Biochemical and pathological findings on sheep and calves dying of experimental cerebrocortical necrosis.

For observing biochemical and morphopathological changes in experimental cerebrocortical necrosis, 6 sheep and 6 calves were given amprolium (600 mg/kg/day). All of the amprolium-dosed animals showed neurological signs and died on days 35 to 57 after the onset of daily administration. They were pathologically confirmed as cerebrocortical necrosis. Total thiamine levels in blood and tissues were markedly reduced at death. Blood total thiamine level decreased significantly on day 7 of amprolium administration, and reached to the level as low as that seen at death about 2 weeks before the onset of abnormal electroencephalograms. Significant decrease in a thiamine-dependent enzyme, erythrocyte transketolase activity, and increase in thiamine pyrophosphate effect were detected about 2 weeks before the onset of abnormal electroencephalograms. Pathological changes and cerebral autofluorescence observed under ultraviolet light were also examined at death.

Biochemical and pathological observations on sheep showing various clinical manifestations of experimental cerebrocortical necrosis.

For observing chronological changes of biochemical and pathological aspects in experimental cerebrocortical necrosis, 14 sheep were given amprolium (600 mg/kg/day), and killed at various clinical stages. At the onset of abnormal electroencephalograms, total thiamine concentrations in the cerebrum, liver, heart and blood were reduced significantly. After anorexia was noted, total thiamine concentrations in them did not decrease further as symptoms developed severely. Autofluorescence and necrotic lesions in the cerebral cortex were observed in animals killed one day after the onset of abnormal electroencephalograms.

Sudden cardiac death in calves with experimental heavy infection of Strongyloides papillosus.

For obtaining the preliminary data on the pathogenesis of sudden death in calves naturally heavily infected with Strongyloides papillosus, we monitored 8 Holstein calves experimentally infected with the larvae on electrocardiographic and pneumographic changes. Six calves died suddenly on days 11 to 17 after infection. Sinus tachycardia had been recorded continuously since 1 to 6 days before death. Heart rates increased gradually until death. Since 1 or 2 days before death, various patterns of tachyarrhythmia and bradyarrhythmia had been observed among patterns of sinus tachycardia. Arrhythmias included serious ventricular premature beat, paroxysmal ventricular tachycardia, complete atrioventricular block and so on. The terminal pattern observed suddenly in all of the cases was ventricular arrhythmias consisting of serial ventricular tachycardia, flutter and fibrillation, which were followed by respiratory arrest. Abnormal pneumograms were not obtained before the terminal ventricular fibrillation. Two of 8 calves recovered from the infection, only one of which showed sinus arrest and the second degree of atrioventricular block transiently. We concluded that calves heavily infected with the larvae died due to sudden cardiac arrest.

Electroencephalographic observation on sheep and cattle with experimental cerebrocortical necrosis.

Nine Suffolk sheep and 4 Holstein cattle were employed to observe electroencephalographic changes in experimental cerebrocortical necrosis. Amprolium (600 mg/kg/day) alone was given intraruminally 6 sheep and 4 cattle, all of which showed neurological signs and abnormal electroencephalograms. Both amprolium and thiamine (200 mg/day) and thiamine (50 mg/day) alone were given 2 and 1 sheep, respectively, as controls, which did not show any abnormal signs. Abnormal electroencephalograms included continuous slow waves and long-lasting spindles, both of which appeared diffusely and were seen subclinically or with neurological signs. The spindles consisted of slow waves or sharp- (or spike-) and-slow-wave complexes with or without convulsive seizures even during the convulsion stage. Conversely, the seizures occurred with the spindles or slow waves.

Intrapressures and oxygen contents of air sacs at deformation of expiratory-oxygen-concentration curve in chickens.

Intrapressures and oxygen contents of air sacs were measured in adult hens showing spontaneous deformation episodes of expiratory oxygen curve. Differential pressures between air sacs were also determined. The deformation resembled that seen at the time of uneven pulmonary ventilation in mammals. To analyse the mechanism responsible for genesis of the deformation episode, an airway was obstructed in the unilateral extrapulmonary primary bronchus by a small balloon. This maneuver caused the expiratory oxygen curve to deform and values of intrapressure and oxygen content of air sacs to change similarly to those of the spontaneous deformation episode. Some of the latter changes in intrapressure and oxygen content caused by obstruction in the left bronchus were different from those caused by obstruction in the right one. The side of airway obstruction at the spontaneous deformation episode could thus be deduced by this result. It was hypothesized that respiratory air from the lung-air sac system on the obstructed side might have flowed through the clavicular air sac to the primary bronchus on the non-obstructed side and vice versa. This condition might induce large respiratory fluctuations of oxygen content in the clavicular air sac, and would be responsible for plateau inclination (deformation) of the expiratory oxygen curve.

Breath-by-breath analysis of expiratory gas concentration in chickens.

Expiratory oxygen and carbon-dioxide concentration were analysed breath by breath in order to examine their wave forms in adult awake hens restrained in various postural positions, including supine, prone and sitting positions. Expired gas was collected at the nostril in almost all the hens. In the sitting position free from vocalization, feeding, drinking, panting, and restlessness, hens showed various forms of stable pattern of oxygen-gas curves. These forms were classified into three types, or the ascending, flat and descending types, with respect to the plateau inclination. The waves of carbon-dioxide were not always a mirror image of those of oxygen. The rate of occurrence of each type varied with the hen's postural position. The wave form was altered with the experimental body-rotation of the hen. When placed between the deflections of stable pattern, the episodes of wave deformation resembling that seen at the time of uneven pulmonary ventilation in mammals could frequently be observed in any hen's posture examined. Cardiogenic oscillation appeared on the plateau of expired-gas curves.

