P. G. Carlier

Lung Fluid Dynamics and Supply Dependency of Oxygen Uptake During Experimental Endotoxic Shock and Volume Resuscitation

Background and MethodsWe studied the effect of volume resuscitation on lung fluid balance and systemic oxygen extraction during septic shock in eight anesthetized dogs. Sepsis was induced using a 2-hr continuous infusion of Escherichia coli endotoxin at 0.25 μg/min-kg. Relationships between oxygen uptake (Vo2) and oxygen supply (Do2) were performed acutely during step wise controlled decrements in cardiac output by progressive inflation of an intracardiac balloon. At each stage, Do2 and corresponding Vo2 were measured independently and the individual critical Do2 level was referred to as the point below which the relationship held. The slope of such a constructed relationship was defined as the maximal oxygen extraction ratio. Lung fluid balance was assessed by measurements of extravascular lung water. All values were studied at baseline, after endotoxin insult, and after reversing hypotension by a 10% dextran infusion. ResultsEndotoxin infusion led to a shock state that associated hypotension (from 135 to 63 mm Hg) with increases in blood lactate (from 0.53 to 3.9 mmol/L). The mean critical Do2 and maximal oxygen extraction ratio were significantly altered from 7.9 to 17.8 mL/min-kg and from 0.81 to 0.38, respectively. After reversing hypotension by 28 mL/kg colloid infusion, the critical Do2 (11.4 mL/min-kg) and maximal oxygen extraction ratio (0.48) were significantly improved. However, restoration of normal values required a state of fluid overload by further dextran infusion (8 mL/kg). At the end of the fluid challenge, extravascular lung water significantly increased from 6.4 to 17.4 mL/kg. ConclusionsThese data suggest that volume loading may reverse endotoxin-induced peripheral perfusion abnormalities. However, substantial pulmonary edema may occur, possibly jeopardizing the beneficial effects of fluid expansion. (Crit Care Med 1991; 19:955)

Pathogenesis and reversibility of the aortic changes in experimental hypertension.

In renal hypertensive female rats (Goldblatt one-kidney, one-clip model) (G 1K-1C), an increase in DNA and collagen synthesis, in the proliferation fraction of smooth muscle cells, and in wet weight were observed in the aorta as early as 4 days after the renal artery was clipped at a time when blood pressure increased rapidly. When blood pressure stabilized at high values, the metabolism of nucleic acid within the aortic media resumed its normal level. When the blood pressure level was corrected either by removal of the clip or by antihypertensive drugs, a modification of the course of the aortic proliferation changes could only be obtained when the treatment was started, at the earliest phase of hypertension. Once the proliferation changes were established, they could not be corrected even after normalization of blood pressure, at least in such short-term experiments. Moreover, some dissociation between the effect of antihypertensive drugs on blood pressure level and on arterial hypertensive disease were observed. These data illustrate the complexity of the mechanisms involved in the response of the vascular wall to high blood pressure and in its correction as well.