A 2 cm long iliac av. fistula is established in 13 dogs. Flow measurements are performed in the fistula limbs and the adjacent arteries immediately (stage I), as well as 3 months (stage II) and 6 to 12 months (stage III) post-shunt. The following results are obtained: 1) In the acute stage, average flow in the distal fistula artery is very small but directed towards the periphery. In stages II and III a progressively increasing retrograde flow directed towards the fistula is regularly measured in the distal fistula artery. 2) Even in the acute stage a considerable retrograde flow is measured in the distal fistula artery when the proximal artery is clamped. Likewise, in stages II and III, this "free" retrograde flow (after occlusion of proximal fistula artery) is 40 to 60% higher than the spontaneous retrograde flow. 3) In chronic av. fistulas, the "free" retrograde flow in the distal fistula artery decreases significantly after occlusion of the adjacent tail artery and the contralateral iliac artery. It can thus be calculated that in chronic iliac av. fistulas the tail artery contributes approximately 44% and the contralateral iliac artery 22% to retrograde arterial fistula flow. The remaining 34% of retrograde flow are mainly derived from collaterals connecting side-branches of the abdominal aorta with the distal arterial limb. 4) These extensive collaterals adjacent to a chronic iliac av. fistula are demonstrated angiographically and by post-mortem vascular casts. 5) In all stages, occlusion of the proximal fistula artery simultaneously increases flow in the tail artery and contralateral iliac artery by more than 50%. This stresses the major contribution of these arteries to retrograde arterial fistula flow. 6) Successive occlusion of the tail artery and the contralateral iliac artery in stages II and III results in a nearly identical per cent decrease in "free" retrograde flow and in pressure (measured in the distal fistula artery). Even in the pre-fistula control stage, this occlusion experiment induces the same relative pressure-drop in the distal iliac artery. The proportional contribution of the collateral pathways to retrograde arterial fistula-flow and -pressure remains unchanged in the chronic stages post-fistula in spite of the tremendous expansion of collateral vessels within one year. These findings indicate that the three main collateral networks adjacent to the iliac artery all expand proportionally to their pre-fistula status in the months following construction of a large iliac av. fistula. This strongly suggests that the extensive interarterial anastomoses in a chronic av. fistula are all preformed collaterals which have gradually expanded.

Acute Disease↗

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Acute and chronic flow-measurements in experimental arteriovenous fistulas.

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Animals↗

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Preload dependence of dP/dt max, VCE max and calculated V max compared to the inotropic sensitivity of these indices of cardiac contractility.

In five canine heart-lung preparations the preload dependence of dP/dt max, V max, VCE max and (dP/dt:P-EDP + C) max was related to the inotropic sensitivity of these indices. V max and (dP/dt:P-EDP + C) max are less affected by preload changes than dP/dt max and therefore should be more suitable for inotropic measurements. But even if the preload changes caused by inotropic interventions are not taken into account, V max shows the same inotropic sensitivity as dP/dt max when the contractile state is reduced and an even lower sensitivity when the contractile state is enhanced. The sensitivity of (dP/dt:P-EDP + C) max, however, is much lower over the whole range of tested inotropic states. If enddiastolic pressure is kept constant during inotropic interventions, dP/dt max is a much more sensitive inotropic index than V max. VCE max usually shows a negative correlation to the diastolic filling of the heart. In the improved inotropic state this correlation can become positive, thus making it impossible to evaluate the influence of the preload dependence on the result. None of the tested parameters shows a higher inotropic sensitivity than dP/dt max, though the preload dependence of dP/dt max is more evident. Therefore, none of these more complicated parameters has any advantage over the simple measure dP/dt max for evaluation of acute changes in contractility.

Animals↗

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Hemorrhagic shock with fixed hypotension and with spontaneous recovery of blood pressure. A comparison of two shock models.

In 26 dogs anesthetized with a barbiturate peripheral blood flow, O2 consumption and acid-base balance have been studied in two kinds of hemorrhagic shock: 1. Hemorrhagic shock with fixed hypotension (hypotensive shock, n = 12) 2. Hemorrhagic shock with spontaneously recovering arterial blood pressure (normotensive shock, n = 14). In both groups the same amount of blood is withdrawn and stored in a reservoir (31-32 ml/kg) to reduce arterial pressure to 40 mm Hg. In hypotensive shock there is a continuous outflow of blood into the reservoir in order to maintain an arterial pressure of 40 mm Hg. After 1 1/2 hours this shift of blood reverses itself spontaneously. In normotensive shock the arterial pressure is allowed to increase after the initial withdrawal of blood. 1 1/2 hours later it reaches a peak of 93 mm Hg after which it starts declining again. The duration of oligemia which the animals control themselves is nearly identical in both groups (4 hours). Both kinds of hemorrhagic shock have a mortality rate of 80%. The survival time is shorter (p less than 0.01) in hypotensive (3 hours) than in normotensive shock (7 1/2 hours). In both kinds of shock heart rate increases to more than 200 beats/min. However, in hypotensive shock it decreases in the late stage of hypovolemia, whereas the increase is continuous in normotensive shock. Cardiac output is significantly higher in the normotensive animals nearly throughout the entire hypovolemic phase although the initial decrease is the same in both groups (71%). Also a greater increase in total peripheral resistance occurs in these animals. The increased cardiac output and total peripheral resistance. A "centralization" of the circulation is also observed in this kind of shock as is made evident by the changes in the relationship between cardiac output and carotid blood flow. Hyperventilation occurs in both kinds of shock. In hypotensive shock respiratory rate decreases at the end of the oligemic phase possibly due to a smaller cerebral blood flow.

Acidosis↗