Antiadrenergic and Antihistaminic Therapy in Hemorrhagic Shock in Dog and Rat

1956 ◽  
Vol 186 (1) ◽  
pp. 79-84 ◽  
Author(s):  
S. Jacob ◽  
Edward W. Friedman ◽  
Sabin Levenson ◽  
Philip Glotzer ◽  
H. A. Frank ◽  
...  
Keyword(s):  
Blood Flow ◽  
Survival Rate ◽  
Blood Loss ◽  
Pressure Gradient ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Venous Pressure ◽  
Survival Period ◽  
Effect Of Treatment ◽  
Antihistaminic Drugs

The influence of pretreatment with dibenamine on the development and course of hemorrhagic shock, and the effect of treatment with dibenamine, rapidly acting antiadrenergic drugs, or antihistaminic drugs after hemorrhagic shock had been allowed to become unresponsive to replacement transfusion, were tested in dogs prepared in advance to permit measurement of portal-caval venous pressure gradient. Preliminary dibenamine administration was also tested in rats submitted to hemorrhagic shock. The conclusions were as follows: 1) The protective effect of dibenamine prior to the induction of hemorrhagic shock in the dog consists mainly of a reduction of the bleeding volume. Intrahepatic vasoconstriction is not reduced. A dog which is not under the influence of dibenamine can tolerate a greater degree of blood loss than a dibenaminized dog. After hemorrhagic shock has been allowed to become refractory to replacement transfusion, antiadrenergic and antihistaminic drugs do not reduce intrahepatic vasoconstriction or increase the survival period or the survival rate. 2) Dibenamine given prior to hemorrhage enables the rat to survive a degree of blood loss which is lethal to the untreated rat. This, in part, appears to be due to better blood flow to the respiratory center.

Splanchnic blood flow in the monkey during hemorrhagic shock

1965 ◽  
Vol 208 (2) ◽  
pp. 265-269 ◽  
Author(s):  
Francis L. Abel ◽  
John A. Waldhausen ◽  
Ewald E. Selkurt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Hemorrhagic Shock ◽  
Hepatic Vein ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Mesenteric Arteries ◽  
Splanchnic Blood Flow

Blood flow in the celiac and superior mesenteric arteries was measured in nine Macaca monkeys during a standardized hemorrhagic shock procedure. Simultaneous pressures were obtained from the hepatic vein, portal vein, and aorta. Each animal was bled rapidly to an arterial pressure of 40 mm Hg and maintained at this level until 30% of the bled volume had spontaneously reinfused. The remaining blood was then rapidly reinfused and the animal observed until death. The results show a lack of overshoot of venous pressure on reinfusion, grossly pale intestines with some microscopic congestive changes, and a decrease in splanchnic conductance throughout the postinfusion period. Hepatic venous pressure exceeded portal pressure in six of the nine animals during the period of hemorrhage. The results are interpreted as indicative of insignificant splanchnic pooling during hemorrhagic shock in this animal.

scholarly journals Heart Protective Effects of Electroacupuncture in an Animal Experimental Study with Delayed Fluid Resuscitation after Hemorrhagic Shock

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Huan Wang ◽  
Zhen Liu ◽  
Yuanshi Liu ◽  
Zhanqi Tong ◽  
Yan Qian ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Blood Loss ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Fluid Resuscitation ◽  
Cardiac Tissue ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Autonomic Nervous

Fluid resuscitation could hardly be performed immediately after fatal hemorrhagic shock in outpatients. We investigated whether electroacupuncture (EA) at Zusanli (ST36) could prevent fatal hemorrhagic shock induced heart failure with delayed fluid resuscitation and whether the protective role of EA is related to the autonomic nervous system. Sixty Sprague Dawley rats were randomly divided into five groups (n=12 each): group of sham hemorrhagic shock (SHAM), group of EA, group of sham EA (SEA), group of delayed fluid resuscitation with EA (EA + DR), and group of delayed fluid resuscitation with SEA (SEA + DR). After blood loss for 6 hours, caspase-3 activity and positive rate of TUNEL in EA + DR group were significantly lower than in other hemorrhagic shock groups (e.g., versus SEA + DR: 0.156±0.039 versus 0.301±0.042; P<0.05). Immediately EA treatment after the blood loss enhanced the protective effect of delayed resuscitation on the cardiac tissue of hemorrhagic shock rats. Considering the significant changes of epinephrine (137.8±6.9 ng/L versus 98.6±7.4 ng/L; P<0.05) and acetylcholine (405±8.6 pmol/L versus 341±10.1 pmol/L; P<0.05) after EA treatment (SEA + DR versus EA + DR), this cardiac protective effect may be related to regulation of the autonomic nervous system.

