Maintain Mean Arterial Blood Pressure Research Articles

Urinary effects of xylazine and general anesthesia in horses

The purpose of this study was to characterize urine flow and biochemical parameters in horses given xylazine (XYL) and anesthetized with ketamine and isoflurane. Nine mares [9 ± 2 (mean ± SE) years; 492 ± 17 kg] were studied. They were anesthetized for 2 hours in support of a campus-approved, laboratory-based orthopedic study. The day prior to anesthesia, a venous blood sample was obtained for biochemical analysis from each unmedicated mare. The urinary bladder was catheterized and emptied, and urine collected over the next three hours to quantitate the pre-drug values. The next day the mares were similarly catheterized. After obtaining urine and venous blood samples, XYL (1.1 mg kg−1 IV) was administered. Anesthesia was induced 5 minutes later with ketamine (2.2 mg kg−1 IV) and diazepam (0.04 mg kg−1 IV) and maintained with isoflurane in O2. Lactated Ringer's solution (10 mL kg−1 hours−1) was administered IV and dobutamine infused as required to maintain mean arterial blood pressure between 70 and 80 mm Hg. Mechanical ventilation maintained PaCO2 between 48 and 52 mm Hg and PaO2 > 200 mm Hg. Blood and urine were collected at 30, 60, and 120 minutes during anesthesia, and at 1 hour postanesthesia. Data were analyzed with RM anova; with p < 0.05. Control urine flow was 0.92 ± 0.17 mL kg−1 hour−1. Urine flow was significantly increased at 30 and 60 minutes following XYL (2.14 ± 0.59 and 2.86 ± 0.97 mL kg−1 hour−1, respectively), but returned to control levels by the end of anesthesia. The most notable biochemical change was an initial significant increase in serum glucose from 121 ± 4 to 167 ± 8 mg dL−1 at 30 minutes post-XYL that was not accompanied by a significant glucosuria (control value 4 ± 1 mg dL−1). We conclude that urine output increases in anesthetized horses following XYL, but this increase is not as a result of glucosuria.

Splanchnic perfusion during controlled hypotension combined with acute hypervolemic hemodilution: a comparison with combination of acute normovolemic hemodilution—gastric intramucosal ph study

Study Objective: To evaluate the effect of controlled hypotension combined with acute hypervolemic or normovolemic hemodilution on the splanchnic perfusion in the clinical setting. Design: Randomized, prospective study. Setting: Inpatient surgery at Nagasaki Rosai Hospital. Patients: 28 ASA physical status I and II patients scheduled for total hip arthroplasty. Interventions: Patients were randomly divided into two groups. Group A (n = 14) received controlled hypotension with acute normovolemic hemodilution (ANH). Group B (n = 14) received controlled hypotension with acute hypervolemic hemodilution (HHD). ANH was produced by drawing approximately 1000 mL of blood and replacing it with the same amount of 6% hydroxyethyl starch solution (HES). HHD was produced by preoperative infusion of 1000 mL of 6% HES without removing blood. The final hematocrit values were 24 ± 2% (mean ± SD) in Group A and 25 ± 3% in Group B. Controlled hypotension was induced with prostaglandin E1 (PGE1) to maintain mean arterial blood pressure at 55 mmHg for 80 minutes. Measurements: Measurements included the gastric pH (pHi), the arterial blood pH (pHa), and plasma lactate. These indices were measured before hemodilution, after hemodilution, 80 minutes after starting hypotension, 60 minutes after recovery from hypotension, and on the first postoperative day. The value of pHi was measured by tonometric method. Main Results: The pHa and lactate values showed no change in either group A or group B throughout the time course. Gastric pHi values in group A showed a significant decrease from 7.424 ± 0.033 to 7.335 ± 0.038 (p < 0.05) after hemodilution, whereas it showed no further decrease at 80 minutes after starting hypotension and 60 minutes after recovery from hypotension. The pHi values in group B showed no significant decrease after hemodilution and no further change at 80 minutes after starting hypotension. Conclusions: HHD does not impair splanchnic perfusion, whereas ANH might cause impairment. Controlled hypotension with prostaglandin E1 would not impair splanchnic perfusion in combination with either HHD or ANH.

Starch-deferoxamine conjugate inhibits hepatocyte Ca2+ uptake during hemorrhagic shock and resuscitation.

