Hemodynamic improvement in hemorrhagic shock by aortic balloon occlusion and hypertonic saline solutions

The initial treatment of uncontrolled hemorrhagic shock from an abdominal source is controversial. The hemodynamic effects of transfemoral diaphragmatic aortic occlusion with a balloon followed by a single bolus of hypertonic saline solutions have been evaluated in 28 dogs. The animals were submitted to pressure-driven hemorrhage for 90 min, according to mean arterial pressure in the abdominal aorta and randomized into four groups, according to the treatment employed at 34 min after hemorrhage. Group 1 dogs (controls) received isotonic NaCl (0.9%, 308 mOsm/l, 4 ml/kg) without aortic occlusion; group 2 underwent aortic occlusion and received isotonic NaCl (0.9%, 308mOsm/l, 4 ml/kg); group 3 were occluded and received hypertonic NaCl (7.5%, 2400mOsm/l, 4 ml/kg); group 4 were occluded and received hypertonic sodium acetate (10.5%, 2400mOsm/l, 4 ml/kg). There were no significant differences between groups at basal measures and also after 30 min of continuous bleeding, when animals presented with severe shock, and significant decreases in mean arterial pressure, cardiac index, systolic index and cardiac filling pressures; the systemic vascular resistance index was increased. Control animals remained in severe shock throughout the experiment and three died. The recovery of mean arterial pressure in aortic-occluded dogs given isotonic NaCl was associated with a marked increase in systemic vascular resistance index, without improvements in cardiac index, systolic index and cardiac filling pressures. In occluded dogs given hypertonic NaCl and NaAc the mean arterial pressure recovery lasted longer, with lower increases in systemic vascular resistance index, while the cardiac index, systolic index and cardiac filling pressures showed a marked albeit transient increase. Injection of hypertonic saline following aortic occlusion produced significantly better hemodynamic profiles and should be seriously considered for the first treatment in severe uncontrolled hemorrhagic shock from an abdominal vascular source.     

Comparison of peripheral and central infusions of 7.5% NaCl/6% dextran 70

Although it had been known for several years that central venous injections of hypertonic salt solutions with added dextran could effectively resuscitate animals from hemorrhagic shock, it was not known whether peripheral injections could result in the same beneficial effects. Chronically instrumented, unrestrained, and unanesthetized sheep were subjected to a moderate degree of hemorrhagic shock and then resuscitated with a 2-minute infusion of 7.5% NaCl/6% dextran 70 in a volume of 5 ml/kg body weight. Infusions were made into the cephalic vein, the femoral artery, or, centrally, the superior vena cava. All three routes of injection promptly reestablished arterial pressure and cardiac output. All gave equivalently good restoration of plasma volume. None of the injections damaged the vessels, as determined either by gross inspection or by histologic examination. Thus the solution was safe and effective when given peripherally. It might be useful in the field resuscitation of hypovolemic patients.     

Effectiveness of hypertonic saline-dextran 70 for initial fluid resuscitation of major burns.

Small-volume resuscitation (4 ml/kg) with hypertonic saline-dextran (HSD) has been shown effective in hemorrhagic shock. In the present study the effectiveness of an initial 4 ml/kg bolus infusion of HSD on cardiovascular function and fluid resuscitation requirements after a major burn injury was evaluated in anesthetized sheep following a 40% BSA scald burn. One hour after injury resuscitation was initiated by a rapid intravenous bolus infusion (4 ml/kg) of either hypertonic saline-dextran (7.5% NaCl in 6% dextran 70) (HSD) or the same volume of normal (isotonic) saline (NS). Lactated Ringer's was later infused as needed to maintain cardiac output at 90% of baseline. HSD rapidly and effectively restored cardiac output and mean arterial pressure significantly better than the same volume of NS. Hemodynamic improvement by HSD was short lived, and need for further fluid therapy was only marginally delayed (HSD 38 +/- 8 min, NS 20 +/- 3 min; p = 0.06) (mean +/- SEM). The total requirements for fluid therapy during the first 6 hr postburn were not reduced by the initial HSD bolus (HSD 3,145 +/- 605 ml, NS 2,905 +/- 495 ml; n.s.), nor was skin edema formation reduced. We conclude that in anesthetized sheep HSD resuscitation was only transiently effective in treating burn shock. This may be attributed to the sustained increase in vascular permeability and continued plasma leak following thermal injury.     

