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H L Borison

Publications and source records attributed to H L Borison.

72 records · Page 4Linked to original sources
PubMed1970

Persistence of the cardio-inhibitory response to brain stem ischaemia after destruction of the area postrema and the dorsal vagal nuclei.

1. In anaesthetized cats, in which the carotid arterial bifurcation had been denervated and the spinal cord transected at the cervical level, reversible bradycardia mediated by the vagus nerves was elicited by temporary arrest of the cranial circulation. Methoxamine was infused intravenously to maintain peripheral vascular resistance, and artificial ventilation was given to avert systemic asphyxia.2. The bradycardia persisted in cats subjected to one or more of the following acute surgical procedures: left vagotomy, mid-collicular decerebration, decerebellation, bulbar transections at the acoustic striae and inferior fovea, and destruction of the area postrema and the underlying dorsal vagal nuclei. Ischaemia-induced bradycardia was invariably abolished after bilateral vagotomy or the administration of atropine.3. Bradycardia could not be elicited by electrical stimulation of the dorsal vagal nuclei, but was evoked by stimulation of deep structures in the vicinity of the nucleus ambiguus even after destruction of the dorsal vagal nuclei.4. Simultaneous application of ischaemia and electrical stimulation of the medullary cardio-decelerator locus produced convergent occlusion of the vagal response. The effect of ischaemia was inhibited by stimulation of a neighbouring region in the medial reticular formation. These interactions indicate that an interneuronal link is involved in the mechanism of ischaemia-induced bradycardia.5. It is concluded that the cardio-decelerator response to ischaemia is initiated upstream to the primary efferent vagal motor neurones and that the cardio-inhibitory fibres do not originate in the dorsal vagal nuclei.

Animals↗
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Phylogenic and neurologic aspects of the vomiting process.

Hindbrain morphology is compared in a variety of animals representing species that vomit and those that do not. Special attention is given to the nucleus of the tractus solitarius (NTS) and its synaptic connections with surrounding structures. The role of the area postrema is examined from the standpoints of containing the chemoreceptor trigger zone (CTZ) for vomiting, of its functional relationship to the blood-brain barrier, and of its significance as part of the circumventricular organ system. A survey is made of the manifold behavioral contributions of NTS to cardiovascular and respiratory regulation, appetite control, arousal, water balance, and digestive and neuroendocrine functions. An overview is presented of neurochemical distribution in the brain stem with respect to aminergic, cholinergic, and peptidergic substances. Finally, causes and prevention of vomiting are discussed in light of the above considerations.

Animals↗
PubMedDate not supplied

Antiemetic activity of N-methyllevonantradol and nabilone in cisplatin-treated cats.

The comprehensive emetic response to xenobiotics can be quantified by monitoring the physiological forces which effectuate vomiting. A unique sequence of thoracic pressure pulses, generated by the somatic muscles of ventilation, can be measured by means of a central venous catheter. This unambiguous emetic endpoint is used to record emetic latency, repetitions and duration of action, all on an established time base and dependent of stomach content. Deslanoside (160 micrograms/kg) produced emesis in 15 cats beginning in 4.4 +/- 1.9 min (mean +/- S.D.). Subsequent emetic episodes were related in time in a log-linear but biphasic manner. Cisplatin (7.5 mg/kg) had an emetic latency of 71 +/- 18 mn in 7 cats. Additional events also had a long-linear temporal relationship for up to 400 min. This quantified emetic profile of cisplatin served as a measure for assessing antiemetic activity of N-metyllevonantradol (Pfizer), nabilone (Lilly) and prochlorperazine. The cannabinoids all evinced dose dependent antiemetic activity in terms of either complete protection, or increased latency to the first emetic episode and reduced number of episodes in those animals not completely protected. By comparison prochlorperazine afforded only minimal protection.

Animals↗
PubMedDate not supplied

Early toxicity of recombinant interleukin-2 in cats.

Studies were conducted in cats to determine whether this species could serve as an animal model for the therapeutic toxicity of recombinant interleukin-2 in humans, and to establish the role of the area postrema in the causation of recombinant interleukin-2-induced vomiting. Injections of recombinant interleukin-2 (3.6 x 10(6) IU/kg, i.m.), given once every 24 hr for one to three days, evoked repeated vomiting in 4 out of 6 area postrema intact cats and in 3 out of 3 area postrema-ablated cats. These results suggest that the area postrema is not essential for the emetic action of recombinant interleukin-2. In anesthetized intact cats, no remarkable changes in ventilation, blood pressure, heart rate or blood pH were observed over 4.5 to 54 hr of continuous physiological recording after i.v. injections of recombinant interleukin-2 to a total dose as high as 27 x 10(6) IU/kg. Cat lymphocytes responded appropriately to the cytokinetic action of human recombinant interleukin-2.

Animals↗