This study investigated whether hepatocyte Ca2+ dysregulation after hemorrhagic shock and resuscitation could be modulated by the iron chelator hydroxyethyl starch-conjugated deferoxamine (HES-DFO). In a randomized experimental study, anesthetized rats (n = 7) were bled for 60 minutes to maintain mean arterial blood pressure at 40 mm Hg. They were then resuscitated with 60% of shed blood and threefold the shed-blood volume as lactated Ringer's solution, 1 mL of pentastarch solution (hydroxyethyl starch 10%) per mL of shed blood, or 1 mL of HES-DFO solution (10%) per mL of shed blood. In isolated hepatocytes, the rate of Ca2+ influx (Ca2+ in), total Ca2+ uptake (Ca2+ up), and membrane Ca2+ flux (Ca2+ flux) were determined by 45Ca incubation. Reduced or oxidized glutathione and malondialdehyde concentrations were assessed fluorometrically. Significant increases of hepatocellular Ca2+ in, Ca2+ up, and Ca2+ flux were observed in rats resuscitated with lactated Ringer's solution compared with control groups (p < 0.05). Although hydroxyethyl starch decreased Ca2+ in but not Ca2+ up, HES-DFO not only prevented the increase of Ca2+ in and Ca2+ up but also inhibited hepatocyte oxidative injury. Iron-catalyzed oxyradical production and membrane peroxidation seem to alter hepatocyte Ca2+ homeostasis after hemorrhagic shock and resuscitation.

Sevoflurane anaesthesia in clinical equine cases: maintenance and recovery

A new inhalant anaesthetic, sevoflurane, was used to maintain anaesthesia in 40 animals (2 mules and 38 horses of 9 breeds) presented for various surgical procedures. Eighteen mares, 11 stallions and 11 geldings underwent 6 orthopaedic and 34 soft tissue operations. Induction of anaesthesia was achieved with combinations of xylazine (0.5–1.1 mg/kg), diazepam (0.03–0.1 mg/kg), butorphanol (0.02 mg/kg), guaifenesin (50–84 mg/kg) and ketamine (1.1 mg/kg). Following tracheal intubation, a surgical plane of anaesthesia was maintained with sevoflurane in oxygen delivered from a precision vaporiser. Temperature, ECG, arterial blood pressure and expired gas composition were monitored. Mechanical ventilation was used in most animals (n=37) because of hypoventilation (P a CO 2 > 7.31 kPa [55 mmHg]). Following surgery, horses were moved to a recovery room and allowed to recover alone (n=36) or with assistance (n=4). Time to sternal recumbency, standing, the time when satisfactory coordination was present (after standing) and the number of attempts to stand were recorded. The quality of recovery was scored on a 1 (best) to 6 (worst) scale. Mean blood pressures at 30, 60, 90, 120 and 150 min of anaesthesia were 72, 73, 74, 75 and 72 mmHg, respectively. Systolic and diastolic pressures at 30, 60, 90, 120 and 150 min of anaesthesia were 97, 97, 94, 96, 93 and 59, 63, 64, 68, 67 mmHg, respectively. Dobutamine was used in 23 horses to maintain mean arterial blood pressure > 60 mmHg. Mean heart and respiratory rates at 30, 60, 90, 120 and 150 min of anaesthesia were 36, 38, 39, 38 and 38 beats/min, and 9, 8, 8, 8 and 8 breaths/min. Mean duration of anaesthesia was 121 rnin (sd: 56 min), mean time to sternal recumbency was 27 min (sd: 13 min), average time to standing (all horses) was 33 min (sd: 12 min) and time to satisfactory coordination was 44 min (sd: 13 min). Most horses (n=37) received xylazine during recovery (mean dose 0.18 mg/kg iv). The median number of attempts to sternal recumbency and standing were 1.0 (range; 1–7) and 2.0 (range; 1–20), respectively, while the median recovery score was 1.5 (range; 14). The ‘depth’ of anaesthesia was easy to control and recoveries were generally very satisfactory.

The Influence of Different Intravascular Volume Replacement Regimens on Renal Function in the Elderly

