ACTH inhibits the development of primary decompensation of the systemic and portal circulation in acute blood loss in rats]

Using the method of contact luminescent biomicroscopy of the liver and intestine coupled with the measurement of systemic blood pressure by micromanometer and ultrasonic registration of blood flow velocity in portal vein and hepatic artery it has been established that in rats with acute decompensatory hemorrhage fragments of ACTH (1-24) and (4-10) improve the state of portal macro- and microcirculation and increase the life span 2-3-fold. ACTH does not influence the dynamics of acute compensatory hemorrhage and the development of the posthemorrhagic microcirculatory disturbances (local microstases, microthromboses, erythrocyte aggregation).     

Lower body negative pressure as a model to study progression to acute hemorrhagic shock in humans.

Hemorrhage is a leading cause of death in both civilian and battlefield trauma. Survival rates increase when victims requiring immediate intervention are correctly identified in a mass-casualty situation, but methods of prioritizing casualties based on current triage algorithms are severely limited. Development of effective procedures to predict the magnitude of hemorrhage and the likelihood for progression to hemorrhagic shock must necessarily be based on carefully controlled human experimentation, but controlled study of severe hemorrhage in humans is not possible. It may be possible to simulate hemorrhage, as many of the physiological compensations to acute hemorrhage can be mimicked in the laboratory by applying negative pressure to the lower extremities. Lower body negative pressure (LBNP) sequesters blood from the thorax into dependent regions of the pelvis and legs, effectively decreasing central blood volume in a similar fashion as acute hemorrhage. In this review, we compare physiological responses to hemorrhage and LBNP with particular emphasis on cardiovascular compensations that both share in common. Through evaluation of animal and human data, we present evidence that supports the hypothesis that LBNP, and resulting volume sequestration, is an effective technique to study physiological responses and mechanisms associated with acute hemorrhage in humans. Such experiments could lead to clinical algorithms that identify bleeding victims who will likely progress to hemorrhagic shock and require lifesaving intervention(s).     

醒脑静注射液对急性脑出血患者FIB和D-二聚体水平的影响

目的:研究醒脑静注射液对急性脑出血患者血浆纤维蛋白原和D-二聚体水平的影响。方法:选取我院神经内科收治的急性脑出血患者90例,随机分为两组,其中对照组45例,予降低颅内压、控制血压、抗感染、营养脑细胞等常规治疗。实验组45例,在常规治疗的基础上加用醒脑静注射液。对比治疗前后患者血浆纤维蛋白原(FIB)、D-二聚体(D1-D)的含量及临床疗效。结果:治疗后,两组患者病情均有所改善,实验组有效率(91.11%)与对照组(82.22%)比较明显较高,差异有统计学意义(P0.05);两组患者血浆FIB含量较治疗前均明显升高,但实验组高于对照组,差异有统计学意义(P0.05);实验组血浆D-D含量明显降低,对照组明显升高,实验组明显低于对照组,差异有统计学意义(P0.05)。结论:醒脑静注射液能够使急性脑出血患者血浆纤维蛋白原含量增加,D-二聚体水平下降,具有良好的临床疗效,值得进一步研究推广。     

Effect of central naloxone on hormone and blood pressure responses to hemorrhage in conscious sheep

The role of the brain opioid system in the control of hypothalamic-pituitary-adrenal activity was studied in 10 conscious sheep with an indwelling cannula in a cerebral lateral ventricle. On separate days, sheep received infusions of artificial CSF (control) and the opiate antagonist, naloxone (100 micrograms/hr) before and during acute moderate hemorrhage (15 ml/kg over 10 min). Infusion of naloxone before hemorrhage raised plasma ACTH and resulted in a significant increase in cortisol compared to the control infusion. In contrast, ACTH and cortisol responses to hemorrhage tended to be blunted by central naloxone infusion. The responses of vasopressin, aldosterone and the catecholamines remained unaffected by naloxone. The fall in blood pressure and the rise in heart rate accompanying hemorrhage were likewise unaltered. These results suggest that brain opioid peptides have an inhibitory effect on basal ACTH secretion but do not play a major role in modulating the hemodynamic or pituitary-adrenal responses to acute moderate hemorrhage in conscious sheep.     

