Effects of adrenaline and vasopressin on cerebral microcirculation at baseline and during global brain ischemia and reperfusion in rabbits.

BACKGROUND: During cardiopulmonary resuscitation, the brain becomes ischemic. Adrenaline and vasopressin have been recommended for use during cardiopulmonary resuscitation. We aimed to investigate the direct effects of adrenaline and vasopressin on the cerebral microvasculature at baseline and during ischemia and reperfusion in rabbits. METHODS: The closed cranial window method was used to visualize the cerebral microcirculation and changes in the pial arteriole diameter in rabbits. Adrenaline and vasopressin were administered topically on the brain tissue. First, the effects of adrenaline and vasopressin on pial arterioles were evaluated in 7 rabbits that were given 4 different concentrations of adrenaline, and another 7 rabbits that received 4 different concentrations of vasopressin. Second, the effects of adrenaline and vasopressin were determined during the global brain ischemia and reperfusion, which was induced by clamping the brachiocephalic, left common carotid, and left subclavian arteries for 15 min. An additional 21 rabbits were randomly assigned to receive artificial cerebrospinal fluid (aCSF) (n = 7), adrenaline 10-5 mol/L (n = 7), or vasopressin 10-7 mol/L (n = 7). Each drug was continuously infused from 5 min after the initiation of ischemia until 120 min after reperfusion. The pial arteriole diameters were recorded before and during ischemia, and after reperfusion. RESULTS: At baseline, adrenaline and vasopressin did not affect the cerebral pial arterioles. During ischemia, vasopressin, but not aCSF and adrenaline constricted the pial vessels. Late in the reperfusion phase, pial diameter became reduced in the vasopressin and aCSF groups whereas pial diameter was higher in the animals treated with adrenaline. CONCLUSIONS: Adrenaline and vasopressin did not affect pial arterioles at baseline. During reperfusion, adrenaline may counteract the cerebral vasoconstriction.

Influence of pneumoperitoneum and head-down maneuver on the cerebral microvasculature in rabbits.

BACKGROUND: With recent advances in robot-assisted techniques, an increasing number of surgeries are being performed with pneumoperitoneum and head-down maneuver (HDM) that may affect the cerebral microcirculation. For the first time, this study investigated the direct influence of pneumoperitoneum and HDM on the cerebral microvasculature in rabbits. METHODS: Adult male rabbits were randomly allocated to the following groups (n = 7 each): control, pneumoperitoneum alone (P), and pneumoperitoneum with HDM (P + HDM) for 120 min. A closed cranial window was installed above the parietal bone to visualize the pial microvasculature. Pial arteriolar diameter and hemodynamic and blood gas parameters were measured during the 140-min observation period. Brain edema was assessed by evaluation of the brain water content at the end of the experiment. RESULTS: Rabbits in the P and P + HDM groups exhibited a similar degree of immediate pial arteriolar dilation following the initiation of both P and P + HDM (P: 1.11 ± 0.03, p = 0.0044 and P + HDM: 1.07 ± 0.02, p = 0.0004, relative changes from the baseline value by defining the baseline as one). In the P + HDM group, pial arteriole diameter returned to the baseline level following the discontinuation of pneumoperitoneum and HDM (1.05 ± 0.03, p = 0.0906, vs. baseline). In contrast, the pial arterioles remained dilated as compared to the baseline level in the P group after discontinuation of pneumoperitoneum. There were no changes in pial arteriole diameter in the animals in the control group. Heart rate, blood gas parameters, and brain water content were not significantly different between the groups. CONCLUSION: The pial arterioles dilated immediately after pneumoperitoneum with or without HDM. The pial arterioles remained dilated 20 min after discontinuation of pneumoperitoneum alone but constricted upon discontinuation of pneumoperitoneum plus HDM. Pneumoperitoneum and HDM for 2 h did not cause brain edema.

Effects of ß1-adrenergic receptor blockade on the cerebral microcirculation in the normal state and during global brain ischemia/reperfusion injury in rabbits.

