Anatomical bases of binaural interaction in auditory brain-stem responses from guinea pig

There is a non-linear interaction of binaural stimulation on auditory brain-stem potentials in both human and animals. The interaction takes the form of the binaurally evoked ABR being of smaller amplitude than the sum of the monaurally evoked ABRs. In the guinea pig this interaction occurs at the time of components P4, N4 and P5. In order to investigate the generator sites of binaural interaction in the ABR, various lesions were made in the brain-stem auditory system in 29 guinea pigs. The effects of those lesions on binaural interaction were as follows: (1) unilateral lesion of lateral lemniscus or bilateral lesions of the inferior colliculi had no significant effect on binaural interaction; (2) transection of the lateral lemnisci bilaterally was associated with a loss of the component of binaural interaction associated in time with N4; (3) a lesion just lateral to the lateral superior olivary complex resulted in an attenuation of the component of binaural interaction associated in time with P4; (4) complete section of the decussating fibers of the trapezoid body or a complete unilateral lesion of the superior olivary complex led to a loss of all components of binaural interaction. These results suggest that binaural interaction in the guinea pig ABR requires the integrity of several distinct portions of the brain-stem auditory pathway, i.e., both lateral lemnisci are required for the interaction occurring at the time of N4; the brain-stem just lateral to the lateral superior olive participates in the interaction at the time of P4. The trapezoid body and superior olivary nucleus are required for binaural interaction at P4, N4 and P5.     

Heme oxygenase does not contribute to control of basal vascular tone in isolated blood-perfused rat lung.

BACKGROUND: Vasoconstriction in pulmonary ischemia-reperfusion injury may involve dysfunction of the physiologic vasodilation of pulmonary arteries. Little is known of the relative importance of heme oxygenase (HO)/carbon monoxide (CO)-dependent vs nitric oxide synthase (NOS)/nitric oxide (NO)-dependent vasodilation of the pulmonary vasculature. We evaluated the significance of HO function on basal pulmonary vascular resistance (PVR) and compared it with the function of NOS. METHODS: Using an isolated blood-perfusion model, lungs of Lewis rats were assigned to 3 groups (n = 6/group). After stabilization, either an inhibitor of HO (tin-protoporphyrin-9 [SnPP-9]) or an inhibitor of NOS (NG-nitro-L-arginine methylester [L-NAME]) was added to the perfusate (50 micromol/liter and 1 mmol/liter as the final concentration, respectively). Lungs receiving saline served as controls. Gas exchange, hemodynamic and respiratory functions and the levels of cyclic 3',5'-guanosine monophosphate (cGMP) in the perfusate were measured. RESULTS: Inhibition of NOS by L-NAME resulted in a significant (p < 0.01) increase in PVR (DeltaPVR: 0.110 +/- 0.012 cm H(2)O/ml. min) within 5 minutes. In contrast, PVR was minimally affected by SnPP-9 (DeltaPVR: 0.005 +/- 0.005 cm H(2)O/ml. min), which was comparable to control lungs (DeltaPVR: 0.012 +/- 0.005 cm H(2)O/ml. min). The level of cGMP in the perfusate 5 minutes after drug application was markedly, but not significantly, lower in the L-NAME group (1.67 +/- 0.74 nmol/liter) when compared with controls (2.69 +/- 0.89 nmol/liter) and SnPP-9-treated lungs (2.65 +/- 0.66 nmol/liter). CONCLUSIONS: NOS but not HO contributes to the control of basal vascular tone in the rat lung.     

Nonfunctioning adrenocortical adenoma: a report of two cases

Two cases of nonfunctioning adrenocortical adenoma are herein reported. The adrenal tumor was found incidentally by computed tomography in both patients. Preoperative evaluation revealed that both patients had neither abnormal values in a variety of adrenal function studies nor any recognizable clinical signs associated with adrenal tumor. Following a definitive diagnosis of nonfunctioning adrenal tumors, surgical extirpation was performed in both cases. Histopathological finding was adrenocortical adenoma. Nonfunctioning adrenocortical tumor will be found more frequently with the increasing use of computed tomography in ordinary clinical practice. The management of nonfunctioning adrenocortical tumor is briefly discussed.     