Active and passive control of hepatic blood volume responses to hemorrhage at normal and raised hepatic venous pressure in cats

1980 ◽  
Vol 58 (9) ◽  
pp. 1049-1057 ◽  
Author(s):  
W. Wayne Lautt ◽  
L. Cheryle Brown ◽  
J. Scott Durham
Keyword(s):  
Blood Flow ◽  
Blood Loss ◽  
Blood Volume ◽  
Passive Control ◽  
Venous Pressure ◽  
Liver Volume ◽  
Passive Flow ◽  
Hepatic Volume ◽  
Volume Response

Hepatic blood volume decreases in response to a rapid hemorrhage (15.3 mL/min) were measured in cats anesthetized with pentobarbital or ketamine–chloralose, by use of in vivo plethysmography alone or in combination with various surgical procedures and vascular circuits. The hepatic blood volume contracts during hemorrhage to compensate for a constant proportion (26 ± 6%) of the blood loss regardless of the extent of the actual blood loss. Following denervation of the liver and α adrenoreceptor blockade (3 mg phentolamine, intraportal) the liver compensation was unaltered. After denervation, nephrectomy, hypophysectomy, and adrenalectomy the liver was still able to compensate for 20 ± 7.4% of the hemorrhage. Decreases in liver volume were linearly related to decreases in total hepatic blood flow that ensued whether the decreased blood flow was induced by hemorrhage or by clamping of the arteries supplying the splanchnic organs (superior mesenteric artery, celiac artery). The hepatic volume response to hemorrhage could be predicted accurately (97 ± 6.6%) simply from the linear passive relationship between flow and volume for a particular animal. However when hepatic venous pressure was experimentally elevated, the volume response to passive flow decrease was markedly reduced whereas the response to hemorrhage and noradrenaline infusion was unimpaired suggesting that active control factors were required to produce normal hepatic volume responses to hemorrhage at raised venous pressure. Phentolamine reduced the response at raised venous pressure but was without effect at normal venous pressure in the same animal, indicating that the hepatic nerves and (or) adrenal catecholamines are of paramount importance in control of the response at raised venous pressure when the passive flow influence is much reduced.

Effects of nifedipine on hepatic venous pressure gradient and portal vein blood flow in patients with cirrhosis

1995 ◽  
Vol 10 (2) ◽  
pp. 198-204 ◽  
Author(s):  
KAZUHIRO OTA ◽  
HIROSHI SHIJO ◽  
HIROSHI KOKAWA ◽  
KATSUHIKO KUBARA ◽  
TETSUHIRO KIM ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Pressure Gradient ◽  
Venous Pressure ◽  
Hepatic Venous Pressure Gradient

Hepatic vascular response to epinephrine

1961 ◽  
Vol 201 (1) ◽  
pp. 58-62 ◽  
Author(s):  
William C. Shoemaker ◽  
L. Newton Turk ◽  
Francis D. Moore
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Pressure Gradient ◽  
Hepatic Blood Flow ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Portal Vein Pressure ◽  
Pronounced Increase ◽  
Epinephrine Administration ◽  
Arterial Blood

Hepatic hemodynamic events were measured before and after epinephrine administration in unanesthetized dogs in which the hepatic vessels had been previously catheterized. Comparisons were made of the response after a single intravenous injection at various doses and after a constant infusion of epinephrine; comparisons were also made between portal vein and femoral vein injections. After femoral venous injection of epinephrine (1–10 µg/kg) there was a marked increase in hepatic blood flow, roughly increasing with the size of the dose. With doses of 25 µg/kg or more, an initial increase in hepatic blood flow was followed by a decreased flow; in some instances death ensued. Epinephrine injected into the femoral vein produced a rise in the arterial blood pressure, followed by a rise in the portal vein pressure, portal-hepatic venous pressure gradient, and mechanical impedance across the hepatic venous bed. When injected into the portal vein under comparable conditions, epinephrine produced little or no change in hepatic blood flow or arterial pressure, but did produce a more rapid and pronounced increase in portal vein pressure, portal-hepatic pressure gradient and hepatic venous impedance.

