Correlation of plasma beta-endorphin levels with mean arterial pressure and cardiac output in hypovolemic shock

Recent studies have been conducted to evaluate the relationship between plasma beta-endorphin (END) levels and the hemodynamic changes that occur in severely stressed animals. Using our canine hypovolemic shock model, END levels were analyzed during the baseline period, at the beginning of treatment (after a period of fixed-pressure hypovolemic shock), and at the end of treatment. Mean arterial pressure (MAP) and cardiac output were also measured at these intervals. Animals were given iv 5 ml of 0.9% NaCl, 4 mg/kg of naloxone (NAL), 30 mg/kg of methylprednisolone (MP), or 4 mg/kg of NAL and 30 mg/kg of MP. A fifth group was composed of nonsteroid-treated animals. Scatterplots were generated and linear regression lines were drawn comparing END with cardiac output and MAP. In the nonsteroid-treated animals, a significant correlation was found between decreases in both MAP and cardiac output and increasing levels of END. The addition of MP did not seem to alter the relationship, suggesting that MP did not affect END release.     

Postreperfusion syndrome: Hypotension after reperfusion of the transplanted liver

Sixty-nine patients undergoing liver transplantation were evaluated to elucidate the relationship between hypotension and physiological changes seen on reperfusion of the grafted liver. Measured variables included hemodynamic profiles, core temperature, serum potassium, ionized calcium levels, arterial blood-gas tensions, and acid-base state. Measurements were taeen 60 minutes after skin incision (baseline), 5 minutes before reperfusion, and 30 seconds and 5 minutes after reperfusion. On the basis of changes in mean arterial pressure (MAP) patients were divided in two groups. Group 1 (n = 49) maintained MAP greater than 70% and group 2 (n = 20) had MAP less than 70% of the baseline value for at least 1 minute within 5 minutes after reperfusion. On reperfusion, changes common to both groups were 27% increase in cardiac filling pressures, 23% base deficit, and 30% serum potassium level and a decrease of 16% in cardiac output and 9% in temperature. Compared with group 1, group 2 had greater decrease in systemic vascular resistance (SVR) (1097 ± 868 and 741 ± 399 dyn · s⁻¹. cm⁻⁵, respectively, P < .05) and higher potassium level (4.5 ± 0.8 and 5.3 ± 0.8 mmol/L,P < .05). Collectively in both groups, there was no correlation between MAP and physiological variables; however, there was a poor correlation with SVR (r = .32, P < .01). Reperfusion hypotension seen in group 2 patients correlated only with a decrease in systemic vascular resistance (r = .5, P < .05). Acute hyperkalemia, hypothermia, and acidosis do not appear to be major causes of reperfusion hypotension.     

Amrinone as an Antidote in Experimental Veraparnil Overdose

Objective: To evaluate the effect of amrinone as a treatment for the hemodynamic effects of verapamil overdose in a canine model.
Methods: This nonblind interventional study was performed in an established canine model of verapamil toxicity, without concurrent control animals. Pentobarbital-anesthetized and instrumented dogs ( n = 8) were maintained and observed for 60 minutes or until death. The animals were overdosed with verapamil, 15 mg/kg IV, over 30 minutes. Hemodynamic parameters, including cardiac index (CI), heart rate (HR), and mean arterial pressure (MAP), were monitored. Completion of the verapamil infusion represented the defined point of toxicity; at that point, all the animals received an amrinone bolus of 2 mgkg IV over 2 minutes followed by an amrinone drip at 10 μg/kg/min. The hemodynamic values at the defined point of toxicity were compared with those obtained postinitiation of the amrinone infusion.
Conclusion: Amrinone appears to reverse the depressed cardiac index associated with verapamil overdose in a canine model while having no significant effect on the hypotension or bradycardia.     

Correlation of Plasma and Peritoneal Diasylate Clomipramine Concentration with Hemodynamic Recovery after Intralipid Infusion in Rabbits

