[Case of Staphylococcus epidermidis endocarditis with a bacterial vegetation suspected by intraoperative alternating pulse].

We report here a case of Staphylococcus epidermidis endocarditis with bacterial vegetation which was suspected by intraoperative alternating pulse on arterial pressure monitoring. A 65-year-old man was diagnosed as lumbar spinal canal stenosis and scheduled for operation. Preoperatively, he had chronic renal failure, mild aortic valve stenosis, and moderate mitral valve regurgitation. Neither inflammatory signs nor vegetations on TEE were observed preoperatively. General anesthesia was induced with propofol and vecuronium, and maintained with oxygen (33%), nitrous oxide and sevoflurane. Two hours after the beginning of operation, alternating pulse was observed suddenly on arterial pressure waves without marked change in hemodynamic parameters. The operation was performed uneventfully and alternating pulse disappeared after changing from prone position to supine. Using a transesophageal echocardiography, large-sized bacterial vegetation (22 x 17 mm) was found in the left ventricle. Second operation was performed to remove vegetation at three weeks after first operation. Alternating pulse is generally considered as a sign of severe left ventricular dysfunction such as dilated cardiomyopathy and aortic stenosis. Therefore, we should be careful about pulse disorder during operation for the patient who is in the state of severe heart failure.

Diabetic patients have an impaired cerebral vasodilatory response to hypercapnia under propofol anesthesia.

BACKGROUND AND PURPOSE: The purpose of this study was to examine the effects of diabetes mellitus and its severity on the cerebral vasodilatory response to hypercapnia. METHODS: Thirty diabetic patients consecutively scheduled for elective major surgery were studied. After induction of anesthesia, a 2.5-MHz pulsed transcranial Doppler probe was attached to the patient's head at the right temporal window, and mean blood flow velocity of the middle cerebral artery (Vmca) was measured continuously. After the baseline Vmca, arterial blood gases, and cardiovascular hemodynamic values were measured, end-tidal CO2 was increased by reducing ventilatory frequency by 2 to 5 breaths per minute. Measurements were repeated when end-tidal CO2 increased and remained stable for 5 to 10 minutes. RESULTS: Significant differences were observed in absolute and relative CO2 reactivity between the diabetes and control groups (absolute CO2 reactivity: control, 2.8+/-0.7; diabetes mellitus, 2.1+/-1.3; P<0.01; relative CO2 reactivity: control, 6.3+/-1.4; diabetes mellitus, 4.5+/-2.7; P<0.01, Mann-Whitney U test). Significant differences were also found between diabetic patients with retinopathy and those without retinopathy in absolute (P=0.002) and relative (P=0.002) CO2 reactivity, glycosylated hemoglobin (P=0.0034), and fasting blood sugar (P=0.01) (Scheffé's test, Mann-Whitney U test). There was an inverse correlation between absolute CO2 reactivity and glycosylated hemoglobin (r=0.69, P<0.001). CONCLUSIONS: Insulin-dependent diabetic patients have an impaired vasodilatory response to hypercapnia compared with that of the control group, and the present findings suggest that their degree of impairment is related to the severity of diabetes mellitus.

Increased plasma concentrations of the mature form of adrenomedullin during cardiac surgery and hepatosplanchnic hypoperfusion.

Adrenomedullin is a potent vasodilatory peptide. Plasma adrenomedullin (AM) concentrations increase during and after cardiopulmonary bypass (CPB). However, the cause of this increase and its site of production have not been identified. We investigated the role of the hepatosplanchnic and cerebral circulations in the increase of plasma AM and investigated whether tissue hypoxygenation is a cause of the AM increase seen during CPB. We measured plasma total AM (AM-T) and the biologically active form of AM, mature AM (AM-m), in seven patients undergoing CPB. Both plasma AM-T and AM-m concentrations increased significantly 60 min after weaning from CPB. At this time point, arterial AM-T and AM-m concentrations were 18-fold and 10-fold larger, respectively, than baseline values measured after the induction of anesthesia. The plasma AM-m concentration and the ratio of AM-m/AM-T in blood from the hepatic vein were significantly larger than those from the radial artery or jugular bulb. The AM-m/AM-T ratio decreased during CPB, suggesting that production of the intermediate form of AM, AM-glycine, is more than that of AM-m. The oxygen tension of the hepatic venous blood (PhvO2) was significantly less during CPB. Plasma AM-m concentrations sampled from the hepatic vein showed a significant negative correlation with PhvO2 at 10 min (r = 0.824; P < 0.02) and 60 min (r = 0.828; P < 0.02) after the onset of CPB. These data suggest that the hepatosplanchnic circulation is an important source of AM-m during CPB. Furthermore, hypoxygenation of the hepatosplanchnic region may be an important cause of this AM-m increase.