Evaluation of an intraosseous infusion device for the resuscitation of hypovolemic shock.

An intraosseous infusion device designed for the prehospital administration of hypertonic saline-dextran solutions was evaluated by resuscitating hemorrhaged conscious sheep. Eight animals underwent 2 hours of hemorrhagic hypotension (50 mm Hg, bled volume = 43 +/- 7 ml/kg). This was followed by the intraosseous infusion of 200 ml (4-5 ml/kg) of 7.5% NaCl-6% dextran 70 into the bone marrow of the sternum. Results were compared to seven control animals (bled volume = 31 +/- 6 ml/kg) resuscitated through a central venous catheter. Despite the small volumes infused, mean arterial blood pressure and cardiac output were rapidly normalized in both groups by 10 minutes post resuscitation (p less than 0.01). Plasma sodium concentration increased an average of 12 mEq/L and plasma volume was rapidly expanded regardless of route. The metabolic acidosis of hemorrhagic shock was rapidly corrected, pulmonary pressures remained normal, and hypoxemia did not occur after intraosseous resuscitation. The device provided safe and rapid vascular access via the sternal bone marrow space. The use of intraosseous infusion of hypertonic saline dextran solutions via the sternal bone marrow may allow prehospital rescuers to consistently incorporate fluid replacement therapy into 'scoop and run' policies by avoiding the time delays associated with failures in IV access.     

The role of lung innervation in the hemodynamic response to hypertonic sodium chloride solutions in hemorrhagic shock

The role of pulmonary innervation in the genesis of hemodynamic responses to hypertonic salt solutions was assessed in an animal model of total lung denervation by total division of the pulmonary hilum followed by reimplantation of the organ. This was performed in 10 mongrel dogs (weighing 12 to 20 kg) randomly assigned to two groups: group I (five dogs) was comprised of animals with catheters placed in the pulmonary artery of the denervated lung; group II (five dogs) was comprised of animals with catheters placed in the pulmonary artery of the intact lung; a control group (group III) (five dogs) was submitted to a sham thoracotomy with catheters inserted in either pulmonary artery. On the seventh postoperative day the mean arterial pressure (MAP) was monitored and severe hemorrhagic shock (MAP = 40 mm Hg) was produced in all animals. After 30 minutes of shock the shed blood was discarded and 5% of the shed volume (+/- 2 ml/kg) was infused through the pulmonary catheter in the form of a hypertonic NaCl solution (2400 mosm/L). MAP continued to be measured for the 30 minutes following the infusion period. A significant rise of MAP was uniformly observed in animals of groups II and III. In group I low elevations of MAP were observed during the infusion period, followed by a return to shock levels on discontinuation of the infusion. The results suggest that selective lung denervation abolished the beneficial cardiovascular effects of hypertonic NaCl infusion during resuscitation from severe hemorrhagic shock without affecting the plasma osmolality pattern.     

Hypertonic solutions in the treatment of hypovolemic shock: a prospective, randomized study in patients admitted to the emergency room.

BACKGROUND. The infusion of small volumes of hypertonic saline solution or hypertonic saline plus dextran 70 is remarkably effective in restoring adequate hemodynamic conditions after hypovolemic shock. This prospective double-blind study compares the immediate hemodynamic effects of a bolus infusion of 7.5% NaCl or 7.5% NaCl plus 6% dextran 70 (both 2400 mOsm/L) in severe hypovolemia. METHODS. One hundred five adult patients admitted in hypovolemic shock (systolic blood pressure less than 80 mm Hg) were revived on arrival to the emergency room and administration of a 250 ml intravenous bolus of hypertonic saline solution (n = 35), hypertonic saline plus dextran (n = 35), or isotonic saline solution (n = 35). This infusion was immediately followed by standard crystalloid and blood replacement until systolic pressure reached 100 mm Hg. Mean arterial pressure (MAP) was measured every 5 minutes, and all intravenous infusions were registered. Plasma volume expansion was calculated from plasma protein concentration measurements. Patients were followed up throughout their hospital course, and results of treatment were recorded. RESULTS. At the end of the infusion period, and 5 and 10 minutes after infusion, MAP was significantly higher in patients receiving either hypertonic solution, compared with the group receiving isotonic solution. All groups showed similar trends toward restoration of hemodynamic parameters thereafter. The calculated plasma volume expansion, immediately after the bolus infusion, was significantly higher (24.1% +/- 1.8% and 24.9% +/- 1.1%) in the hypertonic groups, compared with isotonic groups (7.9% +/- 1.3%). Significantly greater volumes of fluids were required to restore systolic pressure in the patients receiving isotonic saline solution than in the groups receiving hypertonic solution. There were no significant differences between the groups receiving hypertonic solutions. The incidence of complications was low, and the mortality rate was similar in all groups. CONCLUSIONS. Infusion of 250 ml hypertonic saline solution in patients with severe hypovolemia was not related to any complications, nor did it affect mortality rates; it improved MAP significantly, acutely expanded plasma volume by 24%, and reduced significantly the volumes of crystalloids and blood required in their resuscitation.     

