Cone dysfunction and supernormal scotopic electroretinogram with a high-intensity stimulus

An unusual form of scotopic electroretinogram with a bright white stimulus, which consisted of a rectangular a-wave of normal amplitude and a b-wave of supernormal amplitude, was recorded in three patients with cone dysfunction. In addition to poor visual acuity, abnormal color vision and reduced amplitude of the photopic electroretinogram, these patients showed a 2-log unit elevation of the dark-adaptation threshold. Funduscopic examination and fluorescein angiography revealed fine granular pigment disturbances at the mascula. The relationship between the response of the dark-adapted electroretinogram versus stimulus intensity was unique to these patients. The b-wave thresholds were elevated by 1 log unit. The b-waves were reduced in amplitude and markedly delayed in implicit time to dim stimuli, but supernormal in amplitude and normal in implicit time to bright stimuli.Abbreviations GMP guanosine monophosphate     

Tachykinin receptors of the NK2 type involved in the acetylcholine release by nicotine in guinea-pig bladder.

1. The effects of guanethidine and tachykinins on nicotine- and electrical stimulation-induced cholinoceptor responses were studied in isolated urinary bladder from the guinea-pig. 2. Acetylcholine release and the contractile response stimulated by nicotine were partially reduced by a sympathetic nerve blocker, guanethidine. Neurokinin A (but not substance P methyl ester or senktide) enhanced both acetylcholine release and contraction by nicotine in the presence of guanethidine. 3. Frequency-contraction curves (1 to 50 Hz) for electrical field stimulation (EFS) were partially reduced by atropine (1 microM), and after desensitization to alpha,beta-methylene adenosine 5'-triphosphate, the atropine-resistant contraction to EFS was completely abolished. Guanethidine, the tachykinin antagonist [D-Arg1, D-Pro2, Trp7,9, Leu11]-substance P and application of neurokinin A or substance P did not change the contractile response to EFS. Preganglionic nerve stimulation (5 Hz and 20 Hz) also evoked a similar response to EFS and was not influenced at all by guanethidine or neurokinin A. 4. We conclude that the ability of nicotine to release acetylcholine is enhanced both by endogenous tachykinins (probably released from sympathetic nerves) and by exogenously applied tachykinins as a result of interaction with NK2 receptors in the urinary bladder.     

Spontaneous regression of gastric varices after iatrogenic injury to a gastrorenal shunt

We present a patient with gastric varices complicating portal hypertension caused by liver cirrhosis related to hepatitis C virus. The patient underwent balloon‐occluded retrograde transvenous obliteration. The gastric varices almost completely disappeared, without any sclerotic agent being used, after iatrogenic injury of the gastrorenal shunt at the time of the interventional procedure.     

Prefrontal cerebral activity during a simple “rock, paper, scissors” task measured by the noninvasive near-infrared spectroscopy method

We conducted a noninvasive near-infrared spectroscopy (NIRS) study using the game of rock, paper, scissors (RPS) as a simple neurocognitive task for the prefrontal cortex (PFC) in 15 healthy volunteers. We employed an opposite “to lose” RPS task coupled with a normal “to win” RPS task, since the former requires inhibition of behavior, one of the most important functions of the prefrontal cortex. During the NIRS examination, subjects had to present one of the three RPS hands in response to hands displayed randomly on a computer screen every 1.5 s, and were required to show hands that lose to the computer, or that beat the computer. We measured the relative concentrations of oxyhemoglobin (oxy-Hb) using the prefrontal probes of the NIRS system during the tasks. The increases in oxy-Hb during the “to win” RPS task were small, but were quite large and laterally dominant during the “to lose” RPS task. The difference between the two tasks might have been due to the participants’ cognitive conflict with losing on the RPS. We conclude that losing is better than winning on the RPS as a sensitive indicator in the NIRS examination of PFC.     