An analysis on the mechanism responsible for genesis of deformation of expiratory-gas-concentration curves in chickens.

Phenomena associated with a deformation of short-time occurrence and noticed on concentration curves of tidal O2 and CO2 were examined in adult hens sitting quietly in a cage or suspended in prone position. During the episode of deformation, a decrease in arterial oxygen-gas tension was apparent. It was associated with a slight increase in arterial carbon-dioxide-gas tension and a slight acidic shift of arterial blood pH. The episode was associated with increases in intrapressure of the interclavicular and bilateral abdominal air sacs. The tracheal expiratory-gas flow changed in pattern. Hypoventilation due to reduction in tidal volume or respiratory rate could not be detected during the episode. The episode was suddenly terminated at the hen's body movement induced spontaneously or by pinching the comb, at coughlike activity or at no obvious change in behavior in a quietly resting position. Deformation similar to the spontaneous one could be induced by 3 ml-water flushing into the trachea or 0.1% methacholine aerosol inhalation. The mechanism responsible for the genesis of deformation was discussed. It was presumed to be based upon some mechanism, such as mucous accumulation in the lung, rather than upon the pulmonary smooth-muscle contraction.

Mouth breathing in chickens under rebreathing conditions, cervical vagotomy of heat load.

By recording the lower beak movement, open-mouth breathing was monitored in adult hens restrained in a supine position with the cannulated trachea under rebreathing conditions, bilateral cervical vagotomy or heat load. Tidal volume and respiratory carbon-dioxide and oxygen contents were recorded simultaneously. The beak movement can be a significant indication of hypercapnia and/or increase in respiratory CO2 content, but not of hypoxia or decrease in respiratory O2 content. Vagotomy causes big oscillatory movements of the beak, which do not mainly depend on hypercapnic hypoxia induced by the vagotomy. If the dysfunction of the vagus is aggravated progressively, it will be unable for the pattern and amplitude of beak movement to be any differential indication of this dysfunction from hypercapnia and/or increase in respiratory CO2 content seen at respiratory failure. Two patterns of beak movement are noticed. One appears at an early stage of beak movement and at a certain direct level superimposed with or without small beak-oscillation. The other indicates a bigger oscillatory beak movement than the former. This oscillatory movement is synchronous with the inspiration after vagotomy and hypercapnia. This is the case with hyperthermia at a remarkably high breathing frequency. The amplitude of beak movement is not always proportional to the tidal volume. The onset and end of inspiration cannot precisely be indicated by those of a beak movement.

Electrocardiographic observation on goats with urea-ammonia poisoning and a consideration on the main cause of death.

Changes in electrocardiograms, blood pressure, pH, and partial pressure of gases (Po2 and Pco2) in arterial blood were studied in goats poisoned by urea or ammonium compounds under spontaneous and artificial respiration and in nonconvulsive state. Abnormal electrocardiogram patterns, such as ventricular flutter, ventricular premature beat, atrioventricular dissociation, depression of ST-segment and sinus tachycardia, were all observed after the occurrence of tetanic convulsion. The electrocardiogram pattern seen at the respiratory arrest showed sinus or supraventricular tachycardia; respiratory arrest preceded cardiac arrest in all the goats, but one. Blood pressure was markedly elevated, accompanied with tetanic convulsion. Po2 decreased gradually and the level was below 30 mm Hg (37.0 degrees C) at respiratory arrest and the final opisthotonus. Artificial respiration starting at the final opisthotonus could delay the cardiac arrest. Under nonconvulsive urea-poisoning with gallamine triethiodide and with artificial respiration of air or a mixture of air and oxygen to elevate the Po2 level, changes of electrocardiogram, blood pressure, and Po2 were similar to those seen under convulsive urea-poisoning. The main cause of death was discussed and presumed to be respiratory and cardiovascular failure.

Insulin-induced hypoglycemia and the electroencephalogram in goats.

The effect of insulin-induced hypoglycemia on the cortical electroencephalogram was examined in adult goats and kids. Adult goats were injected subcutaneously with 8 or 12 units/kg of insulin or intravenously with 1.2 to 10 units/kg. From a certain level between 15 and 25 mg/dl of blood glucose downwards, marked slowing of electroencephalogram was evident. When the blood glucose level was below 15 mg/dl, abnormal behaviors severer than lassitude appeared. They included inability of standing, twitching of face muscles, writhing, stupor and severe twitching of the head. No tetanic convulsions were observed in the present 8-hour experiments. When kids were injected subcutaneously with 8 units/kg of insulin, they showed the same relations among blood glucose level, electroencephalogram and behavior as the adult goats. They manifested abnormal behaviors, including tetanic convulsions.

Ammonia absorption from the rumen to the systemic circulation with urea poisoning in goats.

To confirm the transfer of ammonia leaking from the rumen content via the liver to the perid by laparotomy. When ammonia leakage from the hepatic vein occurred, it was followed by an increase in ammonia concentration in the jugular vein. There were increases of ammonia concentration in the intestinal vein and in the thoracic duct after urea drenching. These increases suggested neither trapping ammonia in the peritoneal fluid nor responsibility for increases of ammonia in the systemic circulation, respectively. At times when respiration ceased due to urea poisoning, the peritoneal fluids wee in the fluid. The hypothesis of the peritoneal cavity-thoracic duct route of ammonia absorption, presented by some of previous workers on urea toxicity, was not supported in the present study.