Objectives:  Drug sequestration to an expanded plasma lipid phase has been proposed as a potential mechanism of action for lipid emulsions in lipophilic cardiotoxin overdose. The authors set out to document plasma and peritoneal diasylate clomipramine concentration after resuscitation with lipid emulsion in a rabbit model of clomipramine-induced hypotension.
Methods:  Twenty sedated mechanically ventilated New Zealand White rabbits were allocated to receive either 12 mL/kg 20% Intralipid or 12 mL/kg saline solution, following clomipramine infusion to 50% baseline mean arterial pressure (MAP). Hemodynamic parameters and serum clomipramine concentration were determined to 59 minutes. Peritoneal dialysis with 20% Intralipid or saline solution was evaluated for clomipramine concentration.
Results:  Mean arterial pressure was greater in lipid-treated animals as assessed by repeated-measures analysis of variance (F[1,14] = 6.84; p = 0.020). Lipid infusion was associated with elevated plasma clomipramine concentration and reduced initial volume of distribution (Vd; 5.7 [±1.6] L/kg lipid vs. 15.9 [±7.2] L/kg saline; p = 0.0001). Peritoneal diasylate clomipramine concentration was greater in lipid-treated animals (366.2 [±186.2] μg/L lipid vs. 37.7 [±13.8] μg/L saline; p = 0.002).
Conclusions:  Amelioration of clomipramine-induced hypotension with lipid infusion is associated with reduced initial Vd and elevated plasma clomipramine concentration consistent with intravascular drug–lipid sequestration. Concomitant peritoneal dialysis with lipid emulsion enhances clomipramine extraction.     

Contribution of peripheral blood pooling to central hemodynamic disturbances during endotoxin insult in intact dogs

The aim of the present study was to determine possible effects of Escherichia coli endotoxin on peripheral vascular compliance and relate them to concomitant central hemodynamic disturbances. Endotoxin was infused at 0.25 micrograms/kg.min during 2 h in six anesthetized dogs, while six additional animals served as controls. Vascular compliance of the systemic circulation was calculated in intact animals from the changes in CVP after known changes in systemic blood volume. In control dogs, vascular compliance averaged 2.3 ml/mm Hg.kg body weight. During slow endotoxin infusion, cardiovascular effects were measurable only after a certain period of time had elapsed from the start of endotoxin insult and consisted of hypotension associated with systemic vasodilation. Systemic BP decreased gradually from 124 to 68 mm Hg while vascular compliance was finally increased by 100%, when compared to control values. This latter rise was responsible for a reduction in the cardiac preloads. Pulmonary wedge pressure and CVP were decreased from 7.1 to 3.4 and from 4.5 to 2.6 mm Hg, respectively. However, parallel to the decrease in left ventricular preload, endotoxin induced a progressive decrease in left ventricular afterload. Because of the balance in ventricular loading, cardiac output remained almost unchanged. After volume loading (dextran 30 ml/kg), cardiac output was remarkably increased from 3.28 to 6.24 L/min.m2 while peripheral vasodilation was not affected by this maneuver. It is concluded that low dose endotoxin infusion induces in dogs a hemodynamic pattern similar to human sepsis. The left ventricular loading changes are related to an enhanced systemic vascular compliance from 2.3 to 4.5 ml/mm Hg.kg. High flow shock state is encountered provided peripheral blood pooling is compensated by adequate volume replacement.     

Glucagon and Phenylephrine Combination vs Glucagon Alone in Experimental Verapamil Overdose

Objective: To evaluate glucagon and phenylephrine in combination as a treatment for the hemodynamic effects of verapamil overdose. Methods: Pentobarbital–anesthetized and instrumented dogs were overdosed using a previously developed verapamil overdose model (15 mg/kg IV over 30 minutes). The animals were maintained and observed for 90 minutes or until death. Cardiac output (CO), heart rate (HR), and mean arterial pressure (MAP) were monitored. Following the 30–minute verapamil infusion (toxicity), the control animals received no treatment; the glucagon animals received a 5–mg glucagon bolus and a drip of 5 mg/90 minutes; and the glucagon/ phenylephrine animals received the same glucagon therapy plus a phenylephrine drip titrated to 180 (μg/ min over 15 minutes. The groups were compared using analysis of variance: the experimental variables were group and time; the response variables were changes from toxicity for the hemodynamic parameters. Post–hoc comparisons were done with a set at 0. 05. Results: A significant change in CO was seen in the glucagon group (Δ = 2. 6 L/min) and the glucagon/ phenylephrine group (Δ = 1. 9 L/min) compared with the control group (Δ = 0. 8 L/min). The change in CO was significantly larger for the glucagon animals compared with the glucagon/phenylephrine animals. The change in MAP for the glucagon/phenylephrine group (Δ = 24 mm Hg) was significant compared with the control group (Δ = 14 mm Hg). The MAP change for the glucagon group (Δ = 19 mm Hg) was not significantly different from that of either the control or the glucagon/phenylephrine group. The change in glucagon HR (Δ = 6 beats/min) was significant compared with the control group (Δ = –4 beats/min) and the glucagon/phenylephrine group (Δ = –4 beats/min). Conclusion: The glucagon/phenylephrine therapy improved MAP compared with the control, but reduced CO and HR compared with glucagon alone. Glucagon/phenylephrine therapy is not as effective as glucagon alone in reversing the hemodynamic effects of experimental verapamil overdose.     

