Jacob Fine

THE BACTERIAL FACTOR IN TRAUMATIC SHOCK

IN a standardized preparation of hemorrhagic shock we have repeatedly demonstrated that over 80 per cent of animals recover promptly and completely if the blood lost is returned after ninety minute...

CENTRAL VENOUS PRESSURE AND DIRECT SERIAL MEASUREMENTS AS GUIDES IN BLOOD-VOLUME REPLACEMENT

A comparative study in the same patients of the 2 methods for determining the amount of blood needed to obtain optimal blood-volume was conducted. The central venous pressure (CVP) was monitored continuously by an intravenous catheter with its tip in the superior vena cava and connected to a saline-solution manometer with the zero point at 1/2 the anteroposterior diameter of the chest. The measured normal central venous pressure ranged from 2-10 cm of water. The blood-volume was measured with a semi-automatic instrument with which accurate serial determinations of blood-volume were obtained. When the normal blood-volume was not known by direct measurement it was calculated as the product of the patients weight in kg times 65 70 or 75 ml depending on the body habitus and nutritional state of the patient. 6 case reports culled from a study of over 80 patients in shock in whom these 2 measurements were taken serially over a period of many hours are reported. They were selected in order to illustrate the variety of problems encountered in restoring blood-loss. Direct measurement of the blood-volume with the aid of the modern computer devices yields reliable results even in advanced shock and facilitates precise correlation of the deficit yet in patients with or without cardiac disability and particularly those of middle or advanced age monitoring of the CVP combined with serial blood-volume determinations provides the best guide.

Comparative response of normal and cirrhotic rats to intravenously injected bacteria.

Summary Labelled (I131) bacteria infused into portal vein of normal rats were promptly cleared and destroyed with release of ionic I131 and its prompt excretion into the urine. In cirrhotic rats the clearance process was normal, but capacity to destroy bacteria was impaired. This resulted in persistence of ingested bacteria and of “bacteria bound” radioactivity in liver, lung, and spleen, and continued reseeding of the blood stream from such foci.

Detoxification of Endotoxin by Perfusion of Liver and Spleen.

Summary and conclusions The mortality of a dose of a bacterial endotoxin in rabbits, which was 85% when injected into a systemic vein, was reduced to 11% when it was injected via a mesenteric vein, i.e., so that it must traverse the liver before entering the systemic circulation. Bacterial endotoxin (Salmonella enteritidis MLD/80 = 1 mg/kg) in plasma was perfused through the dener-vated dogs spleen in vitro. Corresponding dilutions of infusate and effluent were assayed for detoxification in pertussis-treated mice, and by the immuno-diffusion technic. These assays showed substantial detoxification of the endotoxin in the effluent and of the endotoxin retained by the spleen. Because the degree of dilution of the effluent may have been great enough to reduce the endotoxin content per aliquot below the sensitivity of the bioassay technics, partially purified extracts of spleen were also interacted with endotoxin and detoxification by the same assay technics was demonstrated. These data show that the liver and spleen not only rapidly extract, but also rapidly detoxify bacterial endotoxins. Because of varying degrees of vasoconstriction of the circulation to these organs in the normal animal, the full detoxifying potential of these organs when challenged may not be available.

On the Nature of Tolerance of Endotoxin.

Tolerance of endotoxin has been found to be related to the pinocytic and phagocytic capacity of the reticulo-endothelial system (1–4). Recently the plasma of the tolerant animal has been found to contain a transferable factor that suppresses pyrogenicity and increases the rate of phagocytosis in the recipient (5–7). Such data, though doubtless of considerable significance, do not sufficiently explain what it is that constitutes increased tolerance. We have reported the presence in normal spleen of a protein with an esterase-like behavior (8) which is capable of rapidly degrading endotoxin(9), as indicated by tests: a, for toxicity of endotoxin for the 10-day-old chick embryo, and for the pertussis-treated mouse (10), and b, for the capacity of endotoxin to fix complement on exposure to specific antibody.† That this protein can alter the endotoxin molecule was also demonstrated by its ability to block 2 phage receptor sites on the endotoxin molecule,‡ and by production of multiple precipitation bands, instead of a single one, on Ouchterlony plates. The validity of these tests for assessing the presence or absence of potency in this protein fraction of spleen was affirmed by the finding that the results by more than one of the above 5 methods on any given test sample, though not quantitatively comparable, have nearly always been in the same direction.

Limitations of Antiadrenergic Therapy for Refractory Traumatic Shock.

Conclusion Antiadrenergic therapy by coe-liac blockade or phenoxybenzamine injected via the upper abdominal aorta prevents death from otherwise lethal endotoxic or hemor-rhagic shock if administered within 30 minutes after onset of the shock state. Phenoxybenzamine intravenously is not effective in twice the dose that is effective when it is administered via the upper abdominal aorta. The failure of antiadrenergic therapy can be accounted for by the speed with which severe ischemia inflicts irreversible injury to vascular muscle and to the endotoxin-detoxi-fying mechanisms in the splanchnic tissues.

Gaseous Distention in the Obstructed Small Intestine of Cats

Conclusions Gas formation from malted milk in milk in a closed loop, comprising the stomach and the entire small intestine, is markedly depressed by sulfadiazine, sulfamerazine, sulfamethazine, sulfathiazole and sulfathalidine. There is a definitely less, but still significant depression by sulfasuccidine. Phthalic and succinic acid have no inhibitory effect on gas production. Streptomycin works well in the majority of the experiments, but is a complete failure in others. Penicillin works best of all the drugs tested.