Renal response to hemorrhage in dogs with subacute biliary obstruction

In the present study, we tested the hemodynamic and renal response of 15 sham-operated dogs and 15 dogs with subacute (5-9 days) biliary obstruction to either acute or more chronic hemorrhage. All studies were conducted on sedated but unanaesthetized animals. Both groups were comparable before blood withdrawal with respect to central hemodynamics and renal perfusion. Serum bilirubin was 0.70 +/- 0.09 mg/dL for control dogs and 8.25 +/- 0.14 for experimental dogs (P less than 0.05). In the acute protocol, nine control and seven jaundiced dogs were bled over a period of 30-40 min to lower blood pressure by 19.1 and 19.5%, respectively. Blood volumes required to achieve this drop were 21.3 and 20.05 mL/kg, respectively (P greater than 0.05). Cardiac output declined by an equivalent value for each group and glomerular filtration rate and clearance of p-aminohippurate remained unchanged from control values. In six control and eight experimental dogs, 500 mL of blood was withdrawn over 5 days. Although blood pressure and cardiac output declined for each group by an equivalent amount, renal perfusion remained unchanged for each group from control values. We conclude that acute or chronic hemorrhage of modest degree does not predispose to acute renal insufficiency in dogs with subacute biliary obstruction.     

高血压脑出血患者术后重症监护治疗与早期再出血的相关因素分析

目的:探究高血压脑出血患者术后重症监护治疗与早期(24 h内)再出血的相关因素。方法:回顾性分析2014年1月至2018年10月于中山大学附属第一医院及中山市人民医院行手术治疗并进行重症监护的高血压脑出血患者的相关资料,记录术后早期发生再出血情况,比较其相关因素,包括年龄、性别、术前格拉斯哥昏迷量表(GCS)评分、出血量、术前收缩压、术后收缩压、镇静时间、插管时间、有无使用止血药、血压波动、血压差、有无镇痛情况,分析术后早期再出血的影响因素。结果:本研究共纳入465例患者,其中术后早期再出血患者44例,未再出血患者421例,再出血发生率为9.46%(44/465)。高血压脑出血术后早期再出血患者的术后收缩压、有无镇痛、血压差、血压波动与未再出血患者比较差异具有统计学意义(P0.05)。术后早期再出血患者的年龄、性别及术前GCS评分、出血量、术前收缩压、镇静时间、插管时间、有无使用止血药与未再出血患者比较差异无统计学意义(P0.05)。多因素Logistic回归分析显示,患者血压波动大是术后早期再出血的危险因素,手术前后血压差大、术后使用镇痛治疗是其保护因素。结论:高血压脑出血患者术后血压波动、手术前后血压差及术后镇痛治疗均是早期再出血的影响因素,合理降压及镇痛治疗可减少脑出血术后早期再出血的发生。     

Impaired blood pressure recovery to hemorrhage in obese Zucker rats with orthopedic trauma

We have shown that obese Zucker rats with orthopedic trauma (OZT) exhibit a loss of arteriolar tone in skeletal muscle. We hypothesize that the loss of arteriolar tone in OZT blunts vasoconstrictor responses to hemorrhage, resulting in an impaired blood pressure recovery. Orthopedic trauma was induced with soft tissue injury and local injection of bone components in both hindlimbs in lean (LZT) and OZT (11-13 wk). One day after the orthopedic trauma, blood pressure responses following hemorrhage were measured in conscious control lean, control obese, LZT, and OZT. In another set of experiments, the spinotrapezius muscle of control and trauma animals was prepared for microcirculatory observation. Arteriolar responses to phenylephrine (PE) or hemorrhage were determined. Hemorrhage resulted in similar blood pressure responses in control animals and LZT, but the blood pressure recovery following hemorrhage was blunted in the OZT. In the spinotrapezius, OZT exhibited decreased arteriolar tone and blunted vasoconstrictor responses to PE and hemorrhage. Treatment with glibenclamide improved the blood pressure recovery in the conscious OZT and improved the arteriolar tone, and PE induced vasoconstriction in the spinotrapezius of the OZT. Thus, ATP-dependent K(+) channel-mediated loss of arteriolar tone in OZT blunts the arteriolar constriction to hemorrhage, resulting in impaired blood pressure recovery.     