Plasma acetate levels during hemodialysis

Before dialysis, acetate levels in hemodialyzed patients (0.27--1.1 mmol/1) were more dispersed than in normal subjects (0.20--0.65 mmol/l) and the mean value of plasma acetate was slightly higher (0.52 mmol/l versus 0.31 mmol/l). Though dialysis conditions were almost identical, the acetate kinetics during hemodialysis were very different: in most subjects, plasma acetate concentrations reached a "plateau" (mean value 5.6 mmol/l) whereas in others a continuous rise was observed, suggesting that with patients having chronic renal failure there were important individual or occasional differences in the ability to metabolize acetate. The acetate loads per minute (or mass transfers) were calculated from the blood compartment with plasma values (plasma flow and concentrations), rather than from the dialysate and using the combined calculations (plasma and whole blood values). The results ranged between 2.4 and 4.1 mmol/min. A very important and rapid fall in arterial acetate concentrations occurs in the first 20 min after the end of the dialysis and proves the rapid turnover of the acetate in man.     

Excessive ATP degradation during hemodialysis against sodium acetate

As the initial step in examining the metabolic basis for acetate intolerance, we have tested the hypothesis that excessive adenosine triphosphate (ATP) degradation occurs during hemodialysis against acetate dialysate (compared with the degree of degradation occurring during dialysis against bicarbonate dialysate). Seven patients undergoing long-term dialysis were infused with carbon 14--labeled 8-adenine, and their response to dialysis against acetate was compared with their response to dialysis against bicarbonate. The following changes were observed. During dialysis against acetate, the mean dialysate uric acid--to-creatinine ratio levels were significantly higher than the mean levels observed after dialysis against bicarbonate (p less than 0.001). The mean dialysate uric acid radioactivity--to-creatinine ratio and inosine, hypoxanthine, and xanthine radioactivity--to-creatinine ratio levels were significantly increased during dialysis against acetate (p less than 0.001). There was no significant change in plasma venous hypoxanthine level, but during dialysis against acetate, the arterial hypoxanthine levels (3.7 +/- 1.6 mumol/L) at 60 minutes were significantly higher than the levels observed after dialysis against bicarbonate (1.4 +/- 0.5 mumol/L) (p less than 0.01). These data provide evidence that excessive ATP degradation occurs during hemodialysis against acetate but not during hemodialysis against bicarbonate dialysate.     

BioZ.com监测腰-硬联合麻醉下剖宫产产妇的血流动力学变化

目的：应用无创血流动力学监测仪BioZ.com,探讨腰-硬联合麻醉下剖宫产围术期产妇血流动力学变化.方法：19例择期在腰-硬联合麻醉下行剖宫产的产妇,ASA Ⅰ～Ⅱ级,连接BioZ.com连续监测血流动力学变化,分别在麻醉前,麻醉后5、15 min,胎儿娩出前1 min,胎儿娩出后3 min,术毕时记录心率（HR）、每搏输出量（SV）、平均动脉压（MAP）、心排量（CO）、心脏指数（CI）、体循环阻力（SVR）、胸腔液体量（TFC）、左室射血时间（LVET）.结果：围术期各时点HR、TFC、LEVT无明显变化（P＞0.05）;麻醉后15 min SVR开始下降,术毕时仍显著低于麻醉前（P＜0.01）,SV、CO、CI在麻醉后15 min开始升高（P＜0.05）;MAP除在术毕时显著低于术前（P＜0.01）外,其他时间点的差异无统计学意义.胎儿娩出前后相比,胎儿娩出后产妇的 HR、MAP基本维持稳定,而SV、CO、CI明显升高,SVR则明显下降（P＜0.05）;SV、CO、CI与SVR呈负相关（P＜0.01）,MAP 与SVR呈正相关（P＜0.01）.结论：应用BioZ.com监测剖宫产围术期产妇的血流动力学变化,可为围术期的处理提供更多可靠的依据.     

