Keisuke Amaha

Two-dimensional echocardiographic evaluation of inferior vena cava, right ventricle, and left ventricle during positive-pressure ventilation with varying levels of positive end-expiratory pressure

The effects of intermittent positive-pressure ventilation (IPPV) with 0, 10, and 15 cm H2O of PEEP on inferior vena cava (IVC), right and left ventricular length and septal-lateral dimensions, and cardiac output were examined in 19 patients with respiratory failure using two-dimensional echocardiography. In five patients, cardiac output was also obtained by the thermodilution technique. As PEEP was increased, IVC dimensions increased during both inspiration and expiration, and the IVC collapsibility index decreased. This indicated an increase in venous stasis and decrease in venous return to the right atrium. Increasing PEEP was associated with progressive decreases in cardiac output, and length and septal-lateral dimensions of both ventricles. The decreased cardiac output during IPPV with 10 and 15 cm H2O PEEP may be due to the decreased venous return and ventricular filling. Cardiac output determined by echocardiography was correlated closely to that by the thermodilution technique.

Improvement of renal dysfunction in dogs with endotoxemia by a nonselective endothelin receptor antagonist

OBJECTIVES During endotoxemia, there is a marked and intractable decrease in systemic blood pressure, as well as profound vasoconstriction of the renal artery, thereby leading to septic shock and acute renal failure. The purpose of this study was to elucidate the effect of endothelin-1, a potent endothelium-derived vasoconstrictor peptide, on the hemodynamic and renal vascular changes seen in endotoxemia. DESIGN Prospective, comparative, experimental study. SETTING Laboratory at a university hospital. SUBJECTS Thirty-two male mongrel dogs (12.1+/-0.4 kg) under pentobarbital anesthesia. INTERVENTIONS Four groups of animals were studied: a) the lipopolysaccharide (LPS) group (n = 10), which received LPS (250 ng/kg/min for 2 hrs); b) the TAK-044 (a nonselective endothelinA/ endothelinB receptor antagonist) plus LPS group (n = 12), which received a bolus of TAK-044 (5 mg/kg) 0.5 hr before the start of LPS infusion; c) the TAK-044 plus vehicle group (n = 5), which received the same dose of TAK-044 0.5 hr before the start of vehicle infusion; and d) the control group (n = 5), which received only vehicle infusion. MEASUREMENTS AND MAIN RESULTS Changes in systemic and renal hemodynamics, blood gas, and renal function were measured at baseline, and at 0.5, 1, 2, 3, and 4 hrs. Infusion of LPS resulted in significant decreases in mean arterial pressure, arterial pH, Pao2, base excess, urine volume, renal blood flow, creatinine clearance, and urine osmolality. The administration of TAK-044 before LPS infusion did not affect the LPS-induced hypotension. In contrast, the receptor antagonist prevented LPS-induced metabolic acidosis and hypoxemia, and improved LPS-induced decreases in urine volume, renal blood flow, creatinine clearance, and urine osmolality, whereas TAK-044 or vehicle administered alone resulted in no significant hemodynamic or blood gas changes. Plasma endothelin-1 concentrations significantly increased after LPS infusion, with or without TAK-044. CONCLUSIONS The present study suggests that endothelin-1 plays an important role in the impaired renal hemodynamics and renal function associated with endotoxemia, and that endothelin receptor antagonists may be useful as therapeutic agents for acute renal failure during endotoxemia.

Using the Intubating Laryngeal Mask Airway (lma-fastrach™) for Blind Endotracheal Intubation in Patients Undergoing Cervical Spine Operation

T he intubating laryngeal mask airway (ILMA; LMA-Fastrach, Laryngeal Mask Company, Ltd., Henley on Thames, UK) has been recently introduced as a prototype of the laryngeal mask airway for blind endotracheal intubation (1–3). It allows for an endotracheal tube (ETT) of up to 8.0-mm inside diameter and does not require head and neck manipulations on insertion. The success rate of blind intubation using the ILMA was up to 99.3% in patients with or without airway problems (3). Therefore, the ILMA might be helpful for endotracheal intubation in patients with cervical spine disease. The purpose of this study was to investigate the utility of the ILMA for blind endotracheal intubation in patients undergoing cervical spine surgery.

Middle cerebral arterial blood flow velocity increases during laparoscopic cholecystectomy.

