Tomoo Kanna

Mechanisms of Direct Inhibitory Action of Isoflurane on Vascular Smooth Muscle of Mesenteric Resistance Arteries

Background Isoflurane has been shown to directly inhibit vascular reactivity. However, less information is available regarding its underlying mechanisms in systemic resistance arteries. Methods Endothelium-denuded smooth muscle strips were prepared from rat mesenteric resistance arteries. Isometric force and intracellular Ca2+ concentration ([Ca2+]i) were measured simultaneously in the fura-2-loaded strips, whereas only the force was measured in the &bgr;-escin membrane-permeabilized strips. Results Isoflurane (3–5%) inhibited the increases in both [Ca2+]i and force induced by either norepinephrine (0.5 &mgr;m) or KCl (40 mm). These inhibitions were similarly observed after depletion of intracellular Ca2+ stores by ryanodine. Regardless of the presence of ryanodine, after washout of isoflurane, its inhibition of the norepinephrine response (both [Ca2+]i and force) was significantly prolonged, whereas that of the KCl response was quickly restored. In the ryanodine-treated strips, the norepinephrine- and KCl-induced increases in [Ca2+]i were both eliminated by nifedipine, a voltage-gated Ca2+ channel blocker, whereas only the former was inhibited by niflumic acid, a Ca2+-activated Cl− channel blocker. Isoflurane caused a rightward shift of the Ca2+-force relation only in the fura-2-loaded strips but not in the &bgr;-escin-permeabilized strips. Conclusions In mesenteric resistance arteries, isoflurane depresses vascular smooth muscle reactivity by directly inhibiting both Ca2+ mobilization and myofilament Ca2+ sensitivity. Isoflurane inhibits both norepinephrine- and KCl-induced voltage-gated Ca2+ influx. During stimulation with norepinephrine, isoflurane may prevent activation of Ca2+-activated Cl− channels and thereby inhibit voltage-gated Ca2+ influx in a prolonged manner. The presence of the plasma membrane appears essential for its inhibition of the myofilament Ca2+ sensitivity.

Changes in body temperature following deflation of limb pneumatic tourniquet

Abstract Study Objectives : To investigate changes in both core and peripheral skin-surface temperatures during and after application of a unilateral leg pneumatic tourniquet in adult patients. Design : Prospective, observational clinical study. Setting : University hospital. Patients : 21 ASA physical status I and II adult patients scheduled for elective leg orthopedic surgery with lumbar epidural anesthesia. Interventions : Rectal and fingertip skin-surface temperatures were recorded every minute after steady-state lumbar epidural anesthesia was established. Measurements and Main Results : Significant ( p p Conclusions : Limb tourniquets appear to cause thermal perturbations during epidural anesthesia. The progressive increases in core temperature during tourniquet application presumably resulted from constraint of metabolic heat to the core thermal compartment, and the greater increases in the skin-surface temperature during tourniquet application appear to represent vasodilation in response to the core hyperthermia. On the other hand, redistribution of body heat and the efflux of hypothermic venous blood from the tourniqueted area into systemic circulation following tourniquet deflation probably decreased the core temperature, which might switch off the thermoregulatory vasodilation, leading to the decreases in skin-surface temperature. Recognition of these thermal perturbations are useful in diagnosing intraoperative thermal perturbations.