Use of hypertonic NaCl solutions in primary volume therapy]

The i.v. bolus infusion of 4 ml/kg b.w. of hypertonic (7.2-7.5%) saline solution represents a new concept for primary resuscitation from traumatic-hemorrhagic shock; it is called "small-volume resuscitation". Experimental studies have demonstrated that for the case of a 50% blood loss the infusion of 7.2-7.5% NaCl in a dose equivalent to 1/10 of the blood loss effectively restores cardiac filling pressures and cardiac output and significantly increases systemic pressure. Simultaneous application of a colloid (6-10% Dextran 60/70; 6-10% HAES 200,000/0.5) prolongs the circulatory effect of the hypertonic solution. Moreover, "small-volume resuscitation" by means of 7.2 NaCl/10% Dextran 60 was shown to completely restore nutritional organ blood flow already within only 5 minutes. The superiority of "small-volume resuscitation" using hypertonic-hyperoncotic solution as compared to conventional volume therapy consists of its effects on the microcirculation. Recent clinical trials have revealed the efficacy, practicability and safety of this new therapeutic concept for primary resuscitation from trauma and shock.     

Hypertonic saline solution-hetastarch for fluid resuscitation in experimental septic shock

Hypertonic colloid solutions have been found efficacious in the resuscitation from hemorrhagic/traumatic shock. The present study investigated the hemodynamic, gasometric, and metabolic effects of hypertonic colloids in endotoxic shock in the dog. Thirty minutes after administration of 3 mg/kg normal body weight of Escherichia coli endotoxin, dogs were randomly assigned to receive 10 mL/kg hydroxyethylstarch (HES) either in 0.9% NaCl (HES, 10 dogs) or in 7.5% NaCl (HT-HES, 10 dogs) in 30 min. Thereafter, 0.9% NaCl solution was administered in volumes adequate to maintain pulmonary artery balloon-occluded pressure at baseline levels. Total fluid administered averaged 64 +/- 30 mL/kg (mean +/- SD) in the HES group and 73 +/- 34 mL/kg in the HT-HES group. As these differences were not statistically significant, total sodium load was higher in the HT-HES group. The persistent volume effect was associated with persistently lower hematocrit and protein levels in the HT-HES group. Initial fluid resuscitation with HT-HES resulted in arterial pressure, cardiac filling pressures, cardiac output, stroke volume, and rates of oxygen delivery and oxygen consumption that were greater than those with HES. Vascular resistances were similar. Analysis of left ventricular function curves also indicated an improvement in cardiac performance. However, these effects almost completely vanished during the remainder of the study. In the HT-HES group, serum sodium and osmolality levels increased to 167 +/- 4 mEq/L and 344 +/- 4 mOsm/kg H2O, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of hypertonic sodium chloride during surgical treatment of aortic aneurysms

Thoracoabdominal aortic surgery with aortic clamping is normally associated with major volemic shifts when the clamp is removed. This study compares the hemodynamic effects of hypertonic (HS) and isotonic (IS) solutions of sodium chloride (NaCl) infusions on the severe hypotension which follows aortic unclamping. Five consecutive patients received HS, and five received IS immediately after aortic unclamping. Blood loss, diuresis, and blood and crystalloid infusions were monitored throughout the operation. Blood gases, and pH, and hematocrit, hemoglobin, and plasma electrolyte levels were controlled during and 24 hours after surgery. Systemic arterial pressure, pulmonary arterial and wedge pressures, cardiac output, and systemic and pulmonary vascular resistance were monitored at the start of the operation, during aortic clamping, immediately after unclamping, immediately after HS or IS NaCl infusion and at the end of the operation. Patients who received HS NaCl exhibited higher pulmonary arterial and wedge pressures, higher cardiac index, and lower systemic and pulmonary vascular resistances immediately after the infusion. These patients required less volume transfusion than patients who received IS NaCl, despite slightly higher blood losses. It is concluded that HS NaCl is useful for the treatment of human hemorrhagic shock.     

