Carl F. Rothe

Hepatic venular resistance responses to norepinephrine, isoproterenol, adenosine, histamine, and ACh in rabbits

Changes in hepatic venous resistance were estimated in rabbits from the hepatic venular-inferior vena caval pressure gradient [servo-null micropipettes in 49 +/- 15 (SD) microns vessels] and the total hepatic blood flow (ultrasound probe encircling the hepatic artery and the portal vein). Changes in liver volume, and thus vascular capacitance, were estimated from measures of the liver lobe thickness. Norepinephrine (NE), isoproterenol (Iso), adenosine (Ado), histamine (Hist), or acetylcholine (ACh) was infused into the portal vein at a constant rate for 5 min. NE, Hist, and Ado increased hepatic venular pressure, but only NE and Hist significantly increased hepatic venular resistance. NE reduced the liver thickness, but Hist and Ado caused engorgement. Hepatic blood flow was increased by NE and Ado and decreased by ACh. The influence of intraportal vein infusion of Iso on the liver vasculature, at doses similar to that of NE, was insignificant. We conclude that NE acted on all the hepatic microvasculature, increasing resistance and actively decreasing vascular volume. Hist passively induced engorgement by increasing outflow resistance, whereas the liver engorgement seen with Ado was passively related to the increased blood flow. ACh constricted the portal venules but did not change the liver volume.

Characteristics of Reactive Hyperemia in the Canine Intestine

The isolated ileum of the dog shows a characteristic hyperemia following brief periods of arterial occlusion. The magnitude of this reactive hyperemia depends more upon prolongation of flow related to duration of ischemia, than upon increases of maximal or peak blood flow. Repayment of flow deficit, by the added flow of reactive hyperemia, averaged only 35% in the intestine, far below that found by others in skeletal muscle and in the coronary circulation. Nevertheless, estimates of oxygen debt indicated that this debt was overpaid, even after five minutes of ischemia. A small but consistent increase in weight of the isolated segment was observed during the postocclusion phase. It was found that this weight increase was due largely to increase of the volume of blood in the ileum. The peak of the volume increment appeared slightly later than the peak of flow increase, and for this reason was ascribed to increase in volume of the capacity vessels. In an attempt to assess the respective roles of myogenic vs. metabolic mechanisms in causation of reactive hyperemia, arterial pressure was restored during occlusion by injecting dextran solution into the arterial segment. Pressures in excess of control values did not abolish the hyperemic response. It was concluded that the reactive hyperemia observed in the ileum was chiefly metabolic in origin.

Reflex vascular capacity reduction in the dog.

The maximum degree and time course of active reflex venoconstriction in chloralose-anesthetized dogs was studied. The mean circulatory filling pressure (Pmc) was measured by fibrillating the heart and rapidly pumping blood from the aorta to the vena cava until the systemic arterial pressure equaled the central venous pressure. Ventricular fibrillation was continued for 1 minute and was assumed to induce maximal sympathetic discharge to the capacity vessels. Blood was removed to maintain the Pmc constant at the level determined at 8 seconds after the start of fibrillation. It was necessary to remove 13.8 ml/kg by the end of 1 minute. After autonomic nervous system blockade by hexamethonium only 4.8 ml/kg were removed to hold the Pmc constant. Thus, in conclusion, the maximal degree of active venoconstriction induced by circulatory arrest was 9.0 ml/kg during the 1st minute of cardiac fibrillation. A basal capacity vessel tone was present, equivalent to 10 ml/kg under the experimental conditions used.

Control of Total Vascular Resistance in Hemorrhagic Shock in the Dog

Cardiac output in the dog was measured by indocyanine green dilution in 24 hemorrhagic shock experiments. Total peripheral resistance (TPR) was calculated from the cardiac output and systemic arterial blood pressure. Early in the hypotensive phase resulting from hemorrhage to 50 mm Hg blood pressure, the cardiac output was 19.3±6.6 (SD) % of control and the total peripheral resistance was 199 ±73 (SD) % of control. During the hypotensive phase the peripheral resistance declined significantly. This decline in TPR was associated with a significant decrease in respiration and heart rates, indicating a partial failure of the neurogenic control of the cardiovascular system. Following transfusions of the shed blood, the TPR decreased to the control value, but during subsequent progressive decline in blood pressure, vascular resistance again increased. Occasionally, TPR again fell terminally as the blood pressure decreased below 60 mm Hg. Although there is evidence for partial failure of peripheral resistance vessel tone during severe hypotension and some evidence for this following reinfusion of the shed blood, this failure, when observed, is a minor component of the progressive cardiovascular failure and is not the cause of irreversibility.

Pressure gradients in the splanchnic bed of the monkey during hemorrhagic shock.

Summary Analysis of pressure gradients in the splanchnic bed of the monkey during a standardized hemorrhagic shock procedure has indicated a preponderant increase in intrahepatic resistance with minimal change in mesenteric (intestinal) resistance during oligemia. Following restoration of the bleeding volume, the control pressure relationship was reestablished. The marked elevation of portal venous pressure, so typical of the dog in this phase of the hemorrhagic shock procedure, was not seen in the monkey. Moreover, the intestine of this species appeared pale and ischemic at autopsy, contrasted to the congested and bloody intestine of the dog. The possible significance of the differences in behavior of splanchnic vasculature in the primate and canine species is considered in the light of the etiology of irreversible shock.

Cardiovascular Interactions Tutorial: Architecture and Design

This work examines the design and architecture of a delivery system for a computerized, interactive tutorial on the physiology of the cardiovascular system. Emphasis in this paper is on the mechanisms used to coordinate the users Lab Workbook, subject-oriented Information file, and the cardiovascular interaction (CVI) simulation model. Techniques described are sufficiently generic to allow for different tutorial content and/or different simulation models. Implementation uses Visual Basic and deployment is CDROM-based.

Toward consistent definitions for preload and afterload—revisited

Have you ever wished you could make your curriculum more integrative in nature? Would you like to show your students not only the physiological effects of an infectious disease but also provide a perspective on the microorganism responsible for it and the environment in which it might flourish? Would you like to have a single site where you could search for information on various aspects of the same topic from a variety of disciplines rather than having to surf the net?

Regulation of Hepatic Vascular Capacitance

The mammalian liver is part of the splanchnic bed that provides a highly significant blood reservoir for compensation for loss of blood from the thorax and consequently a decreased cardiac output. Stresses requiring blood volume compensation include: blood or water loss, quiet standing, return from a prolonged bout of zero gravity, thermal stress, or exercise. Hepatic blood volume is changed passively by changes in hepatic arterial or gastrointestinal blood flow or by changes in vena caval pressure. Liver blood volume is also changed actively via reflexes, hormones, or drugs that activate the hepatic venous smooth muscle. Hepatic vascular compliance is about ten times that of the body as a whole, and is changed by active mechanisms. The hepatic unstressed blood volume is markedly changed by hormones. Baroreceptor control of hepatic volume is important in dogs, but not in cats and possibly not in humans. The hepatic venular pressure of rats, rabbits, and puppies is about 40% of the pressure gradient between the portal vein and vena cava. Major areas of uncertainty include: (a) the magnitude of sinusoidal pressure and how it is controlled, (b) the mechanisms controlling hepatic venous resistance, and (c) the mechanisms influencing hepatic vascular capacitance.