Hemodynamic changes in post-suspension rats during gradual hemorrhage

We examined the changes of hemodynamic parameters in nembutal-anesthetized rats during gradual hemorrhage (2 ml/100 g body weight during 30 min). In control rats blood pressure began to decline starting from 3rd min of bleeding and from 5th min it was accompanied by cardiac deceleration. Hindlimb vascular resistance was only slightly increased up to 15th min (by 20-30%) and then began to grow drastically. Less prominent changes of hemodynamics were observed in post-suspension rats. The results indicate that when activity of sympathetic nervous system is blunted with anesthetic post-suspension rats demonstrate higher hemodynamic stability during acute hemorrhage.     

Effect of reinfusions of autologous blood on the systemic and portal circulation in acute blood loss in rats

The experiments on rats using the method of contact luminescent biomicroscopy coupled with the ultrasonic measurement of systemic blood pressure and blood flow velocity in the portal vein and hepatic artery have revealed that portal micro- and macrocirculation reflects the degree of efficacy of acute hemorrhage treatment with autoblood. Autoblood infusion in animals with compensatory type of posthemorrhagic period restored systemic blood pressure and blood flow velocity in the portal vein and hepatic artery, promoting the development of erythrocyte aggregation and local microcirculation disturbances in the central zone of hepatic functional elements.     

Renal SNA as the primary mediator of slow oscillations in blood pressure during hemorrhage

Blood pressure contains a distinct low-frequency oscillation often termed the Mayer wave. This oscillation is caused by the action of the sympathetic nervous system on the vasculature and results from time delays in the baroreflex feedback loop for the control of sympathetic nerve activity (SNA) in response to changes in blood pressure. In this study, we used bilateral renal denervation to test the hypothesis that it is SNA to the kidney that contributes a large portion of the vascular resistance associated with changes in the strength of the slow oscillation in blood pressure. In conscious rabbits, SNA and blood pressure were measured during hemorrhage (blood withdrawal at 1.35 ml. min(-1). kg(-1) for 20 min). Spectral analysis identified a strong increase in power at 0.3 Hz in SNA and blood pressure in the initial compensatory phase of hemorrhage before blood pressure started to fall. However, in a separate group of renal denervated rabbits, although the power of the 0.3-Hz oscillation under control conditions in blood pressure was similar, it was not altered during hemorrhage. Wavelet analysis revealed the development of low-frequency oscillations at 0.1 Hz in both intact and denervated animals. In conclusion, we propose that changes in the strength of the oscillation at 0.3 Hz in arterial pressure during hemorrhage are primarily mediated by sympathetic activity directed to the kidney.     

A possible role for somatostatin in depression of insulin and glucagon levels during hemorrhage

The hypothesis that depression of insulin and glucagon levels during rapid, acute hemorrhage is controlled by somatostatin was supported by hormonal changes measured in the cat. By 5 min of hemorrhage to 50 mmHg (1 mmHg = 133.322 Pa) arterial blood pressure, insulin and glucagon were severely depressed and somatostatin levels rose to 232% of basal levels. Insulin and glucagon suppression was maintained for the 30-min period of hemorrhage. Following return of the blood, somatostatin levels remained high and insulin and glucagon suppression was maintained. The data support, but do not prove, the hypothesis.     