Elderly patients are at risk of developing renal dysfunction. Synthetic colloids are often used perioperatively, but they may have detrimental effects on renal function. In a prospective, randomized study, we assessed the influence of different intravascular volume replacement regimens on renal function in elderly (>65 yr) and younger (< 65 yr) patients without preoperative renal dysfunction who were undergoing major abdominal surgery. Either 6% low molecular weight hydroxyethyl starch (HES) solution (mean molecular weight 70,000 D, degree of substitution 0.5; HES 70/0.5) [each group n = 10]), 6% medium-molecular weight HES (molecular weight 200,000 D, degree of substitution 0.5 (HES 200/0.5) [each group n = 10]), or modified gelatin (molecular weight 35,000 D [each group n = 10]) was administered to maintain mean arterial blood pressure >65 mm Hg and central venous pressure between 10 and 14 mm Hg. After the induction of anesthesia (T0); at the end of surgery (T1); 4 h after surgery (T2); and on the first (T3), second (T4), and third postoperative days (T5), alpha1-microglobulin (alpha1-M), N-acetyl-beta-glucosaminidase, fractional sodium clearance, and creatinine clearance (CC) were measured. Colloids (1300-3000 mL) were infused until the first postoperative day. At T0, urine concentrations of alpha1-M were higher in the elderly than in the younger patients in all groups (P < 0.05). alpha1-M remained increased only in the gelatin group. N-acetyl-beta-glucosaminidase and fractional sodium clearance were not affected during the study period in any groups. At baseline, CC was significantly higher in the younger than in the elderly patients, but CC did not decrease in any of the intravascular volume replacement groups. We conclude that intravascular volume therapy with gelatin and two different HES preparations did not adversely affect renal function in elderly patients without preoperative renal malfunction. We studied the influence of three different intravascular volume replacement regimens on renal function in elderly patients without renal dysfunction who were undergoing major abdominal surgery. Two hydroxyethyl starch and one gelatin preparation were administered perioperatively to maintain stable hemodynamics. As assessed by sensitive markers of renal function, all three regimens can be used safely for volume replacement without risking significant renal dysfunction.

The Influence of Different Intravascular Volume Replacement Regimens on Renal Function in the Elderly

Although hemoglobin-based oxygen carriers (HBOC) are now being investigated, the effects of HBOC solutions during regional anesthesia have never been analyzed. Therefore, we investigated the hemodynamic changes after HBOC infusion during general anesthesia and thoracic epidural anesthesia. Sheep were assigned to three different groups: a) a control group with six unanesthetized sheep; b) six sheep with a halothane anesthesia (2.0 vol.% in oxygen); and c) six awake sheep with a thoracic epidural anesthesia with bupivacaine. After a period of stabilization, all 18 animals received 100 mg/kg of the HBOC pyridoxalated hemoglobin polyoxyethylene conjugate. The infusion of the HBOC caused a significant increase in mean arterial pressure and pulmonary artery pressure in both the control and epidural anesthesia groups. Anesthesia with halothane reduced the effects of the HBOC-solution on mean arterial pressure but did not abolish the increase in pulmonary artery pressure. Our results demonstrate that vasoconstriction caused by HBOC solutions is not abolished by epidural anesthesia, but halothane anesthesia may alter the hemodynamic effects of HBOC solutions. We evaluated the effects of epidural anesthesia and halothane anesthesia on the vasoconstrictive properties of a cell-free hemoglobin solution. The vasoconstriction caused by a cell-free hemoglobin solution was similar in unanesthetized sheep and sheep with thoracic epidural anesthesia and was reduced in sheep with halothane anesthesia.

Differential effects from parapyramidal region and rostral ventrolateral medulla mediated by substance P.

Rostral ventrolateral medulla (rVLM) and parapyramidal region (PPr) serve as important medullary control sites for sympathoexcitation. rVLM and PPr have direct projections to the intermediolateral cell column (IML) that are thought to be important in maintaining mean arterial blood pressure (MAP). Substance P (SP) is found in PPr neurons and in and near the subretrofacial area of the rVLM. At least some of these cells project to the IML. We investigated the involvement of SP at the IML in mediating rVLM- and PPr-evoked pressor responses in the chloralose-anesthetized cat. Pressor responses to electrical and chemical PPr and rVLM stimulation were altered after intrathecal injection, at the level of the T1-T3 spinal cord, of either SP antagonist [D-Pro(2), D-Phe(7), D-Trp(9)]-SP, SP antagonist CP 96,345, or SP antiserum. Although MAP and heart rate responses to PPr stimulation were attenuated by intrathecal SP antagonists or antiserum, MAP responses to rVLM stimulation were augmented. Previous studies have revealed differences in transmitters associated with these two areas, even though the general response of both areas is sympathoexcitatory. The present study implies that the identical substance may increase or decrease the MAP response depending on the pathway activated.