The effects of intraperitoneal CO2 insufflation on middle cerebral arterial blood flow velocity were evaluated in 10 patients undergoing laparoscopic cholecystectomy under general anesthesia with nitrous oxide, oxygen, and isoflurane. Blood flow velocity was measured using transcranial Doppler ultrasonography. During CO2 insufflation, Paco2 and the end-tidal CO2 concentration (PETCO2) increased significantly compared with the preinsufflation baseline value (P < 0.01) while ventilation was kept constant. Cerebral blood flow velocity also increased significantly in comparison with the baseline value (P < 0.01). These values still exceeded baseline values 10 min after deflation of the peritoneal cavity. A significant positive correlation was observed between blood flow velocity and Paco2 (P < 0.001). Our results suggest that intraperitoneal CO2 insufflation during laparoscopic cholecystectomy increases cerebral blood flow and that this is probably due to an increased Paco2.

Endothelin-1 and atrial natriuretic peptide in septic shock

utes are being utilized. 4 Although a recent randomized trial of s tandard and high-dose epinephrine for cardiac arrest outside the hospital failed to reveal a survival advantage for the higher dose protocol, there was a t rend toward improved survival when high-dose epinephrine was administered within 10 minutes after the onset of cardiac arrest, as can be achieved in the catheterizat ion laboratory. 5 There are obvious l imitat ions to this report. I t is not randomized and it is retrospective. The dose of intracoronary epinephrine adminis tered to these pat ients was arbi t rar i ly selected and may not have resulted in the opt imal hemodynamic response. Int racoronary epinephrine was generally selected as a t rea tment of last resort and may have been more effective given earlier during the episode of hypotension. Fur thermore , it was often adminis tered simultaneously with other therapies, and its precise benefit, or even potent ia l harm to pat ients 5 through 8, is impossible to define. However, based on our observations in most pat ients of a rapid increase in arterial blood pressure after the adminis t ra t ion of intracoronary epinephrine, it would seem reasonable to consider its use in cases of refractory hypotension occurring during PTCA when other measures prove ineffective.

Increased Plasma Concentrations of Brain Natriuretic Peptide in Patients With Acute Lung Injury

PURPOSE This study was performed to elucidate the pathophysiological role of brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) in acute lung injury. MATERIALS AND METHODS We sequentially measured plasma concentrations of immunoreactive BNP and ANP in 10 patients (mean age, 63 years (with acute lung injury and compared those with hemodynamic parameters and pulmonary functions. RESULTS Plasma concentrations of immunoreactive BNP and ANP were markedly elevated at entry into the study. Plasma BNP concentrations during the early course (3 days) showed significant (P < .01) positive correlations with systemic vascular resistance index (r = .708) and pulmonary vascular resistance index (r = .573), but a negative correlation with cardiac index (r = .608). Plasma ANP concentrations showed a significant (P < .05) positive correlation with pulmonary capillary wedge pressure (r = .398). Plasma BNP in 4 patients who died and 1 patient with acute renal failure remained elevated during the entire hospital length of stay (12 days). CONCLUSION These findings suggest that circulating BNP plays an important role in acute lung injury along with ANP as a compensatory mechanism for cardiac dysfunction accompanied by increased systemic vascular resistance index and pulmonary vascular resistance index. Circulating BNP may be a sensitive humoral marker for the degree of ventricular dysfunction associated with acute lung injury.

EFFECTS OF CONTINUOUS POSITIVE – PRESSURE VENTILATION ON HEPATIC BLOOD FLOW AND INTRAHEPATIC OXYGEN DELIVERY IN DOGS

The effect of mechanical ventilation with PEEP of 0, 10, and 20 cm H2O (continuous positive-pressure ventilation [CPPV]) on hepatic blood flow (HBF) and intrahepatic oxygen delivery was studied in 26 mongrel dogs anesthetized with fentanyl. Hepatic arterial and portal venous blood flow was measured by an electromagnetic flowmeter. CPPV caused a significant decrease in HBF, which was related to the PEEP level. A linear correlation was seen between HBF and cardiac output. Intrahepatic oxygen delivery decreased more than HBF and cardiac output. The reduced oxygen delivery was due mainly to the decrease in portal venous oxygen content.

The effect of diazepam on the respiratory response to carbon dioxide

Summary and ConclusionsSix healthy adult female volunteers were used in the quantitative assessment of their respiratory responses following intravenous administration of meperidine and diazepam. A modified rebreathing CO2-challenge technique of Eckenhoffet al.,5 previously reported,6 was used for this purpose. The CO2 stimulus response curves obtained confirmed the respiratory depressant response following the use of 0.5 mg./kg. meperidine. Diazepam, at dose levels up to 0.066 mg./kg., produced no statistically significant respiratory response to carbon dioxide detectable by this method(p < 0.025).RésuméSix adultes volontaires du sexe féminin et en bonne santé ont servi à l’évaluation quantitative des réactions respiratoires à la suite d’injection intraveineuse de mépéridine et de diazepam. On a utilisé à cet effet une technique modifiée de Eckenhoff et coll., décrite antérieurement.La courbe des réponses obtenues par la stimulation du CO2 a confirmé que l’usage de 0.5 mg./kg. de mépéridine produissait une dépression respiratoire. Le diazepam, à la dose de 0.066 mg./kg., n’a pas produit de réponse de valeur statistique a la stimulation du CO2 en employant cette méthode (p < 0.025).