Airway troubles related to the double-lumen endobronchial tube in thoracic surgery

Purpose Several case reports indicate critical respiratory complications in relation to the double-lumen endobronchial tube (DLT). A prospective survey for the airway problems in using the DLT is presented. Methods One hundred adult patients undergoing thoracotomy for lung cancer were investigated. Tube malposition and airway obstruction were searched using a fiber-optic scope. The endobronchial cuff was positioned just below the trachcal carina while the trachea was intubated with a DLT (Rüsch). The distances of displacement, from the tracheal carina to the bronchial cuff, were measured during anesthesia using an epidural catheter, which had marks every 5 mm. The distances for correcting the tube position were measured at both the bronchial cuff and the level of the teethPaO₂,PaCO₂ andSPO₂ were also measured. Results Malposition (displacement over 5 mm from the correct position) was found in 42 patients, and 40 of them were in a withdrawal direction, occurring at the postural change and during one-lung ventilation, especially during manipulation of the lung hilum. Correcting distances at the level of the teeth were 15.3–3-times longer than those at the bronchial cuff. Airway deformities and gradual withdrawal of the bronchial cuff were found in association with surgical manipulation. Obstruction occurred at the tips of the tracheal tube in four patients and the bronchial tube in six patients, and at the tip of both in two patients. Hypoxemia (PaO₂<60 mmHg) occurred in four patients and hypercapnea (PaCO₂>60 mm Hg) in two patients. Conclusion Most of the DLT obstructions were associated with withdrawal malposition. Great attention to DLT displacement and airway deformity is advised.     

Interaction of CN-100, a novel non-steroidal anti-inflammatory drug, on biopolymers

Interaction of CN-100, a novel non-steroidal anti-inflammatory drug, with biopolymers were investigated. In collagen induced rat platelet aggregation, the inhibitory effect of CN-100 was almost equipotent as indomethacin (IM) but less potent than that of pranoprofen (PP). The effect of CN-100 on rat platelet aggregation induced by arachidonic acid (AA) was less potent than that of IM and PP. CN-100 inhibited rat platelet functions, serotonin release and malondialdehyde formation, induced by collagen more potently than those induced by AA. In heat-induced rat erythrocyte lysis and Ca2(+)-induced liposome aggregation, the inhibitory effect of CN-100 was less potent than IM but more than those of PP. CN-100 was inhibited with heat denaturation of BSA, and the effect was more potent than IM and PP. The metachromagy based on the binding of an azodye, HABA, to BSA was potentiated weakly by CN-100, but IM had no effect on it. CN-100 and IM increased the fluorescence of the binding of dansyl amide (site I probe) to BSA. These results support that there is considerable interaction between CN-100 and membrane protein, and this effect influences the membrane to increase its stability.     

Mechanisms of pinacidil-induced vasodilatation

The mechanism of the vasodilator effect of pinacidil was examined. Pinacidil (0.1–100 μM) inhibited the increases in cytosolic Ca²⁺ ([Ca²⁺]_i) and muscle tension due to norepinephrine in rat aorta. In contrast, a Ca²⁺ channel blocker, verapamil, inhibited the norepinephrine-stimulated [Ca²⁺]_i more strongly than the contraction. Higher concentrations of pinacidil (3–100 μM) inhibited the verapamil-insensitive portion of the contraction and [Ca²⁺]_i. An inhibitor of ATP-sensitive K⁺ channels, glibenclamide, antagonized the inhibitory effect of low concentrations ( 10 pM) of pinacidol. Pinacidil did not change the contraction induced by Ca²⁺ in vascular smooth muscle permeabilized with Staphylococcus aureus -toxin. Norepinephrine (in the presence of GTP), 12-deoxyphorbol 13-isobutyrate (in the absence of GTP), and treatment with GTP_γS potentiated the contraction of permeabilized smooth muscle induced by the addition of Ca²⁺. Pinacidil (100 μM) inhibited the potentiation due to GTP_γS or noepinephrine but not to phorbol ester. These results suggest that pinacidil has dual effects on vascular smooth muscle contraction. At lower concentrations (>0.1 μM), it decreases [Ca²⁺]_i, possibly by activating ATP-sensitive K+ channels. At higher concentrations (> 3 μM), it may additionally inhibit the receptor-mediated, GTP-binding protein-coupled phosphatidyl inositol turnover.