Treatments to Support Blood Pressure Increases Bleeding and/or Decreases Survival in a Rat Model of Closed Head Trauma Combined with Uncontrolled Hemorrhage

Hemorrhagic hypotension may aggravate the detrimental effects of head trauma on neurologic outcome. Our study examined whether using phenylephrine or large volumes of saline IV to increase mean arterial blood pressure (MAP) to 70, 80, or 90 mm Hg during the combination of head trauma and uncontrolled hemorrhage would improve neurologic outcome. Rats were assigned to one of 17 groups. In Groups 1–5, the variables were head trauma (yes/no), hemorrhage (yes/no), 0 or 3 mL saline per milliliter of blood lost, and no target MAP. In Groups 6–11, hemorrhage was or was not combined with head trauma, and large volumes of saline were given IV to achieve target MAPs of 70, 80, or 90 mm Hg. Groups 12–17 were similar to Groups 6–11 except that phenylephrine was used rather than saline to achieve target MAPs. Saline increased blood loss at 2 h to approximately 16 and 25 mL at a MAP of 80 and 90 mm Hg respectively, increased (worsened) the neurodeficit score but not cerebral edema at 24 h, and decreased survival rate at 2 and 24 h. Because phenylephrine was fatal for 62 of 63 rats, group mean values for blood loss, neurodeficit score, and brain tissue specific gravity could not be calculated. We conclude that supporting MAP with either phenylephrine or large volumes of saline worsened the neurodeficit score and/or survival and did not affect cerebral edema formation in our rat model of head trauma combined with hemorrhage. Implications The results of this study indicate that maintaining mean arterial blood pressure at 70, 80, or 90 mm Hg with either phenylephrine or large volumes of saline worsened the neurodeficit score and/or survival and did not affect cerebral edema formation in our rat model of head trauma combined with hemorrhage.

Treatments to support blood pressure increases bleeding and/or decreases survival in a rat model of closed head trauma combined with uncontrolled hemorrhage.

Hemorrhagic hypotension may aggravate the detrimental effects of head trauma on neurologic outcome. Our study examined whether using phenylephrine or large volumes of saline IV to increase mean arterial blood pressure (MAP) to 70, 80, or 90 mm Hg during the combination of head trauma and uncontrolled hemorrhage would improve neurologic outcome. Rats were assigned to one of 17 groups. In Groups 1-5, the variables were head trauma (yes/no), hemorrhage (yes/no), 0 or 3 mL saline per milliliter of blood lost, and no target MAP. In Groups 6-11, hemorrhage was or was not combined with head trauma, and large volumes of saline were given IV to achieve target MAPs of 70, 80, or 90 mm Hg. Groups 12-17 were similar to Groups 6-11 except that phenylephrine was used rather than saline to achieve target MAPs. Saline increased blood loss at 2 h to approximately 16 and 25 mL at a MAP of 80 and 90 mm Hg respectively, increased (worsened) the neurodeficit score but not cerebral edema at 24 h, and decreased survival rate at 2 and 24 h. Because phenylephrine was fatal for 62 of 63 rats, group mean values for blood loss, neurodeficit score, and brain tissue specific gravity could not be calculated. We conclude that supporting MAP with either phenylephrine or large volumes of saline worsened the neurodeficit score and/or survival and did not affect cerebral edema formation in our rat model of head trauma combined with hemorrhage. The results of this study indicate that maintaining mean arterial blood pressure at 70, 80, or 90 mm Hg with either phenylephrine or large volumes of saline worsened the neurodeficit score and/or survival and did not affect cerebral edema formation in our rat model of head trauma combined with hemorrhage.

Combined medical and surgical treatment after acute spinal cord injury: results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management

The optimal management of acute spinal cord injuries remains to be defined. The authors prospectively applied resuscitation principles of volume expansion and blood pressure maintenance to 77 patients who presented with acute neurological deficits as a result of spinal cord injuries occurring from C-1 through T-12 in an effort to maintain spinal cord blood flow and prevent secondary injury. According to the Intensive Care Unit protocol, all patients were managed by Swan-Ganz and arterial blood pressure catheters and were treated with immobilization and fracture reduction as indicated. Intravenous fluids, colloid, and vasopressors were administered as necessary to maintain mean arterial blood pressure above 85 mm Hg. Surgery was performed for decompression and stabilization, and fusion in selected cases. Sixty-four patients have been followed at least 12 months postinjury by means of detailed neurological assessments and functional ability evaluations. Sixty percent of patients with complete cervical spinal cord injuries improved at least one Frankel or American Spinal Injury Association (ASIA) grade at the last follow-up review. Thirty percent regained the ability to walk and 20% had return of bladder function 1 year postinjury. Thirty-three percent of the patients with complete thoracic spinal cord injuries improved at least one Frankel or ASIA grade. Approximately 10% of the patients regained the ability to walk and had return of bladder function. As of the 12-month follow-up review, 92% of patients demonstrated clinical improvement after sustaining incomplete cervical spinal cord injuries compared to their initial neurological status. Ninety-two percent regained the ability to walk and 88% regained bladder function. Eighty-eight percent of patients with incomplete thoracic spinal cord injuries demonstrated significant improvements in neurological function 1 year postinjury. Eighty-eight percent were able to walk and 63% had return of bladder function. The authors conclude that the enhanced neurological outcome that was observed in patients after spinal cord injury in this study was in addition to, and/or distinct from, any potential benefit provided by surgery. Early and aggressive medical management (volume resuscitation and blood pressure augmentation) of patients with acute spinal cord injuries optimizes the potential for neurological recovery after sustaining trauma.