Visceral pain decreases tolerance to blood loss in conscious female but not male rabbits

Pain is a component of traumatic blood loss, yet little is known about how pain alters the response to blood loss in conscious animals. We evaluated the effects of colorectal distension on the cardiorespiratory response to blood loss in six male and six female conscious, chronically instrumented New Zealand White rabbits. The goal of these experiments was to test the hypotheses that 1) colorectal distension would increase tolerance to hemorrhage (i.e., increase the blood loss required to decrease mean arterial pressure 相似文献   

The hemodynamic consequences of hemorrhage and hypernatremia in two amphibians

1. Graded hypovolemia was induced by hemorrhagic blood loss and graded hypernatremia by salt load in the toad, Bufo marinus, and the bullfrog, Rana catesbeiana. Maximal blood flow rates in the systemic arches and arterial and venous pressures were measured during activity after each stress. 2. Maximal blood flow rates in the B. marinus did not decline until blood loss exceeded 5% of initial body mass. In R. catesbeiana, losses of 2% initial body mass caused a decline (Fig. 1). 3. Maximal heart rates did not change with hemorrhage (Fig. 2). The decline in blood flow rates with hemorrhage was due to declining pulse volumes in both species (Fig. 3). 4. Arteriovenous pressure difference declined with hemorrhage in both species (Fig. 4). Peripheral resistance increased with hemorrhage in parallel with compromised blood flow rates (Fig. 5). 5. Plasma sodium concentration slightly increased with hemorrhage, while plasma protein concentration and hematocrit declined. Lymphatic compensation for hemorrhagic loss is indicated in both species (Fig. 6). 6. Induced hypernatremia compromised blood flow rates in both species at plasma sodium concentrations above 175 mM. The decline in flow rates was principally a result of a decrease in pulse volume, though maximal heart rates also declined (Figs. 2, 3, 7). 7. Induced hypernatremia had no effect on the arteriovenous pressure difference in B. marinus but caused it to decline in R. catesbeiana. Peripheral resistance increased in only B. marinus but not R. catesbeiana (Figs. 4, 5). Hematocrit did not change with salt load, indicative of a constant vascular volume.     

The effect of glucagon on glomerular filtration rate in dogs during reduction of renal blood flow.

Glucagon in small intravenous (i.v.) doses markedly increases glomerular filtration rate (GFR) in normal anesthetized dogs. In this study, the effects of glucagon 5 mug/min (i.v.) on renal hemodynamics was tested in four canine models of acute pre-renal failure (hemorrhage, barbiturate overdose; renal arterial clamping and renal arterial infusions of noradrenaline) and in a model of unilateral acute tubular necrosis at 4 h and 6-7 days following completion of the ischemic insult. Following hemorrhage and barbiturate excess, with arterial blood pressure maintained at 65-70 mm Hg, whole-kidney GFR and clearance rate of p-aminohippurate decreased by 50-70%. During this reduction of perfusion pressure, the subsequent infusion of glucagon increased GFR by 90-130%. In models where arterial pressure was normal during the period of ischemia (clamping and noradrenaline infusion), not only did glucagon significantly increase renal perfusion, but the ischemic kidney proved to be far more sensitive to the hemodynamic effects of glucagon (delta GFR - 120-160%) than the contralateral control (deltaGFR = 30-40%). In three dogs completely anuric following renal arterial clamping, glucagon was able to improve blood flow and restart urine formation. Glucagon, but not dopamine, was able to simulate the beneficial effects of hypertonic mannitol on renal function in dogs with hemorrhagic hypotension. Glucagon was without effect in established acute tubular necrosis. This study, therefore, indicates that, during renal ischemia, glucagon may be quite effective in preserving urine output and perfusion of the kidneys.     

Atriopeptin alters the vasopressin and renin responses elicited by hemorrhage

This study was designed to investigate whether an infusion of atrial peptide is capable of modulating the hormonal and hemodynamic responses elicited by acute hemorrhage. Conscious dogs were bled at a rate of 0.8 ml.kg-1.min-1 until 20 ml of blood/kg body wt had been removed. Two experiments were performed on each dog; in one experiment the animal was given alpha-human atrial natriuretic peptide (alpha-hANP) (50 ng.kg-1.min-1) dissolved in saline; in the other only the saline vehicle was given. Right and left atrial pressures decreased during hemorrhage in all experiments; the absolute decreases were greater when the animals received atriopeptin, but the differences between treatments were statistically significant only for right atrial pressure. Cardiac output decreased (P less than 0.05) and total peripheral resistance increased (P less than 0.05) during hemorrhage when atriopeptin was infused; although these variables showed similar trends when vehicle alone was infused during hemorrhage, no significant changes occurred. Infusion of atrial peptide did not affect the decrease in arterial blood pressure that occurred during hemorrhage. The increase in plasma vasopressin induced by hemorrhage was potentiated, but the increase in plasma renin activity was attenuated when alpha-hANP was infused. Hemorrhage increased circulating aldosterone levels in each experiment, but the response was less pronounced when alpha-hANP was given during the experiment. Intravenous administration of alpha-hANP modulates the hemodynamic responses elicited by hemorrhage, potentiates the rise in plasma vasopressin, and attenuates the rise in plasma renin activity induced by acute blood loss in conscious dogs.     