BACKGROUND: Although recent studies using experimental models of ischemic brain injury indicate that systemically-administered ß1-blockers have potential protective effects on the cerebrovascular system, the precise mechanisms remain unclear. In addition to their cardiovascular effects, water-soluble ß1-blockers can pass the blood-brain barrier and may exert their vascular action on cerebral microvessels. The aim of this study was to investigate the direct effects of ß1-blockade on the cerebral microvasculature both in the normal state and ischemia/reperfusion state using the cranial window method. METHODS: The closed cranial window method was used to visualize the cerebral microcirculation and changes in the pial arteriole diameter in adult male rabbits. In the first experiment, various concentrations of the selective ß1-blocker landiolol were administered into the cranial window to evaluate the dose-response. In the second experiment, the effect of ß1-blockade on the brain during ischemic/reperfusion injury was investigated. Global brain ischemia/reperfusion was induced by clamping the brachiocephalic, left common carotid, and left subclavian arteries for 15 min. Either landiolol or artificial cerebrospinal fluid was infused 5 min after initiation of ischemia through 120 min after reperfusion. Pial arteriole diameter and hemodynamic and physiological parameters were recorded before ischemia, during ischemia, and 5, 10, 20, 40, 60, 80, 100, and 120 min after reperfusion. RESULTS: In the first experiment, topical administration of landiolol at higher concentrations produced slight pial arteriole dilation (10- 8 mol/L: 4.3 ± 3.4%, 10- 6 mol/L: 8.0 ± 5.8%, 10- 4 mol/L: 7.3 ± 4.0%). In the second experiment, the topical administration of landiolol significantly dilated the pial arteriole diameters during ischemia/reperfusion injury (ischemia: 30.6 ± 38.6%, 5 min: 47.3 ± 42.2%, 10 min: 47.8 ± 34.2%, 20 min: 38.0 ± 39.0%). There were no statistical differences in hemodynamic and physiological parameters between the landiolol and control groups. CONCLUSIONS: The blockade of ß1-adrenergic receptors induced significant vasodilation of pial arterioles during ischemia/reperfusion injury. By contrast, only a slight dilation of the arterioles was observed in the normal state, indicating that ischemic cerebral microvessels are more susceptible to the vasodilatory effect induced by selective blockade of ß1-adrenergic receptors than normal microvessels.

The effects of Y-27632 on pial microvessels during global brain ischemia and reperfusion in rabbits.

BACKGROUND: Global brain ischemia-reperfusion during propofol anesthesia provokes persistent cerebral pial constriction. Constriction is likely mediated by Rho-kinase. Cerebral vasoconstriction possibly exacerbates ischemic brain injury. Because Y-27632 is a potent Rho-kinase inhibitor, it should be necessary to evaluate its effects on cerebral pial vessels during ischemia-reperfusion period. We therefore tested the hypotheses that Y-27632 dilates cerebral pial arterioles after the ischemia-reperfusion injury, and evaluated the time-course of cerebral pial arteriolar status after the ischemia-reperfusion. METHODS: Japanese white rabbits were anesthetized with propofol, and a closed cranial window inserted over the left hemisphere. Global brain ischemia was produced by clamping the brachiocephalic, left common carotid, and left subclavian arteries for 15 min. Rabbits were assigned to cranial window perfusion with: (1) artificial cerebrospinal fluid (Control group, n = 7); (2) topical infusion of Y-27632 10-6 mol · L-1 for 30 min before the initiation of global brain ischemia (Pre group, n = 7); (3) topical infusion of Y-27632 10-6 mol · L-1 starting 30 min before ischemia and continuing throughout the study period (Continuous group, n = 7); and, (4) topical infusion of Y-27632 10-6 mol · L-1 starting 10 min after the ischemia and continuing until the end of the study (Post group, n = 7). Cerebral pial arterial and venule diameters were recorded 30 min before ischemia, just before arterial clamping, 10 min after clamping, and 5, 10, 20, 40, 60, 80, 100, and 120 min after unclamping. RESULTS: Mean arterial blood pressure and blood glucose concentration increased significantly after global brain ischemia except in the Continuous group. In the Pre and Continuous groups, topical application of Y-27632 produced dilation of large (mean 18-19%) and small (mean; 25-29%) pial arteries, without apparent effect on venules. Compared with the Control and Pre groups, arterioles were significantly dilated during the reperfusion period in the Continuous and Post groups (mean at 120 min: 5-8% in large arterioles and 11-12% in small arterioles). CONCLUSIONS: Y-27632 dilated cerebral pial arterioles during reperfusion. Y-27632 may enhance recovery from ischemia by preventing arteriolar vasoconstriction during reperfusion.