Endocrine and metabolic responses to plasma volume expansion during halothane anesthesia in ponies.

The study was designed to contribute to identification of the stimulus to adrenocortical activity during halothane anaesthesia in equidae. Two groups of six ponies were premedicated with acepromazine before induction of anaesthesia with thiopentone and maintenance for 120 min with halothane in oxygen. In group H Haemaccel modified gelatine plasma replacer was infused (48+/-13 mL/kg) to maintain mean arterial blood pressure (MABP) close to preanaesthetic values. In group DH, blood pressure was maintained close to preanaesthetic levels with a lower dose of Haemaccel (10 mL/kg) combined with an infusion of dobutamine. Measurements were made before anaesthesia, at 20 min intervals during anaesthesia and 20 and 120 min after anaesthesia. MABP and blood gases, pulse and respiratory rates were measured, and blood was withdrawn for assay of cortisol, adrenocorticotrophic hormone (ACTH), glucose and lactate. Ponies in both groups became hyperoxic, hypercapnic and developed a respiratory acidosis; pulse rate increased in both groups but this was more marked in group H. Haematocrit decreased by 50% in H and by 20% in DH. Cortisol and ACTH did not change significantly during anaesthesia in either group and the area under the time curve (AUC(0-140)) was lower in the DH group. Plasma glucose and lactate remained stable. After the H treatment all ponies had a watery nasal discharge and one pony died from endotoxaemia. This investigation demonstrated that the adrenocortical response to halothane anaesthesia in ponies can be ameliorated by manipulation of ABP using plasma expansion with or without inotrope infusion; however, low dose Haemaccel with dobutamine was safer and more practical. It is suggested that, although hypotension is not the sole stimulus to adrenocortical activity during halothane anaesthesia, it may contribute, probably through an effect on tissue perfusion.

Effect of Controlled Hypotension Combined with Hemodilution on Gastric Intramural pH

Study Objective: To evaluate the effect of controlled hypotension combined with hemodilution on gastric intramural pH in the clinical setting. Design: Randomized, prospective study. Setting: Inpatient surgery at Nagasaki Rosai Hospital. Patients: 30 ASA physical status I and II patients scheduled for total hip arthroplasty. Interventions: Patients were randomly divided into two groups. Group A (n = 15) received controlled hypotension with mild hemodilution. Group B (n = 15) received controlled hypotension with moderate hemodilution. Hemodilution was carried out after induction of anesthesia. Drawn blood was replaced with 6% hydroxyethyl starch solution. Final hematocrit values were 32 ± 2% (mean ± SD) in Group A and 23 ± 2% in Group B. Controlled hypotension was induced with prostaglandin E 1 (PGE 1) to maintain mean arterial blood pressure at 55 mmHg for 80 minutes. Measurements and Main Results: Measurements included gastric intramural pH (pHi), arterial blood pH (pHa), and plasma lactate. These indices were measured before hemodilution, after hemodilution, 80 minutes after starting hypotension, 60 minutes after recovery from hypotension, and on the first postoperative day. The value of pHi was measured by tonometry. The pHa and lactate values showed no change in either Group A or Group B throughout the time course. Gastric pHi values showed no change in Group A throughout the time course. The pHi value in Group B showed a significant decrease from 7.420 ± 0.028 to 7.339 ± 0.034 (p < 0.05) after hemodilution, while it showed no further decrease at 80 minutes after starting hypotension (7.331 ± 0.039) and 60 minutes after recovery from hypotension (7.330 ± 0.048). Conclusion: The results suggest that moderate hemodilution, such as 23% of hematocrit value, might impair oxygenation in gastrointestinal mucosa, whereas controlled hypotension induced by PGE 1 combined with the hemodilution would not increase this impairment.

