PubMed · 14786175
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A JENTZER. 1950-10-12. [Anesthesia].. https://pubmed.ncbi.nlm.nih.gov/14786175/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The novel guanidines N-(3,4-dimethoxy-2-chlorobenzylideneamino)-guanidine (ME 10092) and N-(3,4-dimethoxy-2-chlorobenzylideneamino)-N1-hydroxyguanidine (PR5) were recently reported to exhibit promising cardioprotective activities in myocardial ischaemia and reperfusion in rats. The current study investigated for the first time pharmacological effects of ME10092 in the primate, viz. the Cape baboon Papio ursinus. The effects of ME10092 (1 and 2 mg/kg doses) on the cerebral blood flow, heart rates and the systolic and diastolic blood pressure were investigated after intravenous injection to the baboon under anaesthesia. The cerebral perfusion effects of ME10092 were assessed using Single Photon Emission Computed Tomography according to the split-dose approach and 99mTc-hexamethyl-propylene amine oxime as brain perfusion tracer. The observation that the recovery times from the anaesthesia were unacceptably prolonged excluded doses beyond 2 mg/kg. The data indicate that no cerebral perfusion changes were induced at both the 1 and 2 mg/kg doses of ME10092. Both these doses of ME10092 showed blood pressure and heart rate effects, with the latter being more significant. Decreases in heart rate were seen directly after ME10092 administration reaching levels of about 20% for the 2 mg/kg dose and about 15% for the 1 mg/kg dose at around 6 min post drug administration. A transient decrease in both systolic and diastolic blood pressure was observed for the higher dose. The blood pressure data further suggest an attenuation of the anaesthesia induced increase in pressure usually present in non-intervention studies. ME10092 clearly exhibits mycocardial effects in the non-human primate, similar to the effects previously observed in the ischaemia-reperfusion rat model, where ME10092 showed strong protection.
Despite the widespread clinical use of cryotherapy, there is only limited and inconsistent data on application times. The aim of this study was to determine the changes in tissue temperature and the duration of this effect. In this experimental study, five adult dogs were used. A cold gel pack (10 x 20 cm) was applied transversally over the right leg femoral region. Temperatures were recorded simultaneously: rectal by a mercury thermometer; right leg skin by probe of Nihon Kohden 6000 polygraph; and right leg subcutaneous, intramuscular, and periosteal, and left leg intramuscular temperatures by a fluorooptic biomedical fiber optic (0.6 mm diameter) thermometer connected to a computer system. Total system accuracy was 0.01 degrees C. Cold gel packs were applied for 10, 15, 20, 25, and 30 minutes duration. The results can be summarized as cooling and rewarming data. 1) The superficial tissues such as skin and subcutaneous demonstrated the most rapid and profound cooling effect. The deeper tissues such as bone and muscle exhibited a smaller and more gradual decline in temperature. 2) There was a prolonged rewarming period in all tissues after the removal of the cold gel pack but this period was longer in deeper tissues. According to cold gel pack application time, the rewarming time in intramuscular layers to baseline or plateau temperatures was about: 60 +/- 3 minutes for 10 minutes application, 100 +/- 4 for 15, 130 +/- 5 for 20, 140 +/- 7 for 25, and 145 +/- 8 for 30. It can be concluded from these results that with increased cold gel pack application time, deep tissue temperature decreased and the duration of cooling effect increased. However, the data indicated that the length of application time and the duration of cooling effect were not linearly related. Especially after 20 minutes of application this ratio decreased progressively. There may be implications of these results for clinical practice.
Protease-activated receptor-2 (PAR-2) plays an extensive role in the regulation of digestive exocrine secretion. The present study examined whether PAR-2-related peptides could modulate tear secretion in rats and analyzed the underlying mechanisms. SLIGRL-NH(2), a PAR-2-activating peptide (PAR-2-AP) derived from mouse/rat PAR-2, when administered i.v. in combination with amastatin, an aminopeptidase inhibitor, evoked tear secretion, whereas LRGILS-NH(2), a PAR-2-inactive reversed peptide, had no such effect. In contrast, LSIGRL-NH(2), a partially reversed peptide known to be inactive with PAR-2, caused tear secretion equivalent to the effect of SLIGRL-NH(2). SLIGKV-NH(2), a human-derived PAR-2-AP, also induced significant tear secretion though to a lesser extent, whereas neither VKGILS-NH(2), a reversed peptide, nor LSIGKV-NH(2), a partially reversed peptide, produced any secretion. In desensitization experiments, after the first dose of SLIGRL-NH(2), the second dose of SLIGRL-NH(2) produced no tear secretion, whereas the response to LSIGRL-NH(2) was only partially inhibited by preadministration of SLIGRL-NH(2). Preadministration of LSIGRL-NH(2) abolished the response to subsequently administered LSIGRL-NH(2) but not SLIGRL-NH(2). The tear secretion induced by LSIGRL-NH(2) but not by PAR-2-APs was blocked by atropine or hexamethonium. Mast cell depletion due to repeated doses of compound 48/80 did not alter the effect of SLIGRL-NH(2) or LSIGRL-NH(2). Finally, IGRL-NH(2), a possible core structure of LSIGRL-NH(2), triggered tear secretion in an atropine-reversible manner. Our findings suggest that the PAR-2-APs SLIGRL-NH(2) and SLIGKV-NH(2) cause tear secretion, most likely via PAR-2 and that LSIGRL-NH(2), a PAR-2-inactive peptide, and IGRL-NH(2), its key structure, trigger tear secretion by stimulating parasympathetic nerves via an unidentified target molecule.