Effects of hyperventilation on cerebral oxygen saturation estimated using near-infrared spectroscopy: A randomised comparison between propofol and sevoflurane anaesthesia.

BACKGROUND: Near-infrared spectroscopy estimates cerebral regional tissue oxygen saturation (rSO2), which may decrease under hyperventilation. Propofol and sevoflurane act differently on cerebral blood vessels. Consequently, cerebral blood flow during hyperventilation with propofol and sevoflurane anaesthesia may differ. OBJECTIVES: The first aim of this study was to compare the changes in rSO2 between propofol and sevoflurane anaesthesia during hyperventilation. The second aim was to assess changes in rSO2 with ventilation changes. DESIGN: A randomised, open-label study. SETTING: University of Yamanashi Hospital, Yamanashi, Japan from January 2014 to September 2014. PARTICIPANTS: Fifty American Society of Anesthesiologists physical status 1 or 2 adult patients who were scheduled for elective abdominal surgery were assigned randomly to receive either propofol or sevoflurane anaesthesia. Exclusion criterion was a known history of cerebral disease such as cerebral infarction, cerebral haemorrhage, transient ischaemic attack and subarachnoid haemorrhage. INTERVENTIONS: After induction of anaesthesia but before the start of surgery, rSO2, arterial carbon dioxide partial pressure (PaCO2) and arterial oxygen saturation were measured. Measurements were repeated at 5-min intervals during 15 min of hyperventilation with a PaCO2 around 30 mmHg (4 kPa), and again after ventilation was normalised. MAIN OUTCOME MEASURES: The primary outcome was the difference of changes in rSO2 between propofol anaesthesia and sevoflurane anaesthesia during and after hyperventilation. The second outcome was change in rSO2 after the initiation of hyperventilation and after the normalisation of ventilation. RESULTS: Changes of rSO2 during hyperventilation were -10 ±â€Š7% (left) and -11 ±â€Š8% (right) in the propofol group, and -10 ±â€Š8% (left) and -9 ±â€Š7% (right) in the sevoflurane group. After normalisation of PaCO2, rSO2 returned to baseline values. Arterial oxygen saturation remained stable throughout the measurement period. The rSO2 values were similar in the propofol and the sevoflurane groups at each time point. CONCLUSION: The effects of hyperventilation on estimated rSO2 were similar with propofol and sevoflurane anaesthesia. Changes in rSO2 correlated well with ventilation changes. TRIAL REGISTRATION: Japan Primary Registries Network (JPRN); UMIN-CTR ID; UMIN000010640.

The effects of topical and intravenous JM-1232(-) on cerebral pial microvessels of rabbits.