Effect of low-dose atropine administration on dobutamine dose requirement in horses anesthetized with detomidine and halothane

SUMMARY Objective To determine whether a low dose of atropine is associated with decreased requirement for cardiovascular supportive treatment in horses given detomidine prior to maintenance of general anesthesia with halothane. Animals 3 groups of 10 healthy horses. Procedure Detomidine (20 μg/kg of body weight, IM) was administered to all 30 horses. Then, 10 horses received atropine (0.006 mg/kg, IV) 1 hour after detomidine administration, 10 horses received atropine (0.012 mg/kg, IM) at the time of detomidine administration, and 10 horses served as a control group. Heart rate was measured prior to detomidine administration and at fixed intervals throughout anesthesia. The dobutamine infusion rate necessary to maintain mean arterial blood pressure between 70 and 80 mm of Hg was recorded. Systemic blood pressures, end-tidal halothane, end-tidal CO2, and arterial blood gas tensions were measured at fixed intervals. Results Mean heart rate was higher among horses receiving atropine IV or IM, compared with that in control horses. Horses that received atropine IV had higher systemic arterial blood pressure and required a lower dobutamine infusion rate than did horses of the other groups. Conclusion Detomidine-treated, halothane-anesthetized horses given atropine IV required less dobutamine, compared with horses receiving or not receiving atropine IM. Complications, such as colic and dysrhythmias, from use of higher doses of atropine, were not observed at this lower dose of atropine. Clinical Relevance IV administration of a low dose of atropine prior to induction of general anesthesia may result in improved blood pressure in horses that have received detomidine before anesthesia with halothane. (Am J Vet Res 1997;58:1436–1439)

Combined medical and surgical treatment after acute spinal cord injury: results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management.

The optimal management of acute spinal cord injuries remains to be defined. The authors prospectively applied resuscitation principles of volume expansion and blood pressure maintenance to 77 patients who presented with acute neurological deficits as a result of spinal cord injuries occurring from C-1 through T-12 in an effort to maintain spinal cord blood flow and prevent secondary injury. According to the Intensive Care Unit protocol, all patients were managed by using Swan-Ganz and arterial blood pressure catheters and were treated with immobilization and fracture reduction as indicated. Intravenous fluids, colloid, and vasopressors were administered as necessary to maintain mean arterial blood pressure above 85 mm Hg. Surgery was performed for decompression and stabilization, and fusion in selected cases. Sixty-four patients have been followed at least 12 months postinjury by means of detailed neurological assessments and functional ability evaluations. Sixty percent of patients with complete cervical spinal cord injuries improved at least one Frankel or American Spinal Injury Association (ASIA) grade at the last follow-up review. Thirty percent regained the ability to walk and 20% had return of bladder function 1 year postinjury. Thirty-three percent of the patients with complete thoracic spinal cord injuries improved at least one Frankel or ASIA grade. Approximately 10% of the patients regained the ability to walk and had return of bladder function. As of the 12-month follow-up review, 92% of patients demonstrated clinical improvement after sustaining incomplete cervical spinal cord injuries compared to their initial neurological status. Ninety-two percent regained the ability to walk and 88% regained bladder function. Eighty-eight percent of patients with incomplete thoracic spinal cord injuries demonstrated significant improvements in neurological function 1 year postinjury. Eighty-eight percent were able to walk and 63% had return of bladder function. The authors conclude that the enhanced neurological outcome that was observed in patients after spinal cord injury in this study was in addition to, and/or distinct from, any potential benefit provided by surgery. Early and aggressive medical management (volume resuscitation and blood pressure augmentation) of patients with acute spinal cord injuries optimizes the potential for neurological recovery after sustaining trauma.

Catecholamine and renin-angiotensin response during controlled hypotension induced by prostaglandin E 1 combined with hemodilution during isoflurane anesthesia

Study Objective: To evaluate the catecholamine and renin-angiotensin response during controlled hypotension combined with hemodilution in the clinical setting. Design: Randomized, prospective study. Setting: Inpatient surgery at Nagasaki Rosai Hospital. Patients: 30 ASA physical status I and II female patients scheduled for total hip arthroplasty. Interventions: Patients were randomly divided into three groups. Group A (N = 10) received hemodilution alone. Group B (N = 10) received controlled hypotension alone. Group C (N = 10) received hemodilution plus controlled hypotension. Hemodilution was carried out after induction of anesthesia, in which drawn blood was replaced with 6 % hydroxyethyl starch, and the final hematocrit value was approximately 22%. Controlled hypotension was induced with prostaglandin E 1 (PGE 1) to maintain mean arterial blood pressure at 55 mmHg for 80 minutes. Measurements and Main Results: Measurements included plasma renin activity (RA) and plasma concentrations of angiotensin-II (AG-II), aldosterone (AS), norepinephrine (NE), and epinephrine (EP). These indices were measured before hemodilution, after hemodilution, 80 minutes after starting hypotension, and 60 minutes after recovery from hypotension. Hemodilution alone caused no significant change in the values throughout the time course. Controlled hypotension alone caused significant increases in plasma concentrations of NE (+295%) and EP (+203%) at 80 minutes after starting hypotension, whereas it caused no change in plasma RA and plasma concentrations of AG-II and AS. Hemodilution plus controlled hypotension caused significant increases in plasma RA(+271%) and plasma concentrations of AG-II (+188%), AS (+199%), NE (+279%), and EP (+184%) at 80 minutes after starting hypotension. Conclusion: The combination of hemodilution and PGE 1 induced controlled hypotension causes significant responses, especially in a renin-angiotensin-aldosterone system under isoflurane anesthesia.

