Effect Of Hypovolemic Shock Research Articles

Blood Loss and Shock

This slender gem of a volume on the physiology of blood loss and shock was first published in Great Britain in 1994. One primary goal is reintroduction of the seminal work of Henry Bancroft, professor of physiology at Queen's University of Belfast, Ireland, 1939, who described a stage of hypovolemic shock associated with bradycardia and hypotension. The authors point out that recognition of this phase is ignored in the standard textbook descriptions of hemorrhagic shock. The contributors include eminent cardiovascular physiologists and clinicians, who extensively review the experimental aspects of hypovolemic shock, cardiovascular physiology, the effect of hypovolemic shock on regional perfusion, and selected clinical aspects of hypovolemic shock, including monitoring. The physiologically oriented clinician and the cardiovascular physiologist will especially enjoy the sections on the use of functional hemorrhage models in human studies and the lucid chapter about autoregulation of blood flow. Chapters about cardiovascular sensors, central integration, and

Effects of hypovolemic shock and reperfusion on liver blood flow in the dog.

Liver blood flow was investigated in hypovolemic shock using a modified right heart bypass technique which can obtain accurate portal blood flow. Findings were similar to those previously reported: hepatic blood flow accounted for 34% of cardiac output in this study; 76% of hepatic blood flow was delivered from the portal vein and 24% from the hepatic artery. Hypovolemic shock markedly decreased total liver blood flow by a reduction in portal venous blood flow. The findings of this study provide evidence that mesenteric blood flow is a peripheral circulation circuit where blood flow is restricted during reduced circulatory volume. Development of a hepatic arterial buffer response during hypovolemic shock was confirmed by an increased ratio of hepatic arterial flow to cardiac output. Reduced total hepatic blood flow during hypovolemic shock returned to control flow by an increase in hepatic arterial flow after reperfusion. The results of this study demonstrate that compensated reactions for maintaining liver blood flow mainly due to the hepatic arterial buffer response were functioned both during hypovolemic shock and after elimination of shock.

The effect of hypovolemic shock and reperfusion on the hepatic oxygen supply-uptake relationship in the dog.

The hepatic oxygen supply-uptake relationship was investigated during hypovolemic shock using a right heart bypass technique. The results were dissimilar to those previously reported in that the ratio of liver oxygen delivery to systemic oxygen delivery was significantly decreased during shock. The decreased ratio was due to a significant decrease in the portal venous oxygen delivery when compared to the decrease in the systemic oxygen delivery. The decrease in portal venous oxygen delivery was caused not only by the decrease in portal venous blood flow, but also by the decrease in oxygen content of portal blood. The ratio of hepatic arterial oxygen delivery, on the other hand, was significantly increased during shock. Hypovolemic shock increased the liver oxygen extraction ratio to nearly 100% of the pre-shock value. These findings suggest a hepatic protective mechanism for matching oxygen uptake to rising hepatic oxygen requirements. Liver oxygen delivery returned to pre-shock value after correction of hypovolemia primarily due to a significant increase in hepatic arterial oxygen delivery. A significant negative correlation between the liver oxygen extraction ratio and the oxygen content of hepatic venous blood was observed. The hepatic venous oxygen content appears to be a simple and appropriate index of liver oxygenation in clinical medicine because it is difficult to evaluate the liver oxygen extraction ratio directly.

The effect of hypovolemic shock on pancreatic secretion

A vascular pathogenesis of pancreatitis has been postulated in diabetics, the aged, Ortner's Syndrome, and various low-flow states. This report studies canine pancreatic secretion in a preparation of hypovolemic shock produced by controlled hemorrhage maintained for varying durations. Pancreatic secretion was collected by cannulation of the main pancreatic duct in anesthetized dogs. Secretin was administered by continuous intravenous (i.v.) infusion of 4 U/kg/h. Four 15-min samples of pancreatic juice were collected. Then the dogs were bled by arterial line withdrawing 25-30% of total blood volume or until the mean blood pressure dropped to about 60 mmHg. Blood was collected in heparinized containers for reinfusion. Blood samples for amylase and 15-min samples of pancreatic juice for volume, bicarbonate, and enzymes were obtained during hypovolemia as well as during and following restoration of the blood volume. Hypovolemia induced significant decreases in pancreatic flow, bicarbonate and amylase secretion, parameters which increased after reinfusion but never returned to pre-shock levels. Increasing the period of hypovolemia increased the inhibition of pancreatic flow, increased blood amylase elevation, and resulted in visible pancreatic edema. We conclude that pancreatic secretion is diminished by hypovolemia, that this is initially reversible when hypovolemia is brief, but that the disturbance of function progresses to inflammatory pathology when hypovolemia is prolonged.

Microvessel diameter changes during hemorrhagic shock in unanesthetized hamsters

The effects of hypovolemic shock on the time-dependent diameter changes of small arteries and arterioles were studied in the hamster skin fold window preparation. This experimental model permits the visualization of the microvasculature without the effects of acute surgery, anesthesia, and exposure. In these conditions, all the arterial microvessels showed vasomotion, while the venules and small veins, that were also studied, did not show rhythmic diameter changes. Hemorrhage was induced by the withdrawal of blood through a chronically implanted arterial catheter. The mean arterial blood pressure was reduced to 40 mm Hg in 20 min, and was maintained at this value for an additional 30-min period. Reinfusion of the withdrawn blood was made at 50 min. During the shock period, vasomotion disappeared in all arterial vessels. The small arteries and arterioles, A 1 (70–100 μm, mean diameter), A 2 (40–70 μm, md), and A 3 (15–40 μm, md), contracted by 20 ± 7, 33 ± 10, and 34 ± 11% of the control mean diameter, respectively. A 4 terminal arterioles (<15 μm, md) dilated after the onset of bleeding; their rhythmic diameter changes subsequently stopped and their mean diameter increased by 75 ± 7% of the original value. V 1 small veins (150–200 μm, md) contracted during shock, while V 2 (35–55 μm, md), V 3 (25–35 μm, md), and V 4 (15–25 μm, md) venous vessels did not show any significant change. Reinfusion of shed blood caused the reappearance of vasomotion; control vasomotion patterns recovered after reinfusion. Our results indicate that the microcirculatory responses to hypovolemic shock are dependent on the vessel type; this inhomogeneous reactivity may be due to the different responsiveness of microvessels to the mechanisms elicited by hemorrhage.

Effect of hypovolemic shock on the generalized Shwartzman reaction.

The generalized Shwartzman reaction was produced in rabbits by two intravenous injections of endotoxin given 20-22 h apart. Prior to the second injection of endotoxin, the animals were made hypovolemic by removal of 40% blood volume or reduction of the systolic pressure to 70% of normal whichever came first. This blood removal produced a persistent hypotensive episode. 8/9 rabbits made hypotensive in this manner had evidence of glomerular capillary thrombi compared to 8/8 in a group that did not have blood removed. It is concluded that hypovolemic shock of this magnitude does not prevent the generalized Shwartzman reaction.

The effect of hypovolemic shock on bacterial defense

Studies in man and the dog indicate decreased bacterial resistance after hypovolemic shock. This is due in part to reduced opsonization, in part to increased contact time between bacterium and phagocyte, and in part to reduced phagocytosis as a result of poor opsonization and, perhaps, cellular anoxia. Conventional banked blood restoration seems to aggravate this deficit in the dogs and raises the question of loss of labile opsonins as well as RES blockade by noxious products of blood storage.