scholarly journals Splanchnic and Systemic Hemodynamics in Cirrhotic Patients With Refractory Ascites. Effect of Peritoneovenous Shunting

HPB Surgery ◽  
1991 ◽  
Vol 3 (4) ◽  
pp. 259-269 ◽  
Author(s):  
Corinne Vons ◽  
Antoine Hadengue ◽  
Samuel S. Lee ◽  
Claude Smadja ◽  
Dominique Franco ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Pressure Gradient ◽  
Venous Pressure ◽  
Systemic Hemodynamics ◽  
Refractory Ascites ◽  
Intraabdominal Pressure ◽  
Blood Flows ◽  
Cirrhotic Patients

The splanchnic and systemic hemodynamics of 14 patients with refractory ascites were studied and were compared to those of 15 patients with ascites responding to medical treatment. Among the 14 patients, 10 were grade B and 4 C, according to the Pugh classification. Of the 15 patients, 5 were Pugh B and 10 C. In patients with refractory ascites, free hepatic venous pressure was significantly higher and hepatic venous pressure gradient was significantly lower than in patients with responsive ascites. Hepatic and azygos blood flows were not significantly different between the two groups. Cardiac output was lower in patients with refractory ascites (p < 0.05) than in those with responsive ascites. In patients with refractory ascites, six months after peritoneovenous shunting, there was a significant reduction of wedged and free hepatic venous pressures and azygos blood flow. Cardiac output increased by 20% (p < 0.02). This study shows that hemodynamic alterations in patients with refractory ascites is the consequence of increased intraabdominal pressure due to chronic ascites. Six months after peritoneovenous shunting splanchnic and systemic hemodynamics became similar to those observed in patients without ascites.

scholarly journals The Influence of Zusanli and Nonmeridian Acupuncture Points on the Survival Rate and Intestinal Tissue Features after Fatal Hemorrhagic Shock in Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Xian Shi ◽  
Yuxian Zhong ◽  
Jiarui Yao ◽  
Sen Hu ◽  
Lu Wang ◽  
...  
Keyword(s):  
Survival Rate ◽  
Blood Loss ◽  
Hemorrhagic Shock ◽  
Intestinal Barrier ◽  
The Other ◽  
Intestinal Barrier Function ◽  
Control Group ◽  
Acupuncture Points ◽  
Sprague Dawley ◽  
Intestinal Tissue

Sixty Sprague-Dawley rats were divided into 5 groups: (a) control group (HS); (b) Immediate rehydration group (IFR); (c) ST36 electroacupuncture (EA) delay rehydration group (EA/DFR): EA at ST36 immediately after blood loss with infusion 3 h later; (d) EA nonmeridian rehydration group (SEA/DFR): EA at nonacupuncture sites with rehydration similar to EA/DFR; (e) ST36 EA group (EA): EA at ST36 immediately after blood loss with no rehydration. Forty-five percent of the entire blood volume was taken out to make lethal hemorrhagic shock models. We recorded the survival rate, intestinal tissue DAO content, and microcirculation. The survival rate of the EA/DFR group and the IFR group was significantly higher than that of the other three groups (P<0.05). Twelve hours after blood loss, intestinal tissue DAO content of the EA/DFR group and the IFR group was significantly higher than that of the SEA/DFR group, EA group, and HS group (P<0.05andP<0.01). The mucosal blood flow of the EA/DFR group and the IFR group was significantly higher than the other groups (P<0.05each). We conclude that EA improves the blood pressure and raises the early survival rate of hemorrhagic shock rats, maintains the intestinal barrier function, and improves the degree of intestinal ischemia.