Role of neurosympathetic pathways in the vascular response to sepsis

The aim of this study was to determine the role of sympathetic neural activity in the hemodynamic adaptations to sepsis in pigs with an emphasis on circuit adaptations. A fall in resistance to venous return (RVR) was predicted in contrast to what was previously observed in sympathetically intact animals that had no change in RVR.

We anesthetized and ventilated 13 pigs and gave 5 mg/kg of indomethacin. We measured cardiac output (CO) by thermodilution and measured pulmonary arterial (PAP), pulmonary capillary wedge (Pcw), right atria) pressure (Pra), and arterial pressure (MAP). Intermittent inflation of a 50-mL balloon in the right atrium was used to transiently arrest the circulation for the measurement of mean circulatory filling pressure (MCFP). RVR was calculated from (MCFP — Pra)/CO. Animals were divided into two groups; 6 received 10 mg/kg of the ganglionic blocker, hexamethonium and norepinephrine to maintain MAP; 7 had their spinal cords cut at C-2. After baseline measurements, all animals received 10 μg/kg/h of endotoxin for 2 hours, and hemodynamic measurements were repeated. Plasma samples were obtained for measurements of immunoreactive endothelin-1 (ET-1), which was assayed by a radioimmunoassay.

Hexamethonium had no significant effect on hemodynamics except for an increase in heart rate. After endotoxin, MAP and SVR fell, PAP rose, and CO and RVR did not change. Spinal section resulted in an increase in heart rate and small increase in PAP and MCFP After endotoxin, there was a further increase in heart rate, PAP, and MCFP with a marked fall in MAP and CO. RVR increased from 2.1 ± 0.46 after spinal section to 3.6 ± 54 mm · min/L (P < .05). ET -1 in the hexamethonium group (n = 2) rose from 2.21 ± .14 to 11.5 ± 2.1 pg/ml at 2 hours, and in the spinal group (n = 7) from 2.04 ± 0.77 to 6.85 ± 3.9 pg/mL at 45 minutes.

Spinal section resulted in a more profound fall in blood pressure and less increase in MCFP than in previously studied animals with sympathetic nervous system intact, but there was still an increase in RVR and PAP ET-1 is a possible mediator of the increase in RVR and PAP.     

Comparison of effects of dextran-70 and Ringer's acetate on pulmonary function, hemodynamics, and survival in experimental septic shock

The effects of dextran-70 with NaCl vs. Ringer's acetate on hemodynamics, gas exchange, oxygen transport, and survival were evaluated in a porcine model of pulmonary and circulatory insufficiency induced by a continuous iv endotoxin infusion over 6 h. Dextran and Ringer's acetate were infused continuously to maintain baseline mean left atrial pressure (LAP) throughout the endotoxin period. Twelve pigs receiving endotoxin + Ringer's acetate displayed a progressive 45% decline in cardiac output (Qt) and a two-peaked increase in pulmonary vascular resistance (PVR) with a late increase of 250%. Venous admixture (Qva/Qt) increased progressively more than six-fold and extravascular lung water (EVLW) increased by 55%. Mean arterial BP (MAP) fell by 25%, oxygen delivery by 40%, base excess (BE) ranged between -4.5 and -9 mmol/L at the end of the endotoxin period and four of 12 animals died. Polymorphonuclear cell count (PMN) fell rapidly by 90% and was decreased severely throughout the endotoxin period. By contrast, the 12 pigs that received endotoxin + dextran maintained Qt near baseline and PVR was significantly lower in this group. Qva/Qt increased progressively more than four-fold, but it was significantly lower than in the Ringer's acetate group as was the increase in EVLW (23%). MAP only decreased by 10%, oxygen delivery only decreased by 20%. BE ranged between -1.0 and -3.0 mmol/L at the end of the endotoxin period and all animals survived. PMN fell by 90% at 0.5 h but subsequently tended to return toward baseline, and PMN were significantly increased compared with the Ringer's acetate group.(ABSTRACT TRUNCATED AT 250 WORDS)     

