[in Japanese]

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Using six inert gas elimination method, the change of distribution of ventilation-perfusion ratio (V_A/Q) was observed on 2 cases of the artificial ventilation treatment of acute pulmonary insufficiency.
In case 1 who developed acute pulmonary insufficiency following the cardiac arrest in acute poisoning of agricultural agent and who showed the large intrapulmonary shunting and bimodal V_A/Q imbalance. On the 4th date after the commencement of the artificial ventilation, intrapulmonary shunting was considerably improved and at the 24th date V_A/Q imbalance was also improved.
In case 2 who developed acute pulmonary insufficiency following the multiple rib fracture and pulmonary contusion and who showed unimodal widely distributed V_A/Q imbalance in addition to the large intrapulmonary shunting, the improvement of intrapulmonary shunting was obtained also at the 4th date of artificial ventilation therapy and at 8th date V_A/Q imbalance was improved.
The results obtained were also confirmed by the finding on the chest x ray and those obtained in arterial blood gas analysis.
As a conclusion it will be reasonably stated that in the case of acute pulmonary insufficiency, following the artificial ventilation therapy, the improvement of intrapulmonary shunting will be first obtained then V_A/Q imbalance will be improved.

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A 76 year old woman underwent a subtotal thyroidectomy without event. A postoperative fiberoptic bronchoscopy induced severe laryngospasm. After a period of labored respiration, subcutaneous emphysema developed around the neck and upper thorax while the chest X-ray film showed a right pneumothorax.
An open examination of the surgical wound did not disclose any air leakage from the trachea under the intratracheal positive pressure ventilation.
Since there was no reasonable explanation for the emphysema and pneumothorax, a possible mechanism was suspected in which the air was sucked into the tissues through the drains in the wound by a negative pressure created between the muscle layers during the labored respiration.
To explore the possibility of this mechanism, animal experiments were performed on five mongrel dogs. The dogs were anesthetized and intratracheally intubated.
A transverse incision of about 5cm in length was made in the mid neck area, far from the pleural apex. Several film drains were placed between the muscle layers and around the trachea. After closure of the skin incision, the endotracheal tube was occluded intermittently to prevent instantaneous death. Severe respiratory effort caused an end -inspiratory pressure of about -80mmHg sometime before death.
A necropsy of the dogs revealed emphysema in the loose connective tissues between the fascias, the peritracheal region and the upper mediastinum in all dogs and bilateral pneumothorax in one. Serous membrane was taken from the mediastinum and the rupture point of the membrane was found to be between 40 to 80mmHg.
We believe that the emphysema and pneumothorax found in this patient might have been caused by a rare mechanism, in which the air was sucked into the subdermal and intrafascial loose connective tissue through the drains by a negative pressure during the labored breathing, and transferred to the mediastinum by a pump action of the muscle layers, finally producing pneumothorax.

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During upper abdominal operations, 21 patients were given 20ml of saline epidurally with or without preservative-free morphine, 1mg, via a catheter placed at the spinal level of T_7-8.
Mean requirements of intramuscular administration of pentazocine within 24 hours after surgery in morphine (n=12) and saline (n=9) group were 18.8mg and 66.7mg respectively, which differed significantly between both groups (P<0.001).
Although there seems to be large individual variability in the magnitude of analgesic effect, excellent analgesia was observed 50% of patients receiving morphine.
Present results confirm our previous suggestion that analgesic effect of epidural morphine depends not only the dose of morphine itself but also the volume of saline infused concomitantly.

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The cardiovascular effects of nitroglycerine and sodium nitroprusside during hypotensive anesthesia were studied on 16 cases of cerebral aneurysm.
Under halothane-nitrous oxide-oxygen anesthesia fully stabilized, nitroglycerine or sodium nitroprusside was administered by an infusion pump at the rate of 10μg/kg/min and 2μg/kg/min respectively.
These rate were instantaneously adjusted to reduce the systolic blood pressure to 50-70mmHg.
There were marked fall in arterial blood pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, central venous pressure, systemic vascular resistance and rate pressure product to the similar extent by hypotensive agents.
Cardiac output revealed a tendancy to increase during hypotensive period.
From these results authors concluded that both hypotensive agents reduce arterial blood pressure due to dilatation of peripheral vascular beds.
Cardiac function indicated rather favorable condition during hypotensive period.