Estimation of physiologic ability and surgical stress (E-PASS) for a surgical audit in elective digestive surgery

BACKGROUND: This study was undertaken to establish an equation to estimate mortality with the use of the prediction scoring system designated as the Estimation of Physiologic Ability and Surgical Stress (E-PASS), and to evaluate the system's usefulness in defining quality of care by comparing it with the Physiologic and Operative Severity Score for the enUmeration for Mortality and morbidity (POSSUM) and Portsmouth-possum (P-POSSUM) scoring systems previously generated for surgical audit. METHODS: Patients (n=5212; group A) who underwent elective gastrointestinal surgery were analyzed to establish equations for estimated 30-day and in-hospital mortality rates. The usefulness of E-PASS was evaluated in another series of 1934 patients (group B) who underwent elective digestive surgery in 6 national hospitals. The ratio of observed to estimated mortality rates (OE ratio) of each hospital was defined as a measure of quality. RESULTS: In group A, 30-day and in-hospital mortality rates increased as the Comprehensive Risk Score (CRS) increased, providing equations for estimated mortality rates. There was an excellent correlation between the estimated and observed mortality rates in individual diseases: R=0.958, N=6, P=.0027 for in-hospital mortality; R=0.937, N=6, P=.0059 for 30-day mortality. In all patients of group B, the E-PASS system estimated the 30-day mortality rates by 0.63-fold (linear analysis), whereas the POSSUM score was 11.0-fold (exponential analysis). The E-PASS system estimated the in-hospital mortality rates by 1.2-fold (linear analysis), whereas the P-POSSUM score was 4.5-fold (linear analysis). The OE ratios for 30-day mortality among the 6 hospitals defined by E-PASS correlated well with those defined by POSSUM: R=0.996, N=6, P<.0001. Similarly, the OE ratios for in-hospital mortality defined by E-PASS were also highly correlated with those defined by P-POSSUM:(R=0.929, N=6, P=.0075. CONCLUSIONS: The E-PASS scoring system may be useful in defining surgical quality and may be more accurate than existing systems in evaluating elective digestive surgery.     

Antithrombotic Effect of a New Glycoprotein IIb/IIIa Antagonist, SC-52012A: Studies in two Guinea-pig Thrombosis Models

The antithrombotic effect of a new platelet membrane GPIIb/IIIa antagonist, SC-52012A together with the 5-HT(2) receptor antagonist, ketanserin was studied in two guinea-pig thrombosis models. A segment of the femoral artery was occluded by a platelet-rich thrombus following photochemical reaction between rose bengal and green light which causes endothelial injury followed by platelet adhesion and aggregation at the site of photochemical reaction. SC-52012A, (1-10 μg/kg/min, intravenously (i.v.), dose-dependently prolonged the occlusion time of the artery. Ketanserin, (1 mg/kg, i.v.) or the cyclooxygenase inhibitor, aspirin (100 mg/kg, p.o.) produced no marked effect, but when ketanserin was combined with 3 μg/kg/min SC-52012A, the femoral artery occlusion time was strikingly greater than that produced by the same dose of SC-52012A. In the second model, an AV shunt was established between the carotid artery and the jugular vein and the platelet thrombus formed on a copper wire within the shunt was confirmed and quantified. SC-52012A (1-10 μg/kg/min) and ketanserin (1 mg/kg, i.v.), both produced a significant inhibitory effect on platelet thrombus formation in this model. As the expression of platelet membrane GPIIb/IIIa complex is the final step in the mechanism of platelet aggregation induced by most platelet agonists, inhibitors of this receptor complex may prove to be effective for the control of arterial thrombosis.     

Elevated Von Willebrand factor propeptide for the diagnosis of thrombotic microangiopathy and for predicting a poor outcome

Thrombotic microangiopathy (TMA) is associated with vascular endothelial cell injury and is sometimes linked with poor outcome. Von Willebrand factor (VWF) propeptide (VWFpp) is considered to be a marker of vascular endothelial cell injury. The plasma levels of VWF, VWFpp, and thrombomodulin (TM) were evaluated for their use in the diagnosis of TMA in 75 patients with TMA. There were 30 TMA patients with marked decreases in ADAMTS13 (TMA/ADAMTS13) and 45 without the decrease (TMA/other). The plasma levels of TM, VWF, and VWFpp values were significantly high in patients with TMA, especially TMA/other group. The plasma levels of TM and VWFpp were significantly high in non-survivor with TMA. In the TMA/other group, the plasma levels of VWFpp were negatively correlated with ADAMTS13 activity. The plasma levels of TM correlated with the renal function, but the plasma levels of VWFpp did not. A ROC analysis indicated that VWFpp and TM were useful markers for the prediction of a poor outcome. These findings suggest that VWFpp is an useful marker for the diagnosis of TMA and for the prediction of poor outcome.