Hiroshi Takeshita

Cerebral circulation and metabolism in patients with septic encephalopathy

Cerebral circulation and metabolism in septic encephalopathy have not been well documented. The authors measured cerebral blood flow (CBF) and metabolic rate for oxygen (CMRO2) in six patients with septic encephalopathy associated with multiple organ failure (three to five organs). They found that CBF and CMRO2 were significantly lower than awake control values of 46 +/- 2 to 28 +/- 3 mL/100g/min (mean +/- SEM) and 3.1 +/- 0.2 to 1.2 +/- 0.2 mL/100g/min, respectively. Cerebral vascular resistance (CVR) and cerebral circulatory index (CCI:CBF/CMRO2) were significantly higher than the control values of 2.0 +/- 0.1 to 3.0 +/- 0.4 mm Hg/mL/100g/min and 15.1 +/- 0.8 to 24.2 +/- 3.3, respectively. At the time of cerebral circulatory and metabolic measurements, their consciousness varied between 4 and 10 as evaluated by the Glasgow coma scale. The electroencephalogram showed diffuse slow wave activity and the latency of the auditory brain stem evoked response was prolonged in four of six patients. Computed brain tomography showed either no abnormality or mild atrophy. It is concluded that CBF and CMRO2 are disproportionally decreased during septic encephalopathy in association with dysfunction of the CNS and decreased electrical activity.

Central nervous system complications after cardiac surgery: a comparison between coronary artery bypass grafting and valve surgery.

Central nervous system (CNS) complications (disturbance of consciousness, focal motor deficits, and seizures) after coronary artery bypass grafting (CABG) and cardiac valve surgery were studied retrospectively. The incidence of CNS complications was significantly more frequent in CABG (11%, 71/638) than in valve surgery (7%, 24/345). Major contributory factors of CNS complications were preexisting cerebrovascular disease and cardiopulmonary bypass time. In comparison to previous reports, older age, hypertension, diabetes mellitus, and cerebrovascular disease were more common in the patients undergoing CABG. The preexisting cerebrovascular disease and prolonged cardiopulmonary bypass time probably increase the risk of cerebral embolism and/or cerebral hypoperfusion. We conclude that patients undergoing CABG surgery are at greater risk for neurological damage in comparison to those undergoing valve surgery.

Intracranial pressure following cardiopulmonary resuscitation

Intracranial pressure (ICP) was measured in six patients following cardiopulmonary resuscitation (CPR). The causes of cardiac arrest were respiratory or circulatory problems and the primary intracranial pathology was not detected. The measurement of ICP started 3 to 10 h following CPR except one patient in whom it started on the day 7. Duration of ICP measurement ranged from 2 to 7 days. In five out of six patients, ICP persistently remained below 20 mmHg. In the remaining one patient, ICP elevation associated with seizure activity was observed and ICP ultimately increased to 57 mmHg. Among these, four patients died and two remained in a persistent vegetative state. These results suggest that ICP following CPR does not necessarily increase if the patient has no primary intracranial pathology or seizures.

Nicardipine increases cerebral blood flow but does not improve neurologic recovery in a canine model of complete cerebral ischemia

The effects of the calcium entry blocker nicardipine on CBF, CMRO2, and neurologic outcome following 10 min of complete cerebral ischemia were examined in dogs. In CBF and CMRO2 studies, the CBF in the untreated group (seven dogs) and the nicardipine group (seven dogs; 20 μg kg−1 at 30 min postischemia and a subsequent infusion of 2 μg kg−1 min−1 for 90 min) initially increased to 300–400% and then returned to preischemic values at 30 min postischemia. Thereafter the CBF in the untreated group significantly decreased to 50% of preischemic values for the following 90-min period (hypoperfusion), while the CBF in the nicardipine group did not differ from preischemic values. The CMRO2 in both groups decreased to ∼50–80% of preischemic values after 15 min postischemia and did not differ between the groups throughout the study. In neurologic outcome studies, 18 dogs were divided into three groups (of six dogs each): untreated; saline infusion only, posttreated; nicardipine as in CBF and CMRO2 studies, pretreated; nicardipine 20 μg kg−1 at 2 min preischemia and a subsequent infusion of 2 μg kg−1 min−1 from immediately postischemia to 120 min postischemia. Nicardipine treatment initiated either before or after ischemia failed to improve neurologic outcome at 48 h postischemia. Thus, the increase of postischemic global CBF by nicardipine is not accompanied by neurologic recovery in a canine model of complete cerebral ischemia.