Effects of hemodilution during controlled hypotension on hepatic, renal, and pancreatic function in humans

Study Objective: To evaluate the effects of hemodilution during controlled hypotension on the hepatic, renal, and pancreatic function in the clinical setting. Design: Randomized, prospective study. Setting: Inpatient surgery at Rosai Hospital. Patients: 20 ASA status I and II patients scheduled for total hip arthroplasty. Interventions: Hemodilution was carried out after induction of anesthesia, in which drawn blood was replaced with dextran solution to achieve final hematocrit (Hct) of 31% (Group A = mild hemodilution group, N = 10) or 23% (Group B = moderate hemodilution group, N = 10). In both groups, controlled hypotension was induced with prostaglandin E 1 (PGE 1) to maintain mean arterial blood pressure at 55 mmHg for 80 minutes. Measurements and Main Results: Measurements included arterial ketone body ratio (AKBR, aceto-acetate/3-hydroxybutyrate) for hepatic cellular function, pancreatic phospholipase A 2 (P-PLA 2) for pancreatic cellular function, and urine N-acetyl-β- dglucosaminidase (NAG index) for cellular function of the renal tubule. These indices were measured before hemodilution, after hemodilution, 80 minutes after starting hypotension, 60 minutes after recovery of normotension, and on the first postoperative day. Neither AKBR norP-PLA2 showed a significant change throughout the time course of the study in either group. Urine-NAG index showed a significant increase in moderate hemodilution group at 60 minutes after recovery of normotension (+136%) and on the first postoperative day (+149%) compared with prehemodilution value, whereas it showed no significant change in the mild hemodilution group. Blood urea nitrogen and serum creatinine measured postoperatively were within normal range. Conclusions: PGE 1-induced hypotension combined with moderate hemodilution using dextran, such as 23 % of Hct value, maintains hepatic and pancreatic function but causes damage to the renal tubular cells.

Aerosolized prostacyclin and inhaled nitric oxide in septic shock — different effects on splanchnic oxygenation?

To compare the effects of inhaled nitric oxide and aerosolized prostacyclin (PGI2) on hemodynamics and gas exchange as well as on the indocyanine-green plasma disappearance rate and gastric intramucosal pH in patients with septic shock. Prospective, randomized, interventional clinical study. Intensive care unit in a university hospital. Sixteen patients with pulmonary hypertension and septic shock according to the criteria of the ACCP/SCCM consensus conference all requiring norepinephrine and/or epinephrine to maintain mean arterial blood pressure above 65 mmHg. Patients were randomly assigned to receive either nitric oxide or aerosolized prostacyclin. Nitric oxide was inhaled using a commercially available delivery system, prostacyclin was administered with a modified ultrasound nebulizer. Both nitric oxide and prostacyclin were incrementally adjusted to obtain a 15% decrease of mean pulmonary artery pressure. Hemodynamics and gas exchange as well as indocyanine-green plasma disappearance rate and gastric intramucosal pH were determined at baseline after 90 min in steady state, after 90 min of nitric oxide inhalation or prostacyclin aerosol administration had elapsed in stable conditions, and after 90 min in stable conditions after nitric oxide or prostacyclin withdrawal. Both inhaled nitric oxide and aerosolized prostacyclin selectively reduced the mean pulmonary artery pressure from 35 +/- 4, 30 +/- 4 mmHg (p < 0.05) and 34 +/- 4 to 30 +/- 3 mmHg (p < 0.05) respectively; after removal of nitric oxide and prostacyclin, the mean pulmonary artery pressure returned to the baseline values. Systemic hemodynamics remained unaltered during the vasodilator treatment. While the mean PaO2 was not significantly influenced, it increased in 4/8 of the NO- and 3/8 of the PGI2-treated patients. Neither of the drugs influenced indocyanine-green plasma disappearance rate, but prostacyclin--unlike nitric oxide--significantly increased gastric intramucosal pH (from 7.26 +/- 0.07 to 7.30 +/- 0.05, p < 0.05) which remained elevated in four of these patients after prostacyclin removal, and decreased the arterial-gastric mucosal pressure of carbon dioxide gap from 19 +/- 6 to 15 +/- 4 mmHg (p < 0.05). Our data suggest that aerosolized prostacyclin--unlike nitric oxide--has similar beneficial effects on splanchnic perfusion and oxygenation as intravenous prostacyclin without detrimental effects on systemic hemodynamics. The different effects of prostacyclin and nitric oxide might be explained by the longer half-life of prostacyclin associated with a certain spillover into the systemic circulation.