Midazolam and ketamine inhibit glutamate release via a cloned human brain glutamate transporter.

Purpose: In cerebral ischemia/anoxia, the glutamate transporter runs in reverse and releases glutamate into the extracellular space, causing irreversible neuronal damage. Intravenous anesthetics attenuate overall glutamate release and prevent neuronal injury during anoxia/ischemia, but their effect on the gluatamate transporter is variable.Methods: A human glial glutamate transporter (hGLT-1) cDNA was isolated by screening a human cerebral cortical library. Cloned cDNA was transfected in Chinese hamster ovary cells. The effect of the intravenous anesthetics midazolam (0.3 to 30 µM), ketamine (10 to 100 µM), thiopental (30 to 300 µM), and propofol (3 to 30 µM) on reversed uptake of L-glutamate via hGLT-1 was examined by whole-cell patch-clamp.Results: Midazolam at a concentration 3 µM reduced outward currents arising from reversed L-glutamate uptake via hGLT-1 in a concentration-dependent manner. While, ketamine at 100 µM attenuated the same outward currents, to 53.3±11.4% of those seen in controls without anesthetics (P<0.05 n=5). In contrast, neither thiopental nor propofol showed effects on outward currents mediated by reversed operation of hGLT-1.Conclusions: These results suggest that midazolam and ketamine, but not thiopental and propofol, have a capacity to inhibit glutamate release via GLT-1 directly.RésuméObjectif: Lors d’ischémie/anoxie cérébrale, l’action du transporteur de glutamate est inversée, ce qui libère du glutamate dans le compartiment extracellulaire et cause des dommages neuronaux irréversibles. Les anesthésiques intraveineux réduisent la libération totale de glutamate et préviennent les lésions neuronales pendant l’anoxie/ischémie, mais leur effet varie sur le transporteur de glutamate.Méthode: Un transporteur glial de glutamate humain (TGLh-1) ADNc a été isolé à la suite d’une sélection dans la génothèque corticale cérébrale humaine. L’ADNc cloné a été transféré dans les cellules ovariennes d’un hamster chinois. L’effet des anesthésiques intraveineux midazolam (0,3 à 30 µM), kétamine (10 à 100 µM), thiopental (30 à 300 µM), et propofol (3 à 30 µM) sur la fixation inversée de L-glutamate au moyen du TGL-1 a été examiné selon la technique de «patch-clamp» d’une cellule complète.Résultats: Le midazolam, à 3 µM, a réduit d’une manière dépendante de la concentration le courant sortant provenant de la fixation inversée de L-glutamate au moyen du TGLh-1. La kétamine, à 100 µM, a diminué le même courant sortant à 53,3±11,4 % des témoins sans anesthésique (P<0,05, n=5). Par ailleurs, ni le thiopental ni le propofol n’ont montré d’effets sur le courant sortant dont l’origine serait attribuée à l’opération inversée du TGLh-1.Conclusion: Ces résultats suggèrent que le midazolam et la kétamine, non le thiopental ni le propofol, ont la capacité d’inhiber la libération de glutamate en passant directement par le TGL-1.

Pathologic role of endothelin-1 in septic shock.

To elucidate the pathologic role of endothelin-1 (ET-1) in septic shock, we measured plasma ET-1 concentrations after bacterial lipopolysaccharide (LPS) administration in dogs and determined systemic, pulmonary, and renal hemodynamics and blood gas parameters with or without the nonselective ET receptor antagonist TAK-044. Plasma ET-1 concentrations increased significantly after LPS administration, which correlated positively with mean arterial pressure, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, and central venous pressure. LPS infusion induced hypotension, metabolic acidosis, hypoxemia, and renal dysfunction. TAK-044 prevented LPS-induced metabolic acidosis, hypoxemia, and renal dysfunction, but not hypotension. These findings suggest that increased circulating ET-1 plays a compensatory role in the reversal of systemic vasodilatation in septic shock, but exerts deleterious effects on renal and pulmonary circulation.