Fetal stabilization for antenatally diagnosed diaphragmatic hernia

BACKGROUND/PURPOSE Infants with congenital diaphragmatic hernia have pulmonary hypoplasia resulting in persistent pulmonary hypertension of neonates (PPHN), which is the main contributor to both high mortality and morbidity. The pulmonary artery bed in patients with congenital diaphragmatic hernia (CDH) is underdeveloped and is very sensitive to slight stimuli. It is, therefore, vital to avoid any factors that might increase pulmonary vascular resistance during the perinatal treatment of these patients. Recently, fetal anesthesia for perinatal stabilization in patients with CDH has been reported. However, the efficacy of this method remains controversial. The aim of this study is to analyze the benefits of fetal stabilization using fetal anesthesia in patients with CDH. METHODS The authors have seen 9 cases of antenatally diagnosed CDH and attempted fetal stabilization. The indication for fetal stabilization was a lung thoracic ratio of less than 0.2, without any severe associated anomalies. The protocol for fetal stabilization was (1) monitoring the fetal respiratory movement and heart beat by ultrasonography, (2) the administration of morphine (20 to 30 mg) and diazepam (5 mg) to the mother, (3) the confirmation of any interruptions in fetal movement followed by a cesarean section, (4) pancuronimum (0.5 mg) was given through the umbilical vessels, (5) intubation before clamping of the umbilical cord, and (6) high-frequency oscillatory ventilation (HFO) without bagging. RESULTS The lung-thratic ratio (LTR) was between 0.06 to 0.17 (average, 0.10+/-0.04). Operation was performed in 7 of 9 patients at between 2.5 and 27 hours after birth. The overall survival rate was 66.7% (6 of 9). All of the patients who underwent operation within 5 hours after birth survived. CONCLUSIONS Perinatal stabilization using fetal anesthesia was found to be effective in preventing PPHN and shortening the period of preoperative stabilization. It also improved the survival rate of patients with severe CDH.

Early findings on brain computed tomography and the prognosis of post-cardiac arrest syndrome: Application of the score for stroke patients

AIM To examine whether early findings of the brain computed tomography (CT) evaluated by the modified Alberta stroke programme early CT (m-ASPECT) score is useful for determining the prognosis of post-cardiac arrest syndrome (PCAS) patients or not. MATERIALS From 2003 through 2010, 149 consecutive PCAS patients: (1) with various aetiologies but neither from haemorrhagic stroke nor trauma, (2) who were 15 years old or older and (3) whose brain CT was available were admitted to our intensive care unit. Early findings on all of their CT images were rated with the m-ASPECT scoring system by three raters, and an inter-rater comparison was conducted. Next, the images within 24 h from arrest were collected from 133 patients (89 males, age 60.2±17.6 years), and a relation of the scores with outcome at day 30 of the patients was analysed. RESULTS According to the inter-rater comparison based on a linear regression analysis, agreement between the raters was good (correlation coefficient 0.76-0.88). A receiver operating curve analysis revealed that the m-ASPECT scores within 24 h were a good predictor of poor outcome (dead or vegetative state) with an area under the curve of 0.905. An m-ASPECT score ≤13 was 100% predictive of a poor outcome, with a negative predictive value of 0.57. The m-ASPECT score was the best predictor of poor outcome (odds ratio 45.62) among various factors including cause or duration of arrest. CONCLUSION The m-APSECT score evaluated within 24 h from arrest was found to be the most predictive factor for outcome at day 30.

Detection of retroperitoneal hemorrhage by transesophageal echocardiography during cardiac surgery.

PurposeTo present a case of massive retroperitoneal hemorrhage during cardiopulmonary bypass (CPB) which was detected using transesophageal echocardiography (TEE).Clinical featureA 50-yr-old man suffering from severe mitral regurgitation (MR) was admitted for mitral valvuloplasty. After the beginning of CPB, the volume in the reservoir was noticed to be gradually decreasing. Although venous cannulation had been properly performed, TEE showed an echo free space around the liver, the spleen and in front of the abdominal aorta showed intraabdominal hemorrhage. After cardiac surgery, emergency laparotomy revealed about 5,000 ml of blood in the retroperitoneal space probably as a result of femoral artery cannulation prior to CPB. Hemostasis was achieved, and the patient made complete cardiac and neurological recovery. Retrospective review of the TEE imaging revealed that the kidneys were surrounded by blood bilaterally confirming the diagnosis of retroperitoneal hemorrhage.ConclusionRetroperitoneal hemorrhage during CPB is rare, but may be lethal. Transesophageal echocardiography is a useful monitor not only to evaluate cardiac performance, but also to detect unexpected intraabdominal bleeding during cardiac surgery.RésuméObjectifPrésenter le cas d’une hémorragie rétropéritonéale massive pendant la circulation extracorporelle (CEC), détectée à l’aide de l’échocardiographie transoesophagienne (ETO).Éléments cliniquesUn homme de 50 ans, souffrant de régurgitation mitrale sévère, a été admis pour une valvuloplastie mitrale. Après le début de la CEC, on a noté que le volume du réservoir baissait graduellement. Bien qu’on ait correctement réalisé la mise en place d’une canule veineuse, l’ETO a montré un espace libre d’écho autour du foie, de la rate et, en avant de l’aorte abdominale, indiquant la présence d’une hémorragie intra-abdominale. Après la cardiochirurgie, la laparotomie d’urgence a révélé la présence d’environ 5 000 ml de sang dans l’espace rétropéritonéal, le résultat probable de l’introduction d’une canule dans l’artère fémorale avant la CEC. L’hémostase a été rétablie et le patient a connu une récupération cardiaque et neurologique complète. Létude rétrospective des images de l’ETO a révélé que les reins étaient bilatéralement entourés de sang, ce qui confirme le diagnostic d’hémorragie rétropéritonéale.ConclusionL’hémorragie rétropéritonéale est rare pendant la CEC, mais elle peut être fatale. L’échocardiographie transoesophagienne est un moniteur utile non seulement pour évaluer le rendement du coeur, mais aussi pour détecter des saignements intra-abdominaux inattendus pendant la cardiochirurgie.

