•Acute pulmonary microembolism causes pulmonary vasoconstriction and closure of the terminal airways. We have given reasons to suppose that these effects are not entirely explicable in terms of mechanical obstruction or neurogenic vasoconstriction and we have postulated that the effects of microembolism may be due, in part, to release of some humoral agent.1 "3 The experiments described below were designed to test this hypothesis. Methods MATERIALFourteen technically satisfactory experiments were carried out on 14 pairs of sheep. Members of each pair will be referred to as recipient (A) and donor (B). The mean weight of the recipients (A) was 33.6 kg and that of the donors (B) was 35.0 kg. OPERATIVE PROCEDURESThe supine animals were anesthetized with 10 to 15 mg/kg iv of pentothal sodium (Thiopentone) followed by an intravenous drip of 0.20 to 0.25 mg/kg/min pentothal sodium and 0.15 to 0.20 mg/kg/min heparin given in saline.Following anesthesia the trachea was intubated with a cuffed Magill tube. Catheterization of the pulmonary artery was carried out via a femoral vein and the femoral artery was cannulated. A needle was inserted into the intrapleural space and a small (60 to 100 ml) pneumothorax was induced. Rectal temperature was measured with a thermometer. PRESSURE MEASUREMENTSFemoral arterial, pulmonary arterial, intrapleural, and (whenever a double-lumen catheter was

The cardiopulmonary consequences of coli-lipopolysaccharide and staphylococcus toxin administration were studied in sheep. Circulatory changes consisted mainly of a marked rise in pulmonary arterial and pulmonary arterial wedge pressure (with left atrial pressure unchanged), and a fall in cardiac output and in systemic arterial pressure. Fall in the latter closely followed the onset of pulmonary hypertension. The respiratory response consisted mainly of a severe fall in lung compliance produced by terminal airway closure. Continued perfusion of the nonventilated alveoli resulted in venous admixture. Premedication with antihistaminic, antiserotonin, or adrenolytic agents failed to affect the response. Norepinephrine or hypertensin administered after toxin injection had virtually no effect while isoproterenol treatment reduced pulmonary arterial pressure, increased cardiac output, arterial oxygen saturation, and, in cases of endotoxin shock, promptly raised systemic arterial pressure. Endotoxin-resistant sheep proved nonresponsive to minor pulmonary embolism and to incompatible blood transfusion. It is suggested that a common mediator agent is responsible for the similar cardiopulmonary consequences of these three diverse conditions. Submitted on November 26, 1962

Hemoglobin levels in sheep was found to be related inversely to the logarithm of cardiac index and directly to the calculated systemic and pulmonary arterial resistances over a wide spectrum of hemoglobin concentrations including the normal range. It appeared to be based on changes in blood viscosity produced by a varying red cell concentration. The continuous adjustment of hemoglobin levels and cardiac output may account for the variability of cardiac output values in normal laboratory animals and may represent a mechanism maintaining oxygen delivery to the tissues in the presence of changing oxygen carrying capacity. blood viscosity; vascular resistance; oxygen carrying capacity Submitted on May 15, 1964

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