The effect of hypertonic saline resuscitation on responses to severe hemorrhagic shock by the skeletal muscle, intestinal, and renal microcirculation systems: seeing is believing

BACKGROUND: Decompensated hemorrhagic shock is often refractory to resuscitation, and we show here that it is associated with loss of vascular tone in skeletal muscle precapillary arterioles. We tested the hypothesis that microvascular derangements in the skeletal muscle, intestinal, and renal microcirculation systems would be reversed by initial hypertonic saline-dextran infusion. METHODS: Male Sprague-Dawley rats underwent precollicular brain stem transection without anesthesia for study. Parameters measured by in vivo videomicroscopy included cardiac output, mean arterial pressure, and microvascular responses in the skeletal muscle, ileum, and renal (i.e., the hydronephrotic kidney) microcirculation systems. Hemorrhaged was induced to a mean arterial pressure of 50 mmHg until decompensation occurred. The rats were then initially resuscitated with (1) 4 mL/kg 7.5% NaCl in 6% dextran 70, (2) 33 mL/kg .9% NaCl in 6% dextran 70, or (3) 33 mL/kg .9% NaCl. Twenty minutes later they received shed blood plus 33 mL/kg .9% NaCl to maintain mean arterial pressure at baseline levels. RESULTS: Decompensated hemorrhagic shock decreased cardiac output to between 24% and 35% of baseline values and profoundly decreased microvascular blood flow to between 10% and 19% of baseline. At the completion of resuscitation cardiac output increased to greater than baseline in all groups. Microvascular blood flow increased toward baseline transiently but then progressively deteriorated to between 36% and 69% of baseline in the 3 tissues. There was no significant difference between the three resuscitative fluids. CONCLUSIONS: Despite return of cardiac output to greater than baseline levels, muscle, intestinal, and renal microvascular blood flows remained significantly depressed. Hypertonic saline and/or dextran did not improve these deficits.     

Fluid therapy in burns

Abstract: The dissertation evaluates changes in transcapillary fluid and protein balance in the initial phase after extensive burns, comparing the effects of different regimens for post-burn fluid resuscitation. Studies were performed in anaesthetized rats and sheep. Within 15 min after major thermal injury, cardiac output (CO) was reduced by 40–50%, mainly due to a reduced stroke volume. Mean arterial pressure (MAP) also dropped by 30–40 mmHg. Both lactated Ringer's and plasma improved this postburn circulatory impairment. Rapid bolus infusions of small volumes of very hypertonic saline, 7.5% NaCl (2 400 mosmol/1), have rapidly corrected the circulatory impairment in haemorrhagic shock. Following a rapid bolus infusion of 7.5% NaCl in 6% Dextran 70, CO and MAP were completely restored, but the effect only lasted 30–60 min. When administered by a slow infusion, 7.5% NaCl gave no circulatory improvement. The transcapillary colloid-osmotic gradient was maintained in injured skin following infusion of plasma, whereas it was almost annihilated by infusion of lactated Ringer's. Plasma infusion thus induced a protein-rich edema in injured skin, whereas lactated Ringer's resulted in a generalized edema. Increased interstitial fluid flux can mobilize the interstitial matrix protcoglycan hyaluronan. Following burn injury, plasma concentrations of hyaluronan increased up to ten times above baseline. This observation suggests that at least some of the degradation of structural connective tissue components in thermally injured skin is by lymphatic removal (and subsequent degradation in liver). Increased plasma concentrations of interstitial components have not previously been observed after thermal injury.     

