The use of propofol for induction of anaesthesia in dogs premedicated with acepromazine, butorphanol and acepromazine-butorphanol.

Cardiovascular, pulmonary and anaesthetic-analgesic responses were evaluated in 18 male and female dogs to determine the effect of the injectable anaesthetic propofol used in conjuction with acepromazine and butorphanol. The dogs were randomly divided into three groups. Dogs in Group A were premeditated with 0.1 mg/kg of intramuscular acepromazine followed by an induction dose of 4.4 mg/kg of intravenous propofol; Group B received 0.2 mg/kg of intramuscular butorphanol and 4.4 mg/kg of intravenous propofol; dogs in Group AB were administered a premeditation combination of 0.1 mg/kg of intramuscular acepromazine and 0.2 mg/kg of intramuscular butorphanol, followed by induction with 3.3 mg/kg of intravenous propofol. The induction dose of propofol was given over a period of 30-60 seconds to determine responses and duration of anaesthesia. Observations recorded in the dogs included heart and respiratory rates, indirect arterial blood pressures (systolic, diastolic and mean), cardiac rhythm, end-tidal CO, tension, oxygen saturation, induction time, duration of anaesthesia, recovery time and adverse reactions. The depth of anaesthesia was assessed by the response to mechanical noxious stimuli (tail clamping), the degree of muscle relaxation and the strength of reflexes. Significant respiratory depression was seen after propofol induction in both groups receiving butorphanol with or without acepromazine. The incidence of apnea was 4/6 dogs in Group B, and 5/6 dogs in Group AB. The incidence of apnea was also correlated to the rate of propofol administration. Propofol-mediated decreases in arterial blood pressure were observed in all three groups. Moderate bradycardia (minimum value > 55 beats/min) was observed in both Groups B and AB. There were no cardiac dysrhythmias noted in any of the 18 dogs. The anaesthetic duration and recovery times were longer in dogs premeditated with acepromazine/butorphanol.

[Anoxic-ischemic encephalopathy and myoclonic status epilepticus]. / Encefalopatia anossico-ischemica e stato di male epilettico mioclonico.

The Authors present a case of post-anoxic coma accompanied by myoclonic status. They describe the clinical picture and instrumental data. The outcome seems to be determined by the serious anoxic-pathological damage rather than the myoclonic jerks. They discuss the problem concerning preventive treatment by use of thiopental sodium (T.P.S.) in such cases.

A lamellar complex of lecithin and poly-L-tyrosine.

Complexes of poly-L-tyrosine (PT) with dipalmitoyllecithin, synthetic, (DPL) and with egg lecithin (EL) have been obtained by precipitation from methanol-water solutions. Chemical analysis indicates that both lecithins bind PT up to a limiting ratio of about 4 tyrosine residues/lecithin molecule. DPL-PT complexes have a lamellar structure closely resembling lecithin itself. In fact, DPL and DPL-PT lamellae have very nearly the same thickness as precipitated from methanol-water, although their swelling behavior on resuspension in pure water is different. The complexes crystallize in the form of hexagonal platelets, some monolayers and some with terraced spiral growths, with a thickness of 50-55 A. In X-ray and electron diffraction they yield sharp reflections at 4.14 A which are characteristic of hexagonal packing of phospholipid paraffinic chains. The order-disorder transition temperature of this crystalline lattice, determined by differential scanning calorimetry, is somewhat higher in the complex than in pure DPL. Physical models consistent with these observations are discussed.

Crystallization of DNA from dilute solution.

Hexagonal platelet crystals about 1 mu across and about 150 A thick have been precipitated by the addition of ethanol to solutions of ultrasonically degraded, salmon sperm DNA in sodium cacodylate buffer. X-ray powder diffraction patterns from concentrated slurries of these crystals in mother liquor show intense rings at 23.9 A and at about 3.4 A; the former arise from lateral packing and the latter from an axial periodicity of the DNA helix. Evidence is presented to indicate that native DNA helices crystallize by chain folding and that no irreversible denaturation results from the crystallization process.