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Plasma ADH levels during hepatic resection were measured in 16 patients with hepatoma to evaluate the stress responses under this extensive surgical procedure. 7 patients underwent total gastrectomy were also studied as a control group.
Plasma ADH, osmolality, Mean Arterial Pressure, Pulmonary Capillary Wedge Pressure, Cardiac Output, PaCO₂ and Ccr were measured prior to anesthesia, during and at the end of and 6 hours after operation, respectively. Modified NLA with diazepam-fentanyl-nitrous oxide-oxgen-pancuronium was administered. Ringer lactate 10ml/kg/hr with plasma and glucose was infused intraoperatively.
Plasma ADH rose significantly during operation in both groups and the elevation in this hormone was less prominent in hepatic group, unexpectedly (maximal elevation: 23.3pg/ml in hepatoma and 29.2pg/ml in control). MAP, PCWP, and CO increased during operation in the same way as plasma ADH. Plasma osmolality showed slight elevation and PaCO₂ decreased significantly during operation.
Accordingly, the main stimuli for ADH secretion could be the painful surgical stimuli which might be less potent in hepatic resection than in total gastrectomy.

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We studied the effect of preoperative hydration on the secretion of ADH during surgery. 19 patients undergoing hysterectomy were devided into two groups, Control group and Hydration group, based on the amount of preoperative infusion.
Venous blood samples were obtained
(1) before starting preoperative hydration at 8:00A.M., (2) immediately prior to induction of anesthesia, (3) 15 minutes after induction of anesthesia, (4) 10 minutes after incision, (5) 30 minutes after incision, (6) 60 minutes after incision and (7) immediately after operation.
The ADH levels were (mean±SEM)
(1) 3.1±0.9 (2) 3.2±0.9 (3) 2.7±0.6 (4) 45.1±12.7 (5) 19.5±4.0 (6) 17.9±5.1 and (7) 18.6±4.1pg/ml in the control group and (1) 3.7±0.5 (2) 3.9±0.6 (3) 3.1±0.6 (4) 84.9±30.7 (5) 47.6±14.9 (6) 24.5±5.2 and (7) 23.0±7.0 in the hydration group, respectively. There was statistically no significant difference between the two groups.
Our protocol for preoperative infusion does not seem to have any inhibitory effect on the secretion of ADH during surgery.

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We measured the serum ionized calcium concentration (Ca⁺⁺) in 27 patients who received ACD blood transfusion ranged from 400ml to 4200ml during general anesthesia. Ca⁺⁺ was measured prior to transfusion, at various intervals and at the end of transfusion.
Ca⁺⁺ decreased immediately after the transfusion, from 2.13±0.14mEq/l at the baseline to 1.92±0.20 mEq/l (p<0.05) following the 200ml of transfusion and tended to decrease with additional transfusion up to 600ml of blood. The lowest value of Ca⁺⁺ was 1.78±0.28mEq/l at the 2400-4200ml of transfusion. All values were significant (p<0.05) to baseline, but not significant between each other. We observed no correlation between the rate of transfusion and the decline of Ca⁺⁺.
8 patients who received 1350ml of transfusion on the average, were administered 5ml of 8.5% calcium gluconate after the termination of trantfusion. Ca⁺⁺ increased from 1.72±0.16mEq/l to 2.06±0.21mEq/l (p<0.05) 5min after the administration, and returned to the normal value.

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One hundred and twenty-one subjects, included eleven probands with an episode of malignant hyperthermia, 104 their relatives and normal controls, were examined in biopsied muscle fascicles with caffeine contracture test. The contracture amplitudes (increases in resting tensions) were measured four minutes at 37°C after each caffeine addition in the presence and in the absence of 1% halothane. The grams tension versus log caffeine dose were plotted in duplicate. From dose-response curve the concentration of caffeine required to raise the resting tension of muscle by 1.0g were designated the caffeine specific concentration (CSC) and the caffeine specific concentration with halothane (CSC-H). Halothane potentiated the caffeine contracture in all but especially in higher amplitude in muscle specimens from young male subjects in comparison with those from female subjects.
CSC and CSC-H were significantly less in probands than in normal controls. Also CSC and CSC-H for the near and distant relatives were intermediate between the normals and probands in the average. The abnormal susceptivility of skeletal muscle to caffeine and halothane were suggested to be inherited as a autosomal dominant mode. A trial of determinating the critical values of CSC and CSC-H which discriminating malignant hyperthermia susceptivility from their normal relatives were undertaken.

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