Cerebral Circulatory and Metabolic Stimulation with Nitrous Oxide in the Dog Reconfirmation by the Simultaneous Measurement of Ckrebral Blood Flow using Direct and Kety‐Schmidt Methods

In both the presencc and the absence of nitrous oxide (57%, end‐tidal), cerebral blood flow (CBF) was measured by a direct method in dogs, and compared to an indirect method (Kety‐Schmidt method), using argon as the tracer. Eighteen comparisons were made in five dogs at flows ranging from 45 to 123 ml per 100 g per minute. There was no systematic difference in CBF between the direct and indirect mcthods, and the ratio of direct CBF to indirect CBF was 1.03. The cerebral circulatory and metabolic stimulation effect of N2O in the dog was reconfirmrd.

Responses of EEG, cerebral oxygen consumption and blood flow to peripheral nerve stimulation during thiopentone anaesthesia in the dog.

The effects of sciatic nerve stimulation on the electroencephalogram (EEG), cerebral metabolic rate for oxygen (CMRO2) and cerebral blood flow (CBF) were investigated during thiopentone anaesthesia in dogs. Anaesthetic levels at 15, 35, 65, 95 and 125 minutes after the start of thiopentone infusion (23 mg.kg-1.hr-1) were designated levels I, 11, III, IV and V, respectively. The effects of stimulation for 5 min were tested at each level. At level 1 (plasma thiopentone concentration; 15 ± 2 μg.ml-1), the EEG was activated with stimulation and CMRO2 and CBF increased by a maximum of 16 and 15 per cent, respectively. The increase in CMRO2 and CBF was significant for five and four minutes, respectively, though the increase became less with time. At level II (27 ±3 μg.ml-1), the CMRO2 and CBF increased at one minute by eight and nine per cent, the increase being accompanied by transient EEG activation. At the three deepest levels III, IV and V (37 ± 6, 42 ± 6, 49 ± 6 μg.ml-1). the EEG, CMRO2 and CBF remained unchanged with stimulation. The results suggest the existence of the tight coupling between the EEG, CMRO2 and CBF and of a threshold level of thiopentone to block the response to peripheral stimulation during thiopentone anaesthesia.RésuméLes effets de la stimulation du nerf sciatique sur l’électroencéphalogramme (EEG), consommation d’oxygène par le cerveau (CMRO2) ainsi que le flot cérebral (CBF) ont été investigués lors de l’ anesthésie au thiopentone chez les chiens. Les niveaux d’ anesthésie à 15,35,65,95 et 125 minutes après le début de la perfusion du thiopentone (23 mg-kg-1-hr1) ont été définis comme étant les niveaux I, II, III, IV et V. Les effets d’une stimulation de cinq minutes ont été étudiés à chaque niveau. Au niveau I (concentration plasmatique de thiopentone; 15±2 µg.ml-1), IéEEG a été activeé par la stimulation et la CMRO2 et le CBF ont augmenté de 16 et 15 pour cent respectivement. L’augmentation de la CMRO2 et du CBF a été significative pour cinq et quatre minutes respectivement même si l’augmentation a diminué avec le temps. Au niveau II (27 ± 3 µg.ml-1), le CMRO2 et le CBF ont augmente a une minute de huit et neuf pour cent, I’augmentation étant accompagnée par une activation transitoire de I’EEG. Aux trois niveaux les plus profonds III, IV et V (37 ± 6, 42 ± 6, 49 ± 6µg.ml-1), I’EEG, la CMRO2 et le CBF sont restés inchangés avec la stimulation. Les résultats suggèrent une liaison étroite entre I’EEG, la CMRO2 et le CBF ainsi que les niveaux du thiopentone qui bloqueraient la réponse à une stimulation périphérique.

The effect of ketamine on cerebrospinal fluid pressure.