Sex differences in the respiratory response to hemorrhage in the conscious, New Zealand white rabbit

In conscious animals, the response to hemorrhage is biphasic. During phase 1, arterial pressure is maintained. Phase 2 is characterized by profound hypotension. Despite allied roles, less is known about the integrated cardiovascular and respiratory response to blood loss in conscious animals. We evaluated cardiorespiratory changes during hemorrhage to test the hypotheses that 1) respiratory rate (RR) and blood gases do not change during phase 1; 2) RR increases during phase 2; and 3) RR and blood gas changes during hemorrhage are similar in males and females. We measured mean arterial pressure, RR, and blood gases during hemorrhage in 16 conscious, chronically prepared, male and female New Zealand white rabbits. We removed venous blood until mean arterial pressure was < or =40 mmHg. Sex did not affect mean arterial pressure, heart rate, Pa(O(2)), Pa(CO(2)), or pH during hemorrhage or the blood loss required to induce phase 2. Pa(CO(2)) decreased significantly from 37 +/- 1 to 33 +/- 1 and 29 +/- 1 mmHg (P < 0.001) during phase 1 and 2, respectively. Before hemorrhage, Pa(O(2)) was 87 +/- 2 mmHg. Pa(O(2)) was unchanged in phase 1 (92 +/- 2 mmHg) but increased in phase 2 (101 +/- 2 mmHg; P < 0.001). Body temperature, Pv(CO(2)) (thoracic vena cava), and ventilation-perfusion mismatch (A-a gradient) were unchanged during phases 1 and 2. Neither sex increased RR during phase 1. While males doubled RR during phase 2, RR in females did not change (P < 0.001). Thus, while Pa(CO(2)) decreases in phase 1 and phase 2, the decreases are achieved in different ways across the two phases and in the two sexes.     

Cardiovascular responses to oxygen inhalation after hemorrhage in anesthetized rats: hyperoxic vasoconstriction

Oxygen inhalation is recommended for the initial care of trauma victims. The improved survival seen in early hemorrhage is normally associated with an increase in blood pressure. Although clinical use of oxygen can occur late after hemorrhage, the effects of late administration have not been specifically examined. Anesthetized rats were studied using an isobaric hemorrhage model with target pressures of either 70 or 40 mmHg. At various times after hemorrhage, the feedback control of the blood pressure was stopped and the inspired gas was changed from room air to 100% oxygen. The results show that shortly after hemorrhage to 70 mmHg, oxygen inhalation results in an increase in mean arterial blood pressure of 60 +/- 3 mmHg, which is associated with a large increase in total peripheral resistance from 0.89 +/- 0.05 to 1.25 +/- 0.1 peripheral resistance units. The blood pressure response is essentially unchanged with time, and it is not altered by a 10-min exposure to N(G)-nitro-l-arginine methyl ester. At a target pressure of 40 mmHg, the initial blood pressure response to oxygen is the same, but it gradually decreases as the animal develops a lactic acidosis. We conclude that the therapeutic value of oxygen needs to be separately evaluated for late hemorrhage.     