Infusion of very hypertonic saline to bled rats: membrane potentials and fluid shifts

Anesthetized rats were subjected to a moderate degree of hemorrhagic shock, lowering their mean arterial pressure to approximately 50 mm Hg for approximately 100 min. At the end of the shock period, resting skeletal muscle transmembrane potentials had depolarized from a baseline value of -82 mV to -65 mV; intracellular water had increased by 13%; and intracellular sodium and chloride contents had doubled. Eight rats were then given an infusion of very hypertonic saline (2400 mOsmole/kg, calculated osmolality) in a volume equal to only 10% of the volume of shed blood; another eight rats were given the equivalent amount of sodium and chloride in an isotonic solution (volume equal to 80% of shed blood). The mean arterial pressure in the rats that were given the very hypertonic saline returned to 81 mm Hg, compared to 55 mm Hg in the animals given normal saline. The membrane potentials in the hypertonic group polarized back to near normal- -78 mv--compared to no changes in the normal saline group. Intracellular water returned to preshock values in the hypertonic group as did intracellular sodium and chloride contents. Cellular contents in the normal saline group remained at shock levels. It was concluded that, in rats, infusion of small amounts of hypertonic saline can reverse some of the cellular abnormalities induced by hemorrhagic shock.     

The synergistic effects of pentoxifylline on systemic and regional perfusion after hemorrhage and hypertonic resuscitation

Small volumes of hypertonic saline solution ([HS] 7.5% NaCl) produce systemic and microcirculatory benefits in hemorrhaged animals. Pentoxifylline (PTX) has beneficial effects when administrated after hemorrhagic shock. We tested the hypothesis that the combination of HS and PTX in the initial treatment of hemorrhagic shock provides synergistic hemodynamic benefits. Twenty-four dogs were bled to a target arterial blood pressure of 40 mm Hg and randomized into 3 groups: lactated Ringer's solution (33 mL/kg; n = 6); HS (7.5% NaCl 4 mL/kg; n = 9); and HS+PTX (7.5% NaCl 4 mL/kg + PTX 15 mg/kg; n = 9). Systemic hemodynamics were measured by Swan-Ganz and arterial catheters. Gastric mucosal-arterial Pco2 gradient (D(g-a)Pco2; gas tonometry), portal vein blood flow (ultrasonic flowprobe), and systemic and regional O2-derived variables were also evaluated. HS induced a partial increase in mean arterial blood pressure, cardiac output, and portal vein blood flow. In the HS+PTX group, we observed a significant, but transitory, increase in systemic oxygen delivery (180 +/- 17 versus 141 +/- 13 mL/min) in comparison to HS alone. PTX infusion during hypertonic resuscitation promoted a significant reduction in D(g-a)Pco2 (41.8 +/- 4.8 to 25.7 +/- 3.9 mm Hg) when compared with isolated HS infusion (48.2 +/- 6.4 to 39.4 +/- 5.5 mm Hg). We conclude that PTX as an adjunct drug during hypertonic resuscitation improves cardiovascular performance and gastric mucosal oxygenation.     

Cerebrovascular effects of small volume resuscitation from hemorrhagic shock: comparison of hypertonic saline and concentrated hydroxyethyl starch in dogs

To determine if hypertonic and hyperoncotic resuscitation solutions exerted comparable effects on cerebral hemodynamics following hemorrhagic shock, we compared randomly assigned, equal volumes (6.0 ml/kg) of hypertonic (7.2%) saline (HS) and hyperoncotic (20%) hydroxyethyl starch (HES) for resuscitation from acute experimental hemorrhage in 12 anesthetized dogs. Regional cerebral blood flow (radiolabeled microspheres), intracranial pressure (cisternal catheter), and systemic hemodynamics were recorded. Rapid hemorrhage reduced the mean arterial pressure to 45 mm Hg for 30 min. Resuscitation fluids were infused over 5 min. Both fluids restored mean arterial pressure and cardiac output equally. However, at 60 min following resuscitation, cardiac output decreased in the HS group in comparison to the HES group (1.7 +/- 0.1 vs. 3.1 +/- 0.2 L/min, p <0.05). Cardiac output rapidly declined, however, in the HS group in comparison to the HES group (p <0.05 60 min following resuscitation). Intracranial pressure and cerebral perfusion pressure were similar at all intervals. Regional cerebral blood flow was similar following both fluids. Neither fluid restored cerebral oxygen transport to baseline values. Based on these data, the authors conclude that, following severe hemorrhagic shock of brief duration, systemic and cerebral hemodynamic values are restored equally well by highly concentrated colloid or by hypertonic saline, although hypertonic saline only transiently improves cardiac output.     

Small-volume hypertonic saline dextran resuscitation from canine endotoxin shock.