BACKGROUND: JM-1232(-) is a novel anesthetic agent which acts through gamma-aminobutyric acid receptors. Cerebral pial vascular effects of JM-1232(-) are unknown. We thus evaluated topical and intravenous effects of JM-1232(-) on cerebral pial microvessels in rabbits, and the extent to which carbon dioxide (CO2) reactivity is preserved. METHODS: Closed cranial windows were used to visualize cerebral pial circulation in 29 Japanese white rabbits. In the first experiment, the cranial window was superfused with increasing concentrations of JM-1232(-): 10(-11), 10(-9), 10(-7), 10(-5) mol/L, n = 8 per concentration. In the second experiment, we examined the effects of an intravenous bolus of 1 mg/kg bolus of JM-1232(-), followed by the continuous infusion at 0.3 mg/kg/minute on cerebral pial vascular alteration (n = 9). In the third, we examined CO2 reactivity of cerebral pial vessels under JM-1232(-) (n = 6) or sevoflurane anesthesia (n = 6). RESULTS: Topical application of JM-1232(-) did not change pial venular diameter, and constricted arterials only at the highest concentration. Intravenous administration of JM-1232(-) produced cerebral pial constriction which gradually diminished over time. Under intravenous administration of JM-1232(-) and inhaled sevoflurane, diameters of vessels increased in parallel with CO2 partial pressure. Slopes of linear regression and correlation coefficients in arterioles and venules were comparable for JM-1232(-) anesthesia and sevoflurane anesthesia. CONCLUSIONS: Topical application of JM-1232(-) had little effect on cerebral pial vessels. Intravenous administration produced vasoconstriction of cerebral pial arterioles and venules, however those changes were clinically unimportant. In addition, JM-1232(-) did not impair CO2 responsiveness. At least from the perspective of vascular reactivity, JM-1232(-) thus appears safe for neurosurgical patients.

Optimal doses of sevoflurane and propofol in rabbits.

BACKGROUND: Although sevoflurane and propofol are commonly used anesthetics in rabbits, optimal doses of remain unclear. We thus assessed the optimal hypnotic doses of sevoflurane and propofol, and evaluated the influence of dexmedetomidine on sevoflurane and propofol requirements. METHODS: Twenty-eight Japanese white rabbits were randomly assigned to one of four groups (n=7 each). Rabbits were given either sevoflurane, propofol, sevoflurane+dexmedetomidine, or propofol+dexmedetomidine (injected 30 µg∙kg(-1)∙hr(-1) for 10 min followed by an infusion of 3.5 µg∙kg(-1)∙hr(-1)). Hypnotic level was evaluated with Bispectral Index (BIS), a well-validated electroenchalographic measure, with values between 40 and 60 representing optimal hypnosis. BIS measurements were made 10 minutes after the adjustment of target end-tidal sevoflurane concentration in the sevoflurane group and sevoflurane+dexmedetomidine group, and at 10 min after the change of infusion rate in the propofol group and propofol+dexmedetomidine group. RESULTS: BIS values were linearly related to sevoflurane concentration and propofol infusion rate, with or without dexmedetomidine. Sevoflurane concentration at BIS=50 was 3.9±0.2% in the sevoflurane group and 2.6±0.3% in the sevoflurane+dexmedetomidine group. The propofol infusion rate to make BIS=50 was 102±5 mg∙kg(-1)∙hr(-1) in the propofol group, and 90±10 mg∙kg(-1)∙hr(-1) in the propofol+dexmedetomidine group. CONCLUSIONS: The optimal end-tidal concentration of sevoflurane alone was thus 3.9%, and optimal infusion rate for propofol alone was 102 mg∙kg(-1)∙hr(-1). Dexmedetomidine reduced sevoflurane requirement by 33% and propofol requirement by 11%.

[Femoral nerve block for total knee arthroplasty].

