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Biomedical subjects

H L Borison

Publications and source records attributed to H L Borison.

At least 37 records · Page 2Linked to original sources
PubMed1983

Open-loop comparison of carotid sinus reflex respiratory and circulatory effects in cats.

Isolated control of pressure in the carotid sinus was exercised bilaterally by means of pump-driven autoperfusion in anaesthetized heparinized cats breathing 100% O2. In cats with vagus nerves intact, a rise of intrasinus pressure resulted in a non-adapting fall in arterial blood pressure and a short-lasting depression in tidal volume and frequency of breathing that adapted fully in the steady state. Vagotomy increased the steady-state gain of the intrasinus pressure-vasodepressor relationship and resulted sometimes in a measurable sustained inhibition of breathing, following its initial adaptation, at the upper levels of intrasinus pressure tested. Pharmacological stabilization of the blood pressure with the use of guanethidine plus phenylephrine did not detectably affect the adapting character of the sinus reflex respiratory response. Denervation of the carotid sinuses abolished all responses previously evoked by shifts of intrasinus pressure. It is concluded that the reflex effects of carotid sinus autoperfusion are produced by selective activation of the baroreceptors and that the respiratory adaptation results from signal processing in the central nervous system different from the processing involved in the non-adapting vasodepressor effect.

Adaptation, Physiological↗
PubMed1983

A 1983 neuropharmacologic perspective of space sickness.

Space sickness is generally considered a variant of motion sickness although not fully proved as such. Understanding space sickness requires objective and quantitative characterization of the disorder. Vomiting is a quantifiable physiological event performed by the respiratory muscles which generate the pressures that evacuate the gut. Vomiting from all causes is coordinated by the vomiting center in the medulla oblongata. The emetic chemoreceptor trigger zone (CTZ) in the area postrema is thought to be an indispensable element in the afferent pathway of motion sickness. About 30 potential neurotransmitters exist in the vomiting control mechanism which includes at least eight chemical transmission steps through the reflex pathway of motion sickness. Individual synaptic transmitters do not likely mediate specific functions, but particular combinations of those transmitters might well serve distinct functions. Adaptation to the cause of space sickness probably results from readjustment of a cerebellar circuit or of a humoral factor acting on the CTZ, rather than from stimulus-receptor desensitization. Space sickness must, for purposes of investigation, be treated as a unique disorder engendered by weightlessness until proved equivalent to any emetic syndrome that occurs on earth.

Adaptation, Physiological↗
PubMed1983

Respiratory and cardiovascular depressant effects of nabilone, N-methyllevonantradol and delta 9-tetrahydrocannabinol in anesthetized cats.

Drug effects were examined in cats anesthetized with a mixture of pentobarbital and barbital injected i.p. Respiratory observations were analyzed according to effects produced on 1) chemoregulatory responsiveness determined by changes in tidal volume resulting from CO2 inhalation or measured during isocapnic stabilization, and on 2) mechanoreflex control of respiratory frequency through the vagus nerves. Blood pressure and heart rate were recorded concomitantly. Cardiovascular effects were manifested as dose-related hypotension and bradycardia that were generally response-limited by contrast with the respiratory depressant effects which progressed ultimately to failure. Relative potency of the three agents to produce an elevation of 4% in resting alveolar CO2 fraction was 100 times for N-methyllevonantradol and 10 times for nabilone by comparison with delta 9-tetrahydrocannabinol. Marked slowing of respiratory frequency occurred in vagotomized as well as in nerve-intact cats. Apneustic respiration was not observed in any case. It is concluded that the effects of the cannabinoids resulted from 1) an upward shift in CO2 setpoint of the central chemorespiratory "detector"; 2) decreased gain of the CO2-tidal volume "controller"; 3) depression of the respiratory "oscillator" in the lower medulla; 4) depression of the vasomotor center; and 5) a central vagotonic action in addition to a direct cardiodecelerator action on the heart.