This study evaluated resuscitation of endotoxin shock with 7.5% hypertonic saline dextran (HSD 2400 mOsm) by measuring hemodynamic and regional blood flow responses. Endotoxin challenge (1 mg/kg) in adult dogs caused a significant decrease in mean arterial blood pressure (MABP), cardiac output (CO), left ventricular +/- dP/dt max, and regional blood flow (radioactive microspheres). Cardiocirculatory dysfunction and acid-base derangements persisted throughout the experimental period in untreated endotoxin shock (group 1, n = 10). In contrast both regimens of fluid resuscitation (group 2, n = 11: bolus of 4 mL/kg HSD followed by a constant infusion of lactated Ringer's [LR] to maintain MABP and CO at baseline values; group 3, n = 10; LR alone given as described for group 2) improved regional perfusion and corrected acid-base disturbances similarly in all dogs. Hypertonic saline dextran enhanced all indices of cardiac contraction and relaxation more than LR alone. The total volume of LR required to maintain MABP and CO at baseline values was less in the HSD group (59.2 +/- 6.8 mL/kg) than in the LR alone group (158 +/- 16 mL/kg, p = 0.01). The net fluid gain (infused volume minus urine output and normalized for kilogram body weight) was five times greater in the LR (24.8 +/- 6.2 mL/kg) than in the HSD group (4.6 +/- 1.2 mL/kg, p = 0.01). Lung water was similar in all dogs, regardless of the regimen of fluid resuscitation. Hypertonic saline dextran effectively resuscitates endotoxin shock in this canine model.     

Small-volume resuscitation with hypertonic saline dextran solution

Small-volume hypertonic resuscitation has been proposed as an effective means for restoration of cardiovascular function after hemorrhage at the scene of an accident. We evaluated the cardiovascular, metabolic, and neurohumoral response of resuscitation after hemorrhage using 200 ml of 2400 mosm sodium chloride, 6% dextran 70. Unanesthetized adult sheep were bled to maintain mean arterial pressure at 50 mm Hg for 3 hours, shed blood volume = 42 +/- 7 ml/kg. The sheep were then treated with a single bolus infusion of hypertonic saline dextran (n = 7) or normal saline solution (control group, n = 7) and then observed for a 30-minute period of simulated patient transport during which no additional fluid was given. Hypertonic saline dextran caused rapid restoration of blood pressure and cardiac output within 2 minutes of infusion. Cardiac output remained at or above baseline level, while both O2 consumption and urine output increased to above baseline level during the 30 minutes of simulated patient transport. By comparison 200 ml of normal saline solution caused only a small increase in blood pressure and no improvement in cardiac output or oxygen consumption. After this 30-minute period, both groups were given lactated Ringer's solution as needed to return and maintain cardiac output at its baseline value. The volume of lactated Ringer's solution required to maintain cardiac output was less in the hypertonic group, 371 +/- 168 ml, only one sixth that of the control group, 2200 +/- 814 ml. In summary after 3 hours of hypovolemia, a small volume of hypertonic saline dextran, about 4 ml/kg, fully restored cardiovascular and metabolic function for at least 30 minutes and significantly lowered the total volume requirements of resuscitation.     

等渗透剂量20%甘露醇与3%高渗盐水对大脑半球胶质瘤切除术患者血浆渗透浓度和电解质影响的比较

目的 比较择期大脑半球胶质瘤切除术中应用等渗透剂量的3%高渗盐水(hypertonie saline,HTS)和20%甘露醇(mannitol,M)降颅内压(intracranial pressure,ICP)的同时,患者血浆渗透浓度和电解质的变化及其临床意义. 方法 择期行大脑半球胶质瘤切除术患者40例,根据计算机随机分组表分为高渗盐水组(HTS组)和甘露醇组(M组)(n=20).两组均行静吸复合麻醉,异氟醚呼气末浓度达1 MAC后,在15 min内输注等渗透剂量3%HTS(5.33 ml/kg)或20%M(1 g/kg).记录输注前即刻(T0)、输注后即刻、输注后5、15、30、60、90、120 min(T1～T7)平均动脉压(MAP)、心率(HR),同时采取5 ml动脉血测定血球压积、血浆Na+、K+、Cl浓度、血pH、血浆渗透浓度,同时监测颅内压.结果 两组血浆渗透浓度在输注高渗溶液后均明显升高,在T1达高峰[HTS组:(305.1+4.3)mOsm/L;M组:(304.6±3.5)mOsm/kg](P<0.05),HTS组血浆Na+和cl浓度明显升高,于T1达高峰(152.3+5.2)mEq/kg(P<0.05),M组血浆Na+度降低,在T1达低谷(131.2±3.3)mEq/kg(P<0.05);血浆Cl-浓度在HTS组升高(P<0.05),M组降低(P<0.05).HTS组ICP在T2～T5降低(P<0.05),尤以T1～T2时段降低幅度更为明显,M组ICP在T3～T5降低(P<0.05).结论 在实施择期神经外科手术的患者,单剂静脉输注5.49 mOsm/kg的3%HTS和20%M引起同等程度的血浆渗透浓度上升,并在输注末达到高峰.     