ETAMINE has been reported to produce K marked increases in both cerebrospinal fluid pressure (CSFP) and cerebral blood flow (CBF).1-4 The present study was undertaken to further clarify the relationship between cerebral hemodynamics and CSFP in man anesthetized with ketamine, and to examine the possible modifying effects of hypocarbia. The results indicate that the increase in CSFP induced by ketamine is secondary to an increase in CBF, and that these effects can be minimized or abolished by induced hypocarbia.

Correlation between arterial blood pressure and oxygenation in tetralogy of fallot

To examine the relationship between arterial blood pressure and oxygenation in patients undergoing complete surgical correction of tetralogy of Fallot, a retrospective study of 16 patients was first performed, looking at the correlation between mean arterial blood pressure (MAP) and arterial oxygen tension (PaO2). The correlation between phenylephrine-induced changes in MAP (delta MAP) and those in PaO2 (delta PaO2) was investigated prospectively in seven patients. In the retrospective study, there was a significant correlation between MAP and PaO2 (n = 66; r = 0.55; P less than 0.01), and most data points with a PaO2 less than 50 mm Hg were associated with a MAP less than 60 mm Hg. In the seven patients who received phenylephrine, 10 micrograms/kg, a significant correlation was found between delta MAP and delta PaO2 (n = 10; r = 0.95; P less than 0.01). These results suggest that in tetralogy of Fallot arterial blood pressure is a determinant of arterial oxygenation, and that the risk of serious hypoxia is significant when MAP is less than 60 mm Hg.

PRETREATMENT WITH D-TUBOCURARINE, VECURONIUM, AND PANCURONIUM ATTENUATES SUCCINYLCHOLINE-INDUCED INCREASES IN PLASMA NOREPINEPHRINE CONCENTRATIONS IN HUMANS

We studied in patients the effect of d-tubocurarine, which has sympathetic ganglion blocking action, on succinylcholine-induced increases in plasma levels of catecholamines, and compared it with the effects of vecuronium and pancuronium, which have little sympathetic ganglion blocking action. Thirty-two patients were divided into five groups: seven were given 3 mL saline; seven received 1 mg/kg succinylcholine; and six, seven, and five patients were given 0.08 mg/kg d-tubocurarine, 0.01 mg/kg vecuronium, and 0.01 mg/kg pancuronium, respectively, all of which were injected 5 min before 1 mg/kg succinylcholine. Succinylcholine alone significantly increased plasma norepinephrine concentrations, systolic blood pressure, and heart rate from 187 ± 39 pg/mL (mean ± SEM), 93 ± 2 mm Hg, and 77 ± 4 beats/min to 429 ± 61 pg/mL, 120 ± 7 mm Hg, and 102 ± 6 beats/min, respectively, with onset of fasciculations. Pretreatment with d-tubocurarine, vecuronium, and pancuronium significantly and equally attenuated both the fasciculations and the cardiovascular responses to succinylcholine. These results suggest that the sympathetic ganglion blocking action of neuromuscular relaxants when given before succinylcholine is not an important factor in attenuation of succinylcholine-induced increases in plasma levels of catecholamines.

Lidocaine modifies the effect of succinylcholine on muscle oxygen consumption in dogs

The effects of succinylcholine (SCh: 2 mg/kg) alone and in combination with lidocaine (4.5 mg/kg in two increments) on muscle oxygen consumption (Vo2) and blood flow (MBF) in normal and denervated gastrocnemius muscle were studied in 18 dogs anesthetized with halothane (0.94%, end tidal) to examine the interactions of both drugs at the neuromuscular junction. In an additional five dogs with normal gastrocnemius muscle, the effects of lidocaine alone on Vo2 and MBF were also studied. In normal muscle, Vo2 increased as much as 150% with SCh alone, while with the combination of lidocaine and SCh, Vo2 remained unchanged. MBF remained unchanged with SCh alone and the combined use of lidocaine and SCh. Neither the Vo2 nor MBF was affected by lidocaine alone. In denervated muscle, Vo2 increased as much as 304% with SCh alone and MBF increased 115%. With the combined use of SCh and lidocaine the Vo2 in denervated muscle increased up to 360% with a 290% increase in MBF. These findings indicate different effects of lidocaine on metabolic and circulatory responses to SCh in normal and in denervated muscles in dogs.