Anesthetic management for clipping a giant basilar artery aneurysm with moderate hypothermia, extracorporeal circulation assistance, and propofol infusion.

A 65-year-old female patient underwent surgery to clip a giant basilar artery aneurysm with closed-chest extracorporeal circulation using femorofemoral bypass. Moderate hypothermia (27 degrees C-30 degrees C), retention of spontaneous circulation, and propofol infusion (3-5 mg. kg(-1). h(-1)) were used under general anesthesia. Blood outflow via femoral vein was sufficient to maintain cardiopulmonary bypass and to induce hypothermia. Hemodynamics were controlled with dopamine and noradrenaline. In this case, extracorporeal circulation under moderate hypothermia was used to assist rather than substitute for spontaneous circulation, and spontaneous circulation was maintained at all times. We think that this method had advantages over deep hypothermic circulatory arrest with regard to intraoperative risks and postoperative complications.

G-protein coupled receptor kinase 2 is altered during septic shock in rats.

BACKGROUND: One of the key mechanisms leading to beta-adrenergic receptor-specific desensitization is the phosphorylation of agonist-occupied receptors by the specific beta-adrenergic receptor kinase (GRK2). The present study examines whether GRK2 is altered during septic shock in rats. MATERIALS AND METHODS: Male Wistar rats (7 weeks) weighing between 250 and 300 g were anesthetized with pentobarbital (10 mg/kg ip). Escherichia coli endotoxin (10 mg/kg in 0.3 mL of saline) or saline (0.3 ml) was injected intravenously via the dorsal vein. Hemodynamic parameters and humoral mediators were measured at 2 h after the administration of endotoxin. The hearts were immediately excised to examine beta-adrenergic receptor density and GRK2 level. We also studied the inotropic response to isoproterenol at the same time in other animals. RESULTS: Myocardial beta-adrenergic receptor density in the membrane fraction was decreased after an intravenous administration of 10 mg/kg LPS (LPS group: baseline value; 82 +/- 11 fmol/mg protein; 120 min after LPS; 58 +/- 11 fmol/mg protein, P < 0.05). GRK2 levels in the membrane and cytosolic fraction of the control group did not change. In the LPS group, GRK2 levels in the membrane fraction were increased at 60 and 120 min after the treatment (60 min; control, 4.5 +/- 0.4; pithed control, 4.4 +/- 0.6; LPS group, 6.2 +/- 0.3; pithed LPS group, 5.5 +/- 0.4; 120 min: control, 4.4 +/- 0.3; pithed control, 4.9 +/- 0.7; LPS group, 7.1 +/- 0.3; pithed LPS group, 5.9 +/- 0.4; densitometric unit, respectively: P < 0.05). CONCLUSIONS: GRK2 levels in the membrane fraction are increased during septic shock in rats. GRK2 might play a role in the impairment of the beta-adrenergic receptor signal transduction system.

[The effects of prostaglandin E1 on systemic and cerebral oxygenation before and during cardiopulmonary bypass].

The purpose of this study was to examine the effects of a small dose of prostaglandin E1 on systemic and cerebral oxygenation. Thirty patients for coronary artery bypass graft surgery were randomly divided into two groups: Group 1 received PGE1 25 ng.kg-1.min-1. Group 2 received PGE1 50 ng.kg-1.min-1. After measuring baseline hemodynamics and mixed (SvO2) and juglar (SjvO2) venous oxygen saturations, administration of PGE1 at a rate of 25 ng.kg-1.min-1 or 50 ng.kg-1.min-1 was started before and during CPB. In group 2, mean arterial pressure (MAP) decreased during CPB, while in group 1, MAP was unchanged during CPB. There was no change in SjvO2 both in group 1 and group 2 before and during CPB. The administration of PGE1 at a rate of 25 ng.kg-1.min-1 during CPB was suitable for the maintenance of SvO2 and SjvO2.