BACKGROUND: Femoral nerve block and sciatic nerve block are used to provide intraoperative and postoperative analgesia for total knee arthroplasty. Sciatic nerve block is contraindicated in our hospital, because orthopedists want to assess peroneal nerve function after the surgery. We retrospectively assessed postoperative analgesic effect and complications of the continuous femoral nerve block for total knee arthroplasty. METHODS: We included 19 cases in 17 patients scheduled to undergo total knee arthroplasty under femoral nerve block combined with general anesthesia. Ultrasound-guided femoral nerve block was performed before the surgery. The ultrasound linear probe was used to visualize the femoral nerve. A 22 gauge needle attached to a nerve stimulator, was inserted with in-plane method. Five percent glucose solution was injected through the needle to encircle the femoral nerve. Then, the 22 gauge needle was withdrawn and an 18 gauge needle was inserted with out-of-plane method. Five percent glucose solution was injected through the needle to confirm the needle tip and perineural catheter was inserted through the needle. To achieve femoral nerve block, 0.375% ropivacaine 20 ml was injected through the needle. Perineural infusion with 0.15% ropivacaine at 4 ml x hr(-1) was initiated at the end of the surgery. Intravenous patient-controlled analgesia (IV-PCA) was also conducted postoperatively. We assessed pain at rest with a verbal numeric pain rating score (0-10) including pain on moving, and nausea as well as vomiting. RESULTS: Patients with numeric pain scores at 3 or less were 14 out of 19. Two patients complained of severe pain. There were 4 cases suffering pain on moving. CONCLUSIONS: Femoral nerve separation with 5% glucose solution using in-palne method and catheter placement with out-of-plane method could be useful for perineural catheter placement. Perineural infusion of 0.15% ropivacaine at 4 ml x hr(-1) combined with IV-PCA provided a good postoperative analgesia in patients receiving total knee arthroplasty.

[Assessment of intraoperative hemodynamics, infusion volume, urinary output and dose of circulatory drugs in general anesthesia with transversus abdominis plane block for cholecystectomy].

We retrospectively reviewed intraoperative hemodynamics, infusion volume, urinary output and dose of circulatory drugs in patients undergoing cholecystectomy in 3 types of anesthesia group: General anesthesia (GA group), general anesthesia with epidural anesthesia (EPI group) and general anesthesia with transversus abdominis plane (TAP) block (TAPB group). TAP block was performed using ultrasound-guided subcostal method and 20-30 ml of ropivacaine (0.2-0.3%) was injected to TAP bilaterally. Though, the blood pressure in TAPB group was lower than that in GA group, the degree of low blood pressure was smaller than that in EPI group. Less changes in intraoperative blood pressure, infusion volume and dose of phenylephrine in TAPB group compared to those in EPI group can be the advantage of TAP block alternative to epidural anesthesia.

[Anesthetic management of an emergency open-heart surgery for entrapment of a circular mapping catheter by chordae tendineae with mitral valve damage undergoing atrial fibrillation ablation].

The entrapment of a circular mapping catheter by chordae tendineae during catheter ablation is a very rare but serious complication requiring, in some cases, surgical treatment. We report a case that required open heart surgery for catheter removal and mitral valve repair. A 79-year-old man underwent catheter ablation for paroxysmal atrial fibrillation in other hospital. During the operation, he moved accidentally, despite circular mapping catheter was in the left atrium. The circular mapping catheter was uncontrolable due to resistance interfering with catheter removal, and the patient was brought to our hospital for open heart surgery to remove catheter. General anesthesia was induced and maintained with midazolam, fentanyl. Transesophageal echocardiography was performed to monitor catheter position and mitral valve condition. Transesophageal echocardiography revealed that circular catheter tip was located adjacent to the posterior mitral leaflet and the presence of moderate mitral valve regurgitation. Circular catheter tip was entraped by chordae tendineae and caused posterior mitral leaflet damage. Intracardiac foreign body removal and posterior mitral leaflet repair were completed uneventfully under cardiopulmonary bypass. The postoperative course was uneventful. It is expected that catheter ablation for atrial fibrillation will increase in number. This rare complication of catheter ablation may become a threat to cardiologist, cardiac surgeon and anesthesiologist.

[Anesthetic hazards in an undiagnosed case of retroperitoneal paraganglioma].

We report a patient with undiagnosed retroperitoneal paraganglioma who developed an intraoperative hypertensive crisis. A 64-year-old female was scheduled for right partial mastectomy and removal of an abdominal mass, preoperatively diagnosed as a small intestine GIST. Surgery was performed under general anesthesia combined with epidural anesthesia with close monitoring. Immediately after the surgical manipulation of the abdominal mass, her systolic blood pressure rose to over 200 mmHg. This hypertensive crisis was managed with nicardipine and alprostadil combined with increased infusion rate of remifentanil and propofol. Thereafter, the patient was hemodynamically stable and the postoperative course was uneventful. Pathological examination identified the tumor as extraadrenal paraganglioma. The possibility of paraganglioma should be considered even in asymptomatic abdominal mass, and adequate precautions are required in such cases.