Sevoflurane and bradykinin-induced calcium mobilization in pulmonary arterial valvular endothelial cells in situ: sevoflurane stimulates plasmalemmal calcium influx into endothelial cells.

Kinins locally synthesized in the cardiovascular tissue are believed to contribute to the regulation of cardiovascular homeostasis by stimulating the endothelial cells to release nitric oxide, prostacyclin, or a hyperpolarizing factor via autocrine-paracrine mechanisms. This study was designed to investigate the action of sevoflurane on bradykinin-induced Ca2+ mobilization in endothelial cells in situ. Utilizing fura-2-loaded rat pulmonary arterial valve leaflets, the effects of sevoflurane were examined on bradykinin-induced increases in intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells in situ. In the presence of extracellular Ca2+ (1.5 m M), bradykinin (3–30 &mgr;M) produced an initial phasic and a subsequent tonic increase in [Ca2+]i in a concentration-dependent manner. However, it produced only the phasic increase in [Ca2+]i in the absence of extracellular Ca2+. Sevoflurane (5%, 0.67 m M) inhibited both the phasic and tonic responses to bradykinin. In these experiments, sevoflurane (3–5%) generated sustained increases (approximately 20–40% of the bradykinin-induced maximal increase in [Ca2+]i) in the resting [Ca2+]i level. Sevoflurane still increased [Ca2+]i after depletion of the intracellular Ca2+ stores with ionomycin (0.1 &mgr;M). However, the sevoflurane-induced increase in [Ca2+]i was eliminated by removal of the extracellular Ca2+ and attenuated by NiCl2 (1–3 m M). In conclusion, in the pulmonary arterial valvular endothelial cells, sevoflurane inhibits both bradykinin-induced Ca2+ release from the intracellular stores and bradykinin-induced plasmalemmal Ca2+ influx. In addition, sevoflurane appears to stimulate the plasmalemmal Ca2+ influx and thereby increase the endothelial [Ca2+]i level. Sevoflurane might influence the pulmonary vascular tone through its direct action on the pulmonary arterial valvular endothelial cells.

Geriatric Patients Presenting to the Emergency Department of a Japanese University Hospital

To evaluate the trend of elderly patients visiting the emergency department of a Japanese University Hospital, out patient-based records were reviewed of the emergency department of Kyushu University Hospital from 2000 to 2004. A total number of 7610 emergency patients visited the department during the five year period. The median (25%, 75%) of age was 32 (22, 56). Patients aged 65 years and over accounted for 16% of all attendances. All the patients were classified into 6 groups according to the diagnosis, (1) Respiratory, (2) Circulatory, (3) Central nervous system, (4) Abdominal, (5) Trauma, and (6) Others. The median age in each group was (1) 27 (15, 49), (2) 66 (53, 76), (3) 51 (27, 67), (4) 33 (22, 56), and (5) 26 (20, 46), respectively. There was a statistically significant difference observed, reciprocally except between (1) and (5) (P < 0.05). The patients showed statistically significant difference in the annual transition of the disease (P < 0.0001). In the elderly, the annual transition of the disease showed statistically significant decreases in Circulatory (P = 0.0015) and in Central nervous (P < 0.0001), and an increase in Abdominal (P < 0.0001), respectively. Death rate at the outpatient clinic in the elderly showed much higher than in the younger (P < 0.0001). Admission rate was also much higher in the elderly than in the younger (P < 0.0001). Elderly emergency patients have both internal and external intrinsic factors. They have to be treated carefully since their condition easily deteriorates. Provisions for the problems surrounding the elderly should be made as a nationwide effort.