多巴酚丁胺联用去甲肾上腺素和多巴胺对感染性休克绵羊内脏器官灌注的影响

目的 :观察多巴酚丁胺联用去甲肾上腺素和多巴胺对感染性休克绵羊内脏灌注的影响。方法 :静脉注射内毒素 (L PS)复制绵羊感染性休克模型 ,当收缩压下降至低于 90 .0 0 m m Hg(1m m Hg=0 .133k Pa)或较L PS注射前降低 39.75 m m Hg时记录血流动力学及肠黏膜 p H(p Hi)的基础值。 2 0只绵羊随机分为两组 ,分别静脉注射多巴酚丁胺加去甲肾上腺素和多巴胺 ,调整药物剂量 ,使平均动脉压升高到 90 .0 0 mm Hg,观察药物使用前 (基础值 )及用药后 1、2、3、4 h的血流动力学和内脏灌注指标 p Hi。结果 :在 L PS注射前和基础状态 ,多巴胺组与多巴酚丁胺 +去甲肾上腺素组的血流动力学、氧代谢和肠道 p Hi指标均无明显差异 ;与基础值相比 ,两组动物在用药后血压、心脏指数及氧输送明显升高。多巴胺组用药 4 h动脉乳酸浓度及 p Hi水平与基础值比较无明显改变 ;但动脉 p H值基础水平为 7.4 0± 0 .0 5 ,多巴胺应用 1h后显著降低至 7.2 6± 0 .0 6 (P<0 .0 5 )。应用多巴酚丁胺加去甲肾上腺素后 3和 4 h,动脉乳酸浓度分别为 (2 .3± 1.1) m mol/ L 和 (2 .1± 1.1) m mol/ L,均显著低于基础水平 (4 .0± 1.8) m mol/ L(P<0 .0 5 )。应用多巴酚丁胺加去甲肾上腺素前动物 p Hi为 7.19±0 .0 4 ,用药后 3h,p Hi明显升高到     

Use of Vasopressin in a Canine Model of Severe Verapamil Poisoning: A Preliminary Descriptive Study

OBJECTIVES: The purpose of this preliminary study was to evaluate the effect of arginine vasopressin (AVP) administration in a model of shock induced by calcium channel antagonist overdose and to determine endogenous serum AVP concentrations in calcium channel antagonist-induced shock. METHODS: This was a controlled, randomized laboratory investigation based on a previously described canine model of verapamil toxicity. After induction of verapamil toxicity, animals in both the control and the experimental groups (n = 6 each) received a continuous infusion of verapamil. Experimental animals received an escalating dose of AVP, while control animals received an equal volume of 0.9% saline infusion. The hemodynamic end point was return of mean arterial pressure (MAP) to within 20% of baseline. Surviving animals were killed after 60 minutes. RESULTS: In the treatment group, administration of low-dose AVP (4 mU/kg/min) resulted in further declines in cardiac index and heart rate. No significant change was noted in MAP with low-dose AVP. A slight increase in MAP was noted with both escalating doses of AVP and equivalent volumes of normal saline. By the end of the 60-minute antidote/saline phase, the MAPs of the saline control group and the AVP experimental group were similar. The primary hemodynamic end point was not achieved in either the AVP or the saline control arm. Mean baseline serum AVP concentration in control animals was 5.8 pg/mL, increasing to 225 pg/mL during the toxicity phase. CONCLUSIONS: In an animal model of verapamil-induced shock, endogenous AVP levels increased nearly 40-fold compared with baseline levels. Escalating doses of exogenous AVP worsened cardiac index and failed to return MAP to within 20% of baseline.     

Plasma acetate concentrations during canine haemorrhagic shock.

Acetate, pyruvate, lactate and NEFA concentrations, as well as acid-base-parameters were followed during bleeding, stable hypotension and re-infusion in five dogs. Mean arterial blood pressures were kept at 30 mmHg during the shock phase. An increase in acetate concentrations (P less than 0.01) was found in arterial as well as in venous plasma samples. The maximal mean acetate concentration was 0.19 mmol/l (during reinfusion) as compared to 0.06 mmol/l prior to bleeding. There was no difference between arterial and inferior caval venous concentrations. A definite correlation (r = 0.81, P less than 0.02) was found between blood pyruvate and plasma acetate concentrations. There was no correlation between plasma glucose or NEFA and acetate concentrations or between blood excess lactate and plasma acetate. The plasma acetate accumulation was negligible compared to the concomitant lactate accumulation (1:60), and did not contribute to the metabolic acidosis of shock. The correlation between acetate and pyruvate concentrations may indicate that pyruvate is the main substrate of acetate production in hypovolemic shock.     

