Central and local actions of opioids upon reticulo-ruminal motility in sheep

The effects of opioids and naloxone on cyclical forestomach motility were determined in anaesthetized and conscious sheep. To assess central or peripheral opioid actions, differential routes of administration were used. Possible dynamic effects along the innervating vagovagal reflex arc were investigated electrophysiologically at the cervical level of the vagus nerve. Further, direct influences on the smooth muscle were evaluatedin vitro on isolated longitudinal reticular strips. Additionally, the effects of some spasmogenic agents were studied for comparative purposes. In anaesthetized sheep, opioids depressed in an identical manner both the amplitude of spontaneous cyclical contractions and contractions evoked by electrical stimulation of the distal end of the cut cervical vagus. In conscious sheep, low doses of normorphine and loperamide inhibited frequency and amplitude centrally (20 g/kg and 4 g/kg via carotid artery respectively), whereas locally higher dose levels (200 g/kg and 10 g/kg via coeliac artery respectively) affected only the amplitude of cyclical contractions. Furthermore the opioid peptides Leu-, Met-enkephalin and [D-Ala²-Met⁵]-enkephalinamide preferentially depressed the amplitude of cyclical motility most efficiently if administrated via the coeliac artery. These results indicate the presence both of a central opioid action depressing frequency and amplitude and of a local opioid action depressing only the amplitude of cyclical reticulo-ruminal motility. Opioids did not alter the resting discharge of afferent tension units and similarly failed to modulate tone of reticular stripsin vitro, suggesting that the opioids act locally on the intramural neuronal plexus, possibly by diminishing the output of excitatory transmitter. Whether substance P could play a role as a vagal excitatory transmitter besides the classically implicated acetylcholine has been discussed. The central opioid mechanism is probably not situated within the gastric centres but elsewhere in the brain. Naloxone ( 100 g/kg, jugular vein) stimulated the frequency of cyclical ruminal motility only in well-defined experimental conditions, probably via a central mechanism.     

A fossil noctuid moth egg from the late cretaceous of eastern north america

A moth egg assignable to the family Noctuidae (Lepidoptera) is described from 75-million-year-old sediments from Martha's Vineyard, Massachusetts. This sample, which extends the fossil record of this farnily and modern heteroneuran moths back to the Cretaceous, may provide insight into the coevolution of moths and flowering plants, as well as have implications for the evolution of bats.     

Spasmodic tremor and possible magma injection in long valley caldera, eastern california

Intensive microearthquake swarms with the appearance of volcanic tremor have been observed in the southwest part of Long Valley caldera, southeastern California. This activity, possibly associated with magma injection, began 6 weeks after several strong (magnitude 6+) earthquakes in an area south of the caldera and has continued sporadically to the present time. The earthquake sequence and magmatic activity are part of a broad increase in tectonic activity in a 15,000-square-kilometer region surrounding the "White Mountains seismic gap," an area with high potential for the next major earthquake in the western Great Basin.     

Congenital esophagotracheal fistula as the cause of bloat in a calf

A four day old Holstein calf was presented with a history of recurrent free gas bloat. An exploratory laparotomy was performed and no abnormalities were discovered in the gastrointestinal tract. An esophagotracheal fistula was suspected and confirmed by endoscopy. Surgical correction was performed by ligating the tubular connection between the trachea and esophagus and suturing closed the defects in these structures.     

Examination of the origin of increased equine serum alkaline phosphatase concentrations

Serum alkaline phosphatase activity was found to be increased in 32.6% of equine samples analyzed at the Ontario Veterinary College over an 18 month period. An attempt was made using sensitivity to L-phenylalanine and heat to identify the origin of increased serum alkaline phosphatase isoenzymes present in 44 clinical cases. No difference in sensitivity to either procedure was observed for serum alkaline phosphatase from groups of foals and horses representing different clinical problems. Alkaline phosphatase of osseous tissue origin appeared to be the major source of activity for each group of animals reported.     

Comparison of plasma aldosterone concentration among clinical status groups of dogs with chronic heart failure

The plasma aldosterone concentration (PAC) among clinical status groups of 23 dogs with chronic heart failure was compared at various times after diagnosis of the problem. Eighteen dogs admitted in New York Heart Association (NYHA) class IV clinical status had significant elevations in PAC (P<0.0001), when compared with clinically normal dogs. Five dogs admitted in NYHA class III status and 4 dogs that responded with a change to NYHA class III status had significant elevations in PAC (P<0.01), when compared with clinically normal dogs. In patients with NYHA class IV status, the PAC was significantly greater (P<0.01) than in patients in NYHA class III status. For patients with the poorest prognosis, ie, severe signs of NYHA class IV status, the PAC was not markedly different, when compared with that for patients with a favorable prognosis, ie, recent onset of signs of NYHA class IV status. Patients treated with captopril had significantly lower PAC after therapy (P<0.01), whereas patients treated with hydralazine had significantly higher PAC (P<0.05) after therapy. It was concluded that heart failure in the dog increases PAC, most likely because of renin-angiotensin-aldosterone-system activation, and that the increase is related directly to the clinical status of the patient. Further, it was concluded that treatment of dogs in heart failure with captopril causes a decrease in circulating PAC, whereas treatment with hydralazine causes an increase in circulating PAC.