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Cardiotrophin-1 (CT-1), a member of the interleukin-6 superfamily of cytokines, possesses hypertrophic actions and atrial natriuretic peptide (ANP)-producing activity in vitro. The goal of our study is to elucidate whether CT-1 affects the cardiovascular system in vivo. Intravenous injection of CT-1 (4–100 μg/kg) in conscious rats evoked significant declines in blood pressure and reflex increases in heart rate (HR) in a dose-dependent manner. CT-1 induced no significant change in cardiac output (from 260.7 ± 11.0 to 264.7 ± 26.6 ml ⋅ min− 1 ⋅ kg− 1, P = not significant), which was compatible with the results from isolated perfused rat hearts; HR, change in pressure over time, left ventricular developed pressure, and perfusion pressure were unaffected. Northern blot and RT-PCR analyses revealed that CT-1 increased expression of inducible nitric oxide synthase (iNOS) in lung and aorta but not in heart or liver. Pretreatment with aminoguanidine, a specific iNOS inhibitor, inhibited both iNOS mRNA production and the depressor effect of CT-1. Interestingly, CT-1 increased ventricular expression of ANP and brain natriuretic peptide (BNP). The data demonstrate that CT-1 elicits its hypotensive effect via a nitric oxide-dependent mechanism and that CT-1 induces ANP and BNP mRNA expression in vivo.

We analyzed the effect of a new volatile anesthetic, sevoflurane (2%-5% in oxygen) on the electroencephalogram (EEG) of the neocortex, amygdala, and hippocampus, cortical somatosensory evoked potential (SEP), and brainstem reticular multiunit activity (R-MUA) in cats. Sevoflurane suppressed the background activity of the neocortex more than the amygdala and hippocampus. With increasing concentration of sevoflurane, the cortical EEG progressed from high-amplitude slow waves to a suppression-burst pattern, which was followed by an isoelectric pattern and then spikes with isoelectricity. The amplitude of the SEP was augmented and the R-MUA was suppressed by sevoflurane in a dose-related manner. Repetitive peripheral electrical stimulation induced generalized seizures at 5% sevoflurane in 2 of 13 cats. These results suggest that sevoflurane suppresses the background central nervous system electrical activities in a dose-related manner, leaving the reactive capabilities facilitated at deep anesthesia.

2017

The location of a catheter's tip in the bronchi may be determined using a stethoscope and an audible sound that has a frequency of 558 Hz and a sound pressure of 136 dB for the adult. The device is easy and safe to use, and has been used in a broad range of patients for over 4 yr without sequelae.

The lumbar sympathetic ganglia and their surroundings were examined anatomically in 19 human cadavers. The locations of the ganglia on the lumbar vertebral column at the level of the second and third lumbar vertebral bodies were analyzed statistically using a "ganglion score". The ganglia were most frequently found at the level of the lower third of the second lumbar vertebra, at the L2-3 interspace, and at the level of the upper third of the third lumbar vertebra on both the right and left sides. The points at which the sympathetic chain and the lumbar arteries crossed were at the middle third of the vertebral body in both the second and third lumbar vertebra. These results suggest that the most suitable point for placement of the tip of the needle used for chemical lumbar sympathectomy is not the midpoint of a vertebral body, but rather the lower third of the second vertebral body or the upper third of the third vertebral body.

In helically cut strips of dog cerebral, mesenteric, and femoral arteries contracted with prostaglandin(PG)F2 alpha, trimethaphan (10(-5)-10(-3)M) caused a dose-related relaxation that was not influenced by atropine, propranolol, diphenhydramine, cimetidine, aminophylline, or indomethacin. Trimethaphan-induced relaxation was greater in extracerebral than in cerebral arteries. The relaxation was greater in phenylephrine-contracted arteries than in PGF2 alpha-contracted arteries. On the other hand, hexamethonium did not relax the arteries. Trimethaphan (10(-4)-10(-3)M) shifted the dose-response curve for norepinephrine in mesenteric arteries to the right, but failed to influence the contractile response to 25 mM KCl. Treatment with trimethaphan (10(-4)-10(-3)M) protected alpha-adrenergic receptors from persistent blockade by phenoxybenzamine. Trimethaphan (10(-7)-3 X 10(-6)M) and hexamethonium (3 X 10(-8)-10(-6)M) significantly attenuated the contractile response of mesenteric arteries to nicotine in a dose-dependent manner, but did not alter the response to transmural electrical stimulation. The antinicotinic potency of trimethaphan was approximately one-fourth that of hexamethonium. It is concluded that, unlike hexamethonium, trimethaphan acts directly on vascular smooth muscle to induce vasodilation, more prominently in extracerebral arteries than in cerebral arteries. In high concentrations, trimethaphan appears to possess an alpha-adrenergic blocking action.