Reduction of regional cerebral oxygen saturation coincidental with a perioperative focal motor seizure

previous left hemiparetic attacks, at 3 years 2 months, 1year 5 months, and 8 months before admission. Theonly neurological deficit was a slight sensory distur-bance in the left leg. The brain computed tomographic(CT) scan indicated lacunar infarctions at the bilateralbasal ganglia. However, the Xe-enhanced CT scanfailed to reveal any significant decreases in cerebralblood flow. In addition, cerebral arteriography did notreveal any significant stenotic lesions. She had no appar-ent history of epileptic attacks. In spite of the previousdiagnosis of HT, the blood pressure preoperativelymeasured in the ward was 100–126/64–88mmHgwithout any treatment. She was slightly anemic due togenital bleeding (Hb 10.6g·dl

Changes in Body Temperature Following Deflation of Limb Pneumatic Tourniquet

STUDY OBJECTIVES To investigate changes in both core and peripheral skin-surface temperatures during and after application of a unilateral leg pneumatic tourniquet in adult patients. DESIGN Prospective, observational clinical study. SETTING University hospital. PATIENTS 21 ASA physical status I and II adult patients scheduled for elective leg orthopedic surgery with lumbar epidural anesthesia. INTERVENTIONS Rectal and fingertip skin-surface temperatures were recorded every minute after steady-state lumbar epidural anesthesia was established. MEASUREMENTS AND MAIN RESULTS Significant (p < 0.05) increases in both rectal and fingertip temperatures were observed during tourniquet application for 91 +/- 6 minutes from 36.5 +/- 0.14 degrees C to 37.0 +/- 0.17 degrees C and from 32.6 +/- 0.79 degrees C to 35.5 +/- 0.44 degrees C, respectively. In contrast, both rectal and fingertip temperatures progressively decreased following tourniquet release; significant (p < 0.05) decreases in the rectal and fingertip temperatures were observed 6 and 5 minutes after tourniquet release, respectively. Decreases (approximately maximum) in the rectal and fingertip temperatures 15 minutes after tourniquet release were 0.25 +/- 0.05 degrees C and 1.26 +/- 0.26 degrees C, respectively. In each case, changes in fingertip temperature were approximately six times greater than those in the rectal temperature. CONCLUSIONS Limb tourniquets appear to cause thermal perturbations during epidural anesthesia. The progressive increases in core temperature during tourniquet application presumably resulted from constraint of metabolic heat to the core thermal compartment, and the greater increases in the skin-surface temperature during tourniquet application appear to represent vasodilation in response to the core hyperthermia. On the other hand, redistribution of body heat and the efflux of hypothermic venous blood from the tourniqueted area into systemic circulation following tourniquet deflation probably decreased the core temperature, which might switch off the thermoregulatory vasodilation, leading to the decreases in skin-surface temperature. Recognition of these thermal perturbations are useful in diagnosing intraoperative thermal perturbations.

Limb tourniquet causes thermal perturbations under various types of anesthesia: a report of seven cases

Pneumatic tourniquets are frequently used during limb operations to decrease blood loss and to provide a bloodless surgical field. Deflation of the limb tourniquet is known to cause a number of adverse systemic responses such as systemic hypotension, tachycardia, systemic acidosis with increases in arterial CO2 pressure (Pac%) and lactate, and decreases in arterial oxygen pressure (Pao2) [1-4]. Although Bloch et al. previously demonstrated progressive increases in central temperature following tourniquet application in pediatric patients under general anesthesia [5], little information is available regarding changes in body temperature following tourniquet release. In this report of seven patients who underwent limb surgery under various types of anesthesia, we demonstrate gradual increases in both central and peripheral temperatures during tourniquet application, and progressive decreases in both central and peripheral temperatures following tourniquet release.