The oxidation-antioxidation system in hemorrhagic shock and the infusion therapy with regulators of nitric oxide synthesis in experiment

2019 ◽  
pp. 4-12
Author(s):  
М.И. Ремизова ◽  
Г.В. Гришина ◽  
К.А. Гербут ◽  
Л.Р. Алексанян ◽  
Л.П. Рыбакова
Keyword(s):  
Nitric Oxide ◽  
Survival Rate ◽  
Sodium Chloride ◽  
Blood Loss ◽  
Hemorrhagic Shock ◽  
Antioxidant System ◽  
Infusion Therapy ◽  
Antioxidant Systems ◽  
Oxygen Balance ◽  
Isotonic Sodium Chloride

При различных видах шока, включая геморрагический шок, развивается оксидативный стресс. Большое значение в отношении исхода тяжелой кровопотери имеет состояние оксидантно-антиоксидантной системы организма. Цель работы - изучение в эксперименте состояния кровообращения, кислородного режима организма, а также оксидантно-антиоксидантной системы при геморрагическом шоке и его инфузионной терапии. Методика. Эксперименты проведены на кроликах, находящихся под тиопенталовым наркозом. Геморрагический шок моделировали кровопусканием с снижением АД до 40-60 мм рт. ст. и последующей гипотензией в течение 30-40 мин, после чего начинали инфузию кровезаменителя. Общий объем кровопотери составлял 18,5±0,6 мл/кг массы. Эффективность инфузионной терапии оценивали по показателям системной гемодинамики, микроциркуляции и показателям активности оксидантно-антиоксидантной системы. К инфузионной среде, состоящей из изотонического раствора натрия хлорида и аутокрови, добавляли доноры и стимуляторы синтеза оксида азота - оксаком (0,7 мкмоль/кг) и L-аргинин (200 мг/кг). Результаты. Кровопотеря вызывала выраженные нарушения системной гемодинамики и микроциркуляции с изменением метаболизма и кислородного режима организма. Содержание продуктов пероксидации в крови нарастало, тем значительнее, чем выраженнее были нарушения кровообращения. Выявлены высокие коррелятивные связи между показателями гемодинамики и величинами малонового диальдегида и церулоплазмина в крови животных. Показано благоприятное действие на кровообращение и состояние оксидантно-антиоксидантной системы доноров оксида азота - оксакома и L-аргинина, вводимых в составе инфузионной среды. Заключение. Применение доноров оксида азота при инфузионной терапии геморрагического шока существенно повышает продолжительность жизни животных. В контроле (изотонический раствор натрия хлорида) выживаемость составляла 42%, при добавлении к инфузионной среде оксакома и L- аргинина, соответственно, 77 % и 59%. Different types of shock, including hemorrhagic shock, are associated with oxidative stress. The oxidant-antioxidant system plays a major role during severe blood loss. The aim of these experiments was to study circulation, oxygen regimen and oxidant-antioxidant systems in hemorrhagic shock and infusion therapy. Methods. Experiments were performed on thiopental-anesthetized rabbits. Hemorrhagic shock was induced by blood loss of 18.5±0.6 ml/kg body weight to reduce blood pressure to 40-60 mm Hg for 30-40 min. Then infusion of a volume expander was started. Effectiveness of the infusion therapy was evaluated by indices of systemic hemodynamics, microcirculation, and the oxidant-antioxidant system. The infusion solution consisting of isotonic sodium chloride was supplemented with a nitric oxide (NO) donor, Oxacom® (0.7 µmol/kg), and a NO precursor, L-arginine (200 mg/kg). Results. Blood loss resulted in considerable changes in systemic hemodynamic, microcirculation, metabolism, and oxygen balance. The content of peroxidation products directly depended on the degree of circulatory disorders. Hemodynamic indices were closely correlated with blood levels of malonic dialdehyde and ceruloplasmin. Oxacom® and L-arginine exerted a beneficial effect on circulation and the oxidant-antioxidant system. Conclusion. NO-enhanced infusion therapy increased animal survival. In control experiments (infusion of isotonic sodium chloride), the survival rate was 42% while the sodium chloride solution supplemented with Oxacom® and L-arginine increased the survival rate to 77% and 59%, respectively.

scholarly journals Short-term, Mild Hypothermia Can Increase the Beneficial Effect of Permissive Hypotension on Uncontrolled Hemorrhagic Shock in Rats