Progressive gastric intramucosal acidosis follows resuscitation from hemorrhagic shock.

The time course of gastric intramucosal pH (pHi) during the early phase of resuscitation of hemorrhagic shock has not been adequately characterized. We examined pHi using gastric tonometry catheters in an anesthetized dog model of hemorrhagic shock. Shock was induced in 10 animals to maintain mean arterial blood pressure (MAP) at 40-45 mmHg for 30 min, followed by transfusion of shed blood plus additional saline as needed to maintain MAP at pre-shock values. Five animals served as controls. Baseline pHi values were nearly identical in both groups. Resuscitation promptly restored MAP. Following a precipitous drop of pHi during shock, there was only partial recovery 60 min post-shock, followed by progressive worsening of intramucosal acidosis (7.02 +/- .10 vs. 6.82 +/- .24 at 60 and 210 min post-shock, respectively; p < .002). MAP, heart rate, and pHi did not change significantly during the experiment in the control group. These results indicate that prompt and adequate MAP response to resuscitation failed to prevent significant decreases of pHi in the first few hours post-resuscitation. This finding may be related to persistent splanchnic hypoperfusion or reperfusion injury.

Effects of ketamine on cerebral blood flow velocity in humans Influence of pretreatment with midazolam or esmolol

During normoventilation and 'light', haemodynamically stable, steady-state anaesthesia with isoflurane 0.3%, the effect of ketamine intravenously was investigated in 24 patients randomly assigned to one of the following groups: group 1 (control group) no ketamine, group 2 (ketamine group) ketamine 2 mg.kg-1, group 3 (ketamine/midazolam group) ketamine 2 mg.kg-1 after pretreatment with midazolam and group 4 (ketamine/esmolol group) ketamine 2 mg.kg-1 while maintaining mean arterial blood pressure at a preketamine level with esmolol. Ketamine-induced cerebrovascular changes were measured by means of transcranial Doppler ultrasonography. Control readings in patients without ketamine challenge demonstrated stable cardiovascular and cerebrovascular baseline conditions. Cerebral blood flow velocity and mean arterial blood pressure, however, significantly increased after administration of ketamine without pretreatment. The increase in cerebral blood flow velocity could not be blocked by maintaining mean arterial blood pressure at baseline value with esmolol. In contrast, the effects of ketamine on cerebral blood flow velocity and mean arterial blood pressure were prevented by prior administration of midazolam. The results suggest that ketamine may significantly influence intracerebral haemodynamics via a direct drug effect rather than via a secondary effect due to changes in arterial carbon dioxide and/or mean arterial blood pressure.

Effect of low-dose endotoxin on pulmonary vascular permeability following acute hemorrhagic shock.

The purpose of the current study was to determine the effect of low-dose Escherichia coli lipopolysaccharide (LPS) on pulmonary vascular permeability when administered after hemorrhagic shock (40% of baseline cardiac output) followed by resuscitation. Animals were monitored for 3-4 h after LPS infusion. Thirty minutes prior to termination of the experiment, 3 mCi of 125I-human serum albumin was injected intravenously to calculate a permeability index from the left lung lavage and plasma 125I ratios. The two control groups were (1) shock only (no LPS, n = 4), and (2) LPS only (no shock, n = 8). The permeability index for the shock-only group was 0.0015 +/- 0.0007 (mean +/- SE) and that for the LPS-only group was 0.0035 +/- 0.0014. The permeability index for the experimental group (shock followed by LPS, n = 10) was 0.0071 +/- 0.0030 (p > 0.05). Similarly, there was no difference in the wet-to-dry ratios between the three groups. The shock+LPS group required more intravenous fluids to maintain mean arterial blood pressure at control values than the LPS-only group (p < 0.003). We conclude that hemorrhagic shock and resuscitation do not lead to an acute increased permeability of the lung when it is subsequently challenged by a low dose of bacterial LPS.