Hemodynamic effects of blood loss during a passive response to a stressor in the conscious rabbit

In the conscious rabbit, exposure to an air jet stressor increases arterial pressure, heart rate, and cardiac output. During hemorrhage, air jet exposure extends the blood loss necessary to produce hypotension. It is possible that this enhanced defense of arterial pressure is a general characteristic of stressors. However, some stressors such as oscillation (OSC), although they increase arterial pressure, do not change heart rate or cardiac output. The cardiovascular changes during OSC resemble those seen during freezing behavior. In the present study, our hypothesis was that, unlike air jet, OSC would not affect defense of arterial blood pressure during blood loss. Male New Zealand White rabbits were chronically prepared with arterial and venous catheters and Doppler flow probes. We removed venous blood until mean arterial pressure decreased to 40 mmHg. We repeated the experiment in each rabbit on separate days in the presence and absence (SHAM) of OSC. Compared with SHAM, OSC increased arterial pressure 14 +/- 1 mmHg, central venous pressure 3.3 +/- 0.4 mmHg, and hindquarter blood flow 34 +/- 4% while decreasing mesenteric conductance 32 +/- 3% and not changing heart rate or cardiac output. During normotensive hemorrhage, OSC enhanced hindquarter and renal vasoconstriction. Contrary to our hypothesis, OSC (23.5 +/- 0.6 ml/kg) increased the blood loss necessary to produce hypotension compared with SHAM (16.8 +/- 0.6 ml/kg). In nine rabbits, OSC prevented hypotension even after a blood loss of 27 ml/kg. Thus a stressful stimulus that resulted in cardiovascular changes similar to those seen during freezing behavior enhanced defense of arterial pressure during hemorrhage.     

应激性高血糖与急性自发性脑出血患者术后并发症和早期预后的相关性研究

目的:探讨应激性高血糖与自发性脑出血患者术后并发症及早期预后的关系。方法:回顾性分析我院收治的自发性脑出血患者358例,根据入院时血糖水平、糖化血红蛋白(HbAlc)及既往有无糖尿病史分为血糖正常组(96例)、应激性高血糖组(107例)及糖尿病组(155例),记录和比较各组入院时的血糖、格拉斯哥昏迷评分(GCS)、平均出血量及入院后30 d时各组的术后并发症发生情况、格拉斯哥预后评分(GOS)的差异。结果:糖尿病组入院时血糖水平、平均出血量、重型患者所占比率、脑出血破入脑室、颅内再出血、颅内感染、肺部感染、尿路感染及上消化道出血发生率、GOS分级植物状态或死亡发生率均明显高于应激性高血糖组(P0.05),GOS分级良好率低于应激性高血糖组(P0.05);而应激性高血糖组入院时血糖水平、平均出血量、重型患者所占比率、脑出血破入脑室、颅内再出血发生率、GOS分级植物状态或死亡发生率均明显高于血糖正常组(P0.05)。结论:自发性脑出血患者入院时应激性高血糖与患者的病情显著相关,可加重急性脑出血的不良预后。     

Detrimental effects of complement activation in hemorrhagic shock.

The complement system has been implicated in early inflammatory events and a variety of shock states. In rats, we measured complement activation after hemorrhage and examined the hemodynamic and metabolic effects of complement depletion before injury and worsening of complement activation after hemorrhage and resuscitation [with a carboxypeptidase N inhibitor (CPNI), which blocks the clearance of C5a]. Rats were bled to a mean arterial pressure of 30 mmHg for 50 min and were then resuscitated for 2 h. Shock resulted in significant evidence of complement consumption, with serum hemolytic activity being reduced by 33% (P < 0.05). Complement depletion before injury did not affect hemorrhage volume (complement depleted = 28 +/- 1 ml/kg, complement intact = 29 +/- 1 ml/kg, P = 0.74) but improved postresuscitation mean arterial pressure by 37 mmHg (P < 0.05) and serum bicarbonate levels (complement depleted = 22 +/- 3 meq/ml, complement intact = 13 +/- 8 meq/ml, P < 0.05). Pretreatment with CPNI was lethal in 80% of treated animals vs. the untreated hemorrhaged group in which no deaths occurred (P < 0.05). In this model of hemorrhagic shock, complement activation appeared to contribute to progressive hypotension and metabolic acidosis seen after resuscitation. The lethality of CPNI during acute blood loss suggests that the anaphylatoxins are important in the pathophysiological events involved in hemorrhagic shock.