2012 ◽  
Vol 116 (6) ◽  
pp. 1288-1298 ◽  
Author(s):  
Tao Li ◽  
Xiulai Lin ◽  
Yu Zhu ◽  
Lijie Li ◽  
Liangming Liu
Keyword(s):  
Oxygen Consumption ◽  
Survival Rate ◽  
Energy Metabolism ◽  
Blood Loss ◽  
Beneficial Effect ◽  
Hemorrhagic Shock ◽  
Mitochondrial Function ◽  
Mild Hypothermia ◽  
Short Term ◽  
Hypotensive Resuscitation

Background Our previous and other studies have shown that hypotensive or hypothermic resuscitation have beneficial effects on uncontrolled hemorrhagic shock. Whether hypothermia can increase the beneficial effect of hypotensive resuscitation on hemorrhagic shock is not known. Methods Two-hundred and twenty Sprague-Dawley rats were used to make uncontrolled hemorrhagic shock. Before bleeding was controlled, rats received normotensive or hypotensive resuscitation (target mean arterial pressure at 80 or 50 mmHg) in combination with normal (37°C) or mild hypothermia (34°C) (phase II). After bleeding was controlled, rats received whole blood and lactated Ringer's solution resuscitation for 2 h (phase III). The animal survival, blood loss, fluid requirement, cardiac output, and coagulation functions, as well as vital organ function, mitochondrial function, and energy metabolism of liver, kidney and intestines, were noted. Results Short-term, mild hypothermia before bleeding was controlled increased the beneficial effect of hypotensive resuscitation. Hypothermia further decreased blood loss, oxygen consumption, and functional damage to the liver, kidney, and intestines during hypotensive resuscitation, protected mitochondrial function and energy metabolism (activity of Na(+)-K(+)-ATPase), and further improved survival time and survival rate (hypothermic/hypotensive combined group: survival rate, 9/10; survival time, 616 min; normothermic/normotensive group: 1/10, 256 min; hypothermic/normotensive group: 4/10, 293 min). Hypothermia slightly inhibited coagulation function. Conclusion Mild hypothermia before bleeding is controlled can increase the beneficial effect of hypotensive resuscitation on uncontrolled hemorrhagic shock. The mechanism underlying the benefits of short-term hypothermia may be related to the decrease in oxygen consumption and metabolism, and protection of mitochondrial and organ functions.

scholarly journals Electroacupuncture Improves the Survival Rate and Organ Function in a Rat Model of Hemorrhagic Shock

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Yuxian Zhong ◽  
Guochen Xu ◽  
Yushou Wu ◽  
Huiping Zhang ◽  
Haibin Wang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Survival Rate ◽  
Hemorrhagic Shock ◽  
Fluid Resuscitation ◽  
Diamine Oxidase ◽  
Mucosal Blood Flow ◽  
Tissue Perfusion ◽  
Organ Function ◽  
Organ Protection ◽  
Arterial Blood

Electroacupuncture (EA) at ST36 can improve the survival rate in rats after hemorrhagic shock (HS). The current study investigated rats with 60% blood loss. 144 rats were divided into four groups: hemorrhage without fluid resuscitation (HS), EA after hemorrhage without fluid resuscitation (EA), hemorrhage with delayed resuscitation (DFR), and EA after hemorrhage with delayed resuscitation (EA + DFR). The survival rate and biological parameters 0, 3, 12, and 24 h after HS were investigated. The 24 h survival rate of EA + DFR was significantly higher than that of DFR. 12 h after hemorrhage, the level of mean arterial blood pressure of EA + DFR was significantly higher than that of DFR, and the levels of renal blood flow, intestinal mucosal blood flow, and hepatic blood flow of EA + DFR were also significantly higher than those of DFR. Three hours after hemorrhage, the levels of lactate, PaCO2, alanine aminotransferase, and creatinine of groups receiving EA were significantly lower than those of non-EA groups, and the levels of pH, PaO2, and diamine oxidase of groups receiving EA were significantly higher. EA at ST36 can improve the 24 h survival rate and produce the experimental antishock effects on tissue perfusion and organ protection from fatal HS.

Sign in / Sign up

Export Citation Format

Share Document