Rock and sediment dataset of petit-spots in the northwestern Pacific.

Rock and sediment samples were collected from petit-spots in the northwestern Pacific. The sampling was conducted using deep-submergence vehicle (DSV) Shinkai 6500 and its mother ship, research vessel (RV) Yokosuka during YK20-14S and YK21-07S cruises. The collected rock samples are basalt and peperite. Some of the basalts include small mantle xenoliths (∼3 cm in diameter). The dataset of rock and sediment samples from the petit-spots located on >130 Ma northwestern Pacific plate are presented herein. The peperites are a reaction product between petit-spot magma and wet sediment, and the mantle xenoliths are fragmented mantle materials transported by the petit-spot magmas. Therefore, the petit-spot samples are of significant importance to elucidate modification process of the surface condition by petit-spot magma and to characterize the deep lithospheric mantle. The dataset presented herein provides in a sense a unique insight into the whole Pacific plate just before its subduction beneath the Japan arc.

High doses of oseltamivir phosphate induce acute respiratory arrest in anaesthetized rats.

It has been reported that one of the serious adverse events after the treatment of oseltamivir phosphate (OP) for influenza patients is sudden death resulting from cardiorespiratory arrest. To investigate the aetiology of such an adverse consequence, we examined effects of OP (expressed as free base) on blood pressure and ventilation in anaesthetized rats with vagotomy. Intravenous OP (30-200 mg/kg) caused dose-dependent hypotension and bradycardia in spontaneously breathing animals. Concomitantly with changes in blood pressure, the tracheal airflow increased. The ventilatory rate hastened during the injection and then transiently slowed around 1 min. after the administration (transient hypopnea). Thereafter, it gradually returned to control. The hypopnea increased with increasing dose and ventilatory arrest occurred at 200 mg/kg. Intraduodenal OP (500-1000 mg/kg) provoked cardioventilatory arrest 72-218 min. after the injection. Oseltamivir carboxylate (100-200 mg/kg, i.v.), an active metabolite of OP, had no significant effect on ventilation and blood pressure. In artificially ventilated animals, intravenous OP caused slowing of the respiratory rate around 1 min. after the injection in a dose-dependent manner. This effect of OP waned in 5 min. after the administration. The amplitude of phrenic nerve discharge was not changed at lower doses (30-100 mg/kg). The phrenic nerve stopped to discharge immediately after higher doses (150-200 mg/kg). We demonstrated that OP causes central suppression of the respiratory function in rats and suggest a relationship between the OP-induced cardiorespiratory arrest and sudden death observed in influenza patients after taking OP.

M3-receptor activation counteracts opioid-mediated apneusis, but the apneusis per se is not necessarily related to an impaired M3 mechanism in rats.

AIMS: Morphine slows the respiratory cycle due to a predominant prolongation of inspiration (apneusis) by postponing the spontaneous termination of inspiration (inspiratory off-switching). The present study investigates whether the morphine-induced apneusis results from impairment of cholinergic mechanisms in the central respiratory network. MAIN METHODS: The efferent discharge was recorded from the phrenic nerve in artificially ventilated and anesthetized rats with vagotomy. All drugs were injected intravenously. KEY FINDINGS: The phrenic nerve displayed an augmenting discharge during inspiration and arrest of discharge during expiration in normal condition. Administration of morphine (0.3-10.0mg/kg) dose-dependently provoked apneusis characterized by a long-lasting, plateau inspiratory discharge of the phrenic nerve. It shortened the expiratory duration. Subsequent administration of physostigmine (0.1mg/kg) restored the morphine-induced apneusis to eupnea with a partial recovery of the augmenting inspiratory discharge. This modification of physostigmine was blocked by a non-specific muscarinic antagonist scopolamine (3.0mg/kg), leading to re-prolongation of inspiration. A similar antagonism was affected by an antagonist of M3 cholinergic receptors, 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, 1.0 and 10.0mg/kg) but not by an antagonist of M1 cholinergic receptors, pirenzepine (1.0 and 10.0mg/kg). SIGNIFICANCE: These results demonstrate that the activation of endogenous M3 cholinergic mechanisms counteracts the morphine-induced apneusis.