Influence of hemorrhage on propofol pseudo-steady state concentration

BACKGROUND: A small induction dose has been recommended in cases of hemorrhagic shock. However, the influence of hemorrhage on the amplitude of plasma propofol concentration has not yet been fully investigated during continuous propofol infusion. The authors hypothesized that the effect of hemorrhage on plasma propofol concentration is variously influenced by the different stages of shock. METHODS: After 120 min of steady state infusion of propofol at a rate of 2 mg x kg(-1) x h(-1), nine instrumented immature swine were studied using a stepwise increasing hemorrhagic model (200 ml of blood every 30 min until 1 h, then additional stepwise bleeding of 100 ml every 30 min thereafter, to the point of circulatory collapse). Hemodynamic parameters and plasma propofol concentration were recorded at every step. RESULTS: Before total circulatory collapse, it was possible to drain 976 +/- 166 ml (mean +/- SD) of blood. Hemorrhage of less than 600 ml (19 ml/kg) was not accompanied by a significant change in plasma propofol concentration. At individual peak systemic vascular resistance, when cardiac output and mean arterial pressure decreased by 31% and 14%, respectively, plasma propofol concentration increased by 19% of its prehemorrhagic value. At maximum heart rate, when cardiac output and mean arterial pressure decreased by 46% and 28%, respectively, plasma propofol concentration increased by 38%. In uncompensated shock, it increased to 3.75 times its prehemorrhagic value. CONCLUSIONS: During continuous propofol infusion, plasma propofol concentration increased by less than 20% during compensated shock. However, it increased 3.75 times its prehemorrhagic concentration during uncompensated shock.     

Initial management of severe hemorrhage with an oxygen-carrying hypertonic saline solution

We tested the hypothesis that the combination of polymerized bovine hemoglobin (PBHg) with hypertonic saline may be beneficial for the initial management of hemorrhagic shock in 22 mongrel dogs (15 +/- 1 kg) bled to a mean arterial pressure (MAP) of 40 mm Hg in 5 min and maintained at this level for 45 min (shed blood volume approximately 50 ml/kg). Animals were treated with a 4 ml/kg bolus over 4 min of one of the following fluids: whole blood, 7.5% NaCl (HS), 13 g/dl of PBHg, or 7.5% NaCl combined with polymerized bovine hemoglobin (HS-PBHg). No additional intervention was performed, and the animals were followed for 60 min after treatment. PBHg and HS-PBHg produced a sustained, significant increase in MAP. Cardiac output was transiently increased only after HS and HS-PBHg. A partial increase in superior mesenteric artery blood flow was observed, particularly after HS-PBHg. We concluded that small volumes of PBHg alone restore MAP, but not blood flow. The combination of PBHg with hypertonic saline provides improvements in cardiac output and mesenteric blood flow, suggesting a potential benefit for the initial management of major blood loss.     

Renal, cerebral, and pulmonary effects of hypertonic resuscitation in a porcine model of hemorrhagic shock

To determine the safety and efficacy of a hypertonic solution for hypovolemic resuscitation, we compared the acute and delayed effects of hypertonic sodium lactate solution (514 mOsm) to Ringer's lactate solution (274 mOsm) in a porcine model of hemorrhagic shock. Cardiovascular, pulmonary, renal, and cerebral functions were examined in mature swine after their blood volume had been reduced by 40%. Hemorrhage produced significant decreases in blood pressure, cardiac output, and creatinine clearance, which were reversed with resuscitation. Resuscitation with Ringer's lactate solution required significantly more fluid and produced a significantly greater increase in intracranial pressure than did hypertonic sodium lactate solution. HSL produced significant increases in serum sodium and osmolality, which resolved within 48 hours. Hypernatremia and hyperosmolality were not associated with renal or cerebral dysfunction and were corrected through increased sodium excretion, free water intake, and a negative free water clearance.