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Aggregate anaphylaxis was induced in eight ovalbumin-sensitized monkeys (Macaca irus). Hemodynamics, blood flow distribution and myocardial performance were studied. Following challenge, severe circulatory shock developed. Systemic arterial and left atrial pressures decreased and pulmonary arterial and right atrial pressures increased. There was a tenfold increase in pulmonary vascular resistance, and cardiac output was markedly reduced (-75%). A redistribution of the blood flow to vital organs (brain, heart and liver) occurred, at the expense of flow to other regions (muscles, kidneys, pancreas and spleen). There was also a redistribution of the blood flow within the myocardium, resulting in an unchanged right ventricular blood flow, despite a decrease in total myocardial blood flow. Right ventricular stroke work was reduced in spite of high filling pressures, whereas the decrease in left ventricular stroke work coincided with low filling pressures. It is concluded that the initial main cause of the low outflow state was an increased resistance in the pulmonary circulation followed by acute right heart failure.

Recently, it has been observed that, when a patient is breathing a nitrous oxide-oxygen mixture and the cuff of the tracheal tube is filled with air, nitrous oxide may diffuse into the cuff and thereby cause an increase in volume and pressure. In the present investigation, different gas mixtures were used to fill the cuff, and repeated measurements of pressure, and occasionally of volume, were made during anaesthesia. Both large-volume and small-volume cuffs were studied. A considerable increase in volume and pressure took place in both types of cuffs. The changes were directly proportional to time for the first few hours. If the cuff was inflated with nitrous oxide-oxygen, no pressure increase occurred, and this was also true for the air-filled cuff if halothane anaesthesia was given.

Mechanisms inducing a low cardiac output (CO) state in IgE-mediated (cytotropic) anaphylactic shock in anesthetized Macaca irus monkeys were studied. 7 monkeys were sensitized by 2 i.v. injections of a human reaginic serum containing a high concentration of IgE antibodies against dog albumin. Anaphylactic shock was elicited 48 h after the last sensitization dose, by an i.v. injection of dog albumin. The severe anaphylactic shock which developed was characterized by an initial phase consisting of increased CO (+16%, mean value, 1 min after challenge), pulmonary hypertension and systemic vasodilatation followed by a phase consisting of decreased CO (-67%), a fall in mean arterial pressure from 113 to 45 mmHg, decreases in left and right arterial pressures (-5.3 and -3.2 mmHg, respectively) and increases in pulmonary vascular (+364%) and total peripheral (+30%) resistances. These changes were recorded 5 min after challenge and the values then remained essentially unaltered during the rest of the 30-min observation period. Pulmonary vascular resistance was only increased by 140% at the end of that period. Myocardial blood flow was maintained during shock at the expense of flow to other organs. However, initially there was a redistribution of blood flow within the left ventricular myocardium, resulting in a relative decrease in subendocardial flow. This finding was not related either to occasional S-T changes in the electrocardiograms or to the level of decreased CO. The oxygen supply to the myocardium was reduced in shock but the reduction was always smaller than the corresponding decrease in heart work. Two additional monkeys sensitized with an IgE fraction from the human serum showed a smaller amount of specific IgG in their serum prior to challenge than the other monkeys. The response to challenge was milder, but resembled the initial vasodilatory reaction in monkeys sensitized with serum. These data on cytotropic anaphylaxis in the monkey show that the main cause of decreased CO and thus of the shock state is a decreased venous return, primarily due to peripheral blood pooling and, to a smaller extent, extravasation of plasma. No appreciable involvement of the heart in the induction of shock was detected.

Aggregate anaphylaxis was induced by intravenous injection of the specific antigen in eight ovalbumin-sensitized monkeys. Changes in respiratory mechanics, acid-base status and blood gases were studied during the following half hour. Within 1 minute after challenge, a short period of respiratory depression, probably reflex-mediated, was observed. This was followed by hyperventilation, and arterial PCO2 decreased. There was a rapid increase in pulmonary resistance (Rpulm) and a concomitant decrease in pulmonary dynamic compliance (Cdyn), suggesting constriction of smooth muscles in the lung. Rpulm returned to the control value but Cdyn remained depressed, as a result of constriction of small airways and pulmonary congestion. Oxygen saturation in arterial blood decreased slightly due to a marked desaturation of mixed venous blood and increased venous admixture. Progressive metabolic acidosis developed, indicating poor tissue oxygenation and perfusion. The changes observed in this study were not severe enough to cause any major disturbance of the gas exchange in the lungs, despite a severe anaphylactic shock.

Seven monkeys were passively sensitized intravenously (i.v.) with human serum containing IgE antibodies specific to dog albumin. I.v. administration of the antigen resulted in an immediate increase in pulmonary resistance (Rpulm) with a concomitant decrease in pulmonary dynamic compliance (Cdyn). Initially these changes in the respiratory system resulted in pronounced effects on venous admixture, arterial oxygen saturation (SaO2) and arterial pH. After 30 min, as Rpulm and Cdyn returned towards control levels, the blood gas changes were mainly due to low cardiac output. There was a transient increase in hematocrit, a decrease in plasma fibrinogen and a transient reduction in the number of circulating leukocytes. The anaphylactic reaction resulted in a 10- to 30-fold increase in plasma adrenaline with time and in a substantial but less marked increase in plasma noradrenaline and dopamine. Probably as a consequence of the increase in plasma catecholamine, there was a rise in plasma cyclic AMP, glucose and glycerol. No increase in plasma histamine levels was found. In two animals sensitized with purified IgE a reaction which was less severe but had the same general pattern was observed. The findings show that IgE-mediated anaphylaxis in the monkey results in a bronchoconstriction leading to a profound respiratory disturbance characterized by decreased SaO2 due to increased venous admixture. After 30 min these variables were normalized and the shock state was dominated by poor tissue perfusion due to a low cardiac output.

As a marker of brain cell injury, adenylate kinase (AK) was measured in cerebrospinal fluid (CSF) in 10 patients given anaesthesia with isoflurane-induced hypotension for corrective surgery of dentofacial deformities. Nine out of 10 patients displayed a marked increase in CSF-AK postoperatively compared with preoperative values. The postoperative mean value displayed a 400% increase compared to the corresponding preoperative value. This difference was statistically significant (P = 0.001). The rise in CSF-AK was most probably the result of an enhanced efflux of AK into CSF subsequent to a presumed hypoxic injury to brain cells.