbital, ketamine, and fentanyl. The results suggest that clinically relevant concentrations of anesthetics and opioids modulate the activity of LC neurons induced by biogenic amines, excitatory amino acids, and acetylcholine.

Does propofol enhance GABA-mediated inhibition?

The effects of propofol on synaptic transmission were characterized and compared with pentobarbital in the rat hippocampal slice preparation. Hippocampal CA1 population spike after stimulation of Schaffer collaterals indicated that the postsynaptic response was primarily mediated by non-N-methyl-D-aspartate class glutamate receptors since it was abolished by the presence of 6,7-dinitroquinoxaline2,3-dione (DNQX). Propofol and pentobarbital depressed CA1 population spike amplitude in a dose dependent fashion. Dose-response curves for population spike amplitudes were determined for propofol and pentobarbital and the concentrations producing a half-maximum response (ED50) were 110 μM and 160 μM for propofol and pentobarbital, respectively. By contrast, when GABAA-mediated inhibition was blocked by addition of 100 μM pictotoxin, propofol, in concentrations up to 400 μM had no significant effect on population spike amplitudes. These results suggest that propofol attenuates synaptic transmission in the central nervous system in part by enhancing GABAA-mediated inhibition and not by depressing glutamate-mediated excitation, as occurs with pentobarbital.

Hemodynamic effects of nicardipine-induced hypotension during enflurane/nitrous oxide anesthesia in man

Hemodynamic effects of nicardipine-induced hypotension during enflurane/nitrous oxide were evaluated in 10 surgical patients. An infusion of nicardipine was titrated to maintain mean arterial pressure at 60 to 70 mmHg under enflurane 1.5 to 2.0 vol% and nitrous oxide 60 vol%. Mean arterial pressure was well controlled with the nicardipine infusion, whereas cardiac index increased with decreased systemic vascular resistance. Heart rate increased concomitantly with decreased blood pressure, which indicated that enflurane 1.5 to 2.0 vol% did not suppress baroreceptor reflex during nicardipine administration. However, rate-pressure-product was not increased by the nicardipine. Right and left ventricular systolic work indices were not increased by the nicardipine. Right ventricular ejection fraction was not also changed by the nicardipine. Although serum norepinephrine level increased during the nicardipine infusion, the values remained within physiological ranges. Our results suggest that nicardipine-induced hypotension may be safely performed during enflurane/nitrous oxide anesthesia because neither ventricular work nor myocardial oxygen demand was increased by nicardipine.