Effect of methylprednisolone on naloxone's hemodynamic response in canine hypovolemic shock

Previous studies have suggested that methylprednisolone (MP) pretreatment attenuates the usual hemodynamic response to naloxone (NAL) treatment of hypovolemic shock. In this study, both drugs were given concurrently during shock to evaluate hemodynamic changes, plasma endorphin-like activity (PELA), and survival. Twenty-six dogs were bled to a mean arterial pressure (MAP) of 40 to 45 mm Hg, which was maintained for 45 min. Animals were then treated with iv 0.9% NaCl (NS), 5 ml; NAL, 4 mg/kg; MP, 30 mg/kg; or NAL, 4 mg/kg, plus MP, 30 mg/kg. Animals treated with NAL and/or MP had significantly (p less than .05) improved MAP, cardiac output, and myocardial contractility compared with NS-treated animals. NAL and MP each significantly lowered PELA levels and both NAL and NAL plus MP significantly improved survival.     

The effect of acetate and bicarbonate hemodialysis on protein and lipid metabolism in patients with chronic kidney failure

In 26 patients with chronic renal failure undergoing hemodialysis, use was made of an acetate solution (40 mmol/l) and in 7 patients, of a bicarbonate solution (35 mmol/l). The control group was made up of 20 healthy volunteers. In addition to better tolerance, the bicarbonate dialysis favoured adequate correction of acid-base balance, normalization of hypercholesterolemia, lowering of the rate of protein degradation. Among patients on the acetate dialysis, subgroups with normal (9 persons) and delayed (17 persons) acetate utilization were distinguished. A close relationship was discovered between blood acetate concentration before procedure and the rate of urea generation (r = +0.79, p less than 0.05). It is assumed that the acetate dialysis intolerance is determined by protein hypercatabolism under the conditions of delayed utilization of acetate by the peripheral tissues.     

Hemodynamic status susceptible to slowing of heart rate during thermodilution cardiac output determination in anesthetized patients

To identify hemodynamic variables that might indicate susceptibility to slowing of heart rate (HR) and to mean arterial pressure (MAP) decrease caused by cold injectate during thermodilution (TD) cardiac output determination, we measured hemodynamic variables in 32 anesthetized patients undergoing major surgery. A total of 608 cardiac output determinations were evaluated for any relationship between the magnitude of HR decreases and basal hemodynamic variables. The magnitude of HR decrease was pronounced in low cardiac index (CI), low mean pulmonary artery pressure (MPAP), and high systemic vascular resistance index (SVRI). Although there was some decrease in MAP associated with cold injectate, neither changes in SVRI nor those in the other hemodynamic variables correlated with the decreases in MAP. These results suggest that decreased CI and MPAP associated with elevated SVRI may be more susceptible to slowing of HR during cardiac output determination by TD in anesthetized patients.     

Immediate hemodynamic effects of high-dose furosemide in normovolemic and hypovolemic dogs

We investigated whether the large dose (7 mg/kg) of iv furosemide often recommended for patients with oliguric acute renal failure impaired hemodynamic function in dogs. Six normovolemic and six hypovolemic animals were anesthetized, intubated, and ventilated. Femoral and pulmonary artery catheters were inserted. After a stable baseline period, the animals received 7 mg/kg of iv furosemide over 30 sec. Mean systemic artery pressure (MAP), mean pulmonary artery pressure (MPAP), CVP, and ECG were continuously monitored. Cardiac output and mean pulmonary arterial occlusion (wedge) pressures (WP) were recorded 2, 6, 12, 18, 24, 30, and 46 min after injection. Neither group demonstrated significant immediate changes in MAP, CVP, MPAP, heart rate (HR), cardiac output, or systemic and pulmonary vascular resistances (SVR and PVR, respectively). Later in the observation period, cardiac output decreased and SVR and PVR increased significantly. The changes were probably associated with decreased plasma volume causing compensatory increases in baroreceptor activity and vascular tone.     

Hemodynamic effects of pentobarbital therapy for intracranial hypertension

Barbiturate therapy has been employed for reduction of increased intracranial pressure (ICP) after acute brain injury and also for cerebral resuscitation. However, this treatment may be complicated by hypotension with an adverse impact on survival. We, therefore, investigated the acute hemodynamic effects of pentobarbital (PB) when administered in loading doses of 4-7 mg/kg and maintenance doses of 1-4 mg/kg. After pentobarbital therapy, HR, mean arterial pressure (MAP), and rectal temperature were significantly reduced. Four episodes of hypotension and 6 episodes of oliguria were observed during the initial 12 h of therapy in close relationship to reduced cardiac output, stroke volume, and MAP. These abnormalities were corrected by infusion of colloid-containing fluids. We postulate that increases in venous capacitance, hypovolemia, and decreased barostatic reflexes, rather than depression of myocardial function, accounted for the hemodynamic abnormalities.