[Low doses of ketamine have no effect on bispectral index during stable propofol-remifentanil anesthesia].

BACKGROUND: Ketamine is associated with an increase in the bispectral index (BIS) values that can lead to an overdose of hypnotic agents. We investigated the effect of ketamine on BIS values during general anesthesia with a target-controlled infusion (TCI) of propofol and infusion of remifentanil. METHODS: Forty-five ASA I or II patients undergoing gynecological surgery were included in this study. After 5 min of steady-state anesthesia (BIS at 35-45) without surgical stimulation, patients received either a bolus administration of ketamine 0.2 mg x kg(-1) (LK group) or ketamine 0.5 mg x kg(-1) (HK group). Patients in the control group received no intervention. BIS values were recorded every minute until 15 min after ketamine administration. RESULTS: After ketamine administration, BIS value in HK group increased significantly compared with that at baseline. There were no significant changes for BIS values in LK group and control group over time. BIS values in HK group were significantly higher than those in the LK group and control group after ketamine injection. BIS values were not statistically different between LK group and control group. CONCLUSIONS: Under stable propofol and remifentanil anesthesia, a small dose of ketamine did not increase the BIS value over the next 15 min.

[Case of spinal anesthesia for pyrolomyotomy in a former preterm infant with chronic lung disease].

A former premature infant (1,795 g) with chronic lung disease underwent pyrolomyotomy under spinal anesthesia. She had been managed with artificial ventilation for 2 months after birth and had developed chronic lung disease. She showed frequent apnea with desaturation several times per day and 21 x min(-1) of oxygen had been administered. She began projectile vomiting 1 month after extubation and then was diagnosed as hypertrophic pyrolic stenosis by ultrasonography. She was transferred to our hospital to have pyrolomyotomy. After admission to pediatric intensive care, she was managed with nasal-DPAP to prevent apnea. Surgery was completed on the second day after admission under spinal anesthesia using 1.0 mg x kg(-1) of hyperbaric bupivacaine. Spinal puncture was accomplished with 19 mm of 27 G needle after removal of lidocaine patch which had been applied 1 hour before. After the outflow of clear CSF was confirmed, the anesthetics was administered. After we confirmed the anesthesia level up to T5, surgery was commenced. She was managed with mask CPAP to prevent deasaturation under spontaneous respiration during surgery. She required nasal-CPAP to prevent apnea after surgery and she was transferred back to the referred hospital on the 3rd postoperative day without any sequela.

[General anesthesia for cesarean section in a patient with moyamoya disease].

We described our management of a patient with moyamoya disease who presented for emergency cesarean section. A 29-year-old primigravida (162 cm, 61 kg) who had been diagnosed as having moyamoya disease at age 24, underwent urgent cesarean section at 35 weeks of gestation. Because she was medicated with aspirin, general anesthesia was selected. Anesthesia was induced with thiamylal and was maintained with sevoflurane in air oxygen mixture and fentanyl before delivery. After delivery, anesthesia was maintained with midazolam and fentanyl. Ventilation and depth of anesthesia were adjusted according to the end-tidal carbon dioxide tension and bispectral index, respectively. Hypertension caused by tracheal intubation was successfully prevented by nicardipine, which was ineffective for intraoperative hypertension. On the other hand, landiolol was effective for treating intraoperative hypertension and tachycardia. The cesarean delivery was uneventful and a healthy 2104 g neonate was delivered with Apgar score of 7 and 9 at 1 and 5 min, respectively. Landiolol was effective for treating intraoperative hypertension and tachycardia. Monitoring of depth of anesthesia, blood pressure, and ventilation would be essential for cesarean section under general anesthesia in patients with moyamoya disease.