Anesthesia, General↗
PubMed1982

Noninvasive documentation of emesis in cats.

Chest and abdominal wall movements were assessed as objective indicators of emesis. Thirty-six vomiting episodes in one intact and four decerebrate cats were monitored either by an inductive plethysmograph or by magnetometers applied to the chest and abdomen. The plethysmographic method was found to be the more suitable of these two monitoring techniques because it produced stable, artifact-free recordings with excellent signal differentiation. The occurrence of emesis was validated by simultaneously recording thoracic central venous pressure. Unlike the intrathoracic pressure measurement, spasmodic movements of chest and abdomen did not differentiate retching from expulsion. However, rhythmic abdominal excursions recorded during vomiting were several times greater than those occurring during any other activity. Surprisingly, these movements indicated an increase in abdominal dimensions during vomiting in contrast to the reduction in size observed during sneezing and coughing. We believe that recording of abdominal movements that accompany vomiting might potentially serve as a noninvasive research tool for the study of emesis in cancer chemotherapy.

Abdominal Muscles↗
PubMed1982

Vomiting induced by cyclophosphamide and phosphoramide mustard in cats.

Cyclophosphamide and phosphoramide mustard produce significant vomiting. Cyclophosphamide is metabolized to phosphoramide mustard, which may ultimately contribute to vomiting after cyclophosphamide administration. The role of the chemoreceptor trigger zone (CTZ) in vomiting caused by these agents is unknown. We studied the emetic syndromes produced by iv and intracerebroventricular cyclophosphamide and phosphoramide mustard in unanesthetized normal and CTZ-ablated cats. Iv cyclophosphamide produced vomiting unpredictably, with a mean latency of 54 +/- 9 mins (mean +/- SE) in cats that vomited. A dose-response relationship was found for phosphoramide mustard-induced emesis. A dose of 200 mg/kg was consistently effective, with a mean latency of 127 +/- 6 mins. Neither agent produced predictable emesis by the intracerebroventricular route of administration. One of four CTZ-ablated cats vomited after 300 mg/kg of cyclophosphamide. Since cyclophosphamide was an unpredictable emetic stimulus, it was not possible to further evaluate the effect of CTZ ablation on cyclophosphamide-induced vomiting. However, CTZ-ablated cats given 200 mg/kg of phosphoramide mustard vomited significantly less frequently (P = 0.05 by chi-square test) and with a longer latency than nonablated animals. A temporary, severe neurotoxic reaction was observed in cats receiving greater than or equal to 3400 mg/kg of cyclophosphamide, which may have had an inhibitory effect on emesis. Phosphoramide mustard was found to be a potent emetic stimulus in cats and may contribute to the emetic response following cyclophosphamide administration. Analysis of latency data suggests that in the cat other cyclophosphamide metabolites may also contribute to the emetic syndrome.

Animals↗
PubMed1981

Apneustic respiration normalized by an atypical cholinergic drug action in cats.

Cats were anesthetized with a mixture of pentobarbital and barbital given intraperitoneally and vagotomized. All animals were pretreated with atropine i.v. which blocked conventional muscarinic receptors and at the same time revealed atropine-insensitive sites whose stimulation by the cholinergic drug, bethanechol, was earlier found to produce respiratory analepsis. Respiration was recorded by pneumotachograph and intrapleural cannula. Apneustic breathing was produced by placing electrolytic lesions in the pneumotaxic area or by injecting a local anesthetic agent into the cerebrospinal fluid. Experiments were performed under isocapnic conditions. Bethanechol, administered intracerebro-ventricularly, restored regular breathing and increased the tidal volume in a dose-related manner within minutes of its injection. In cats with lesions, the expiratory pause generally decreased first and was followed by shortening of the inspiratory plateau. In cats made apneustic by intracerebro-ventricular injection of procaine, bethanechol acted competitively to normalize the distorted waveshape. The central excitant drug pentylenetetrazol was given intravenously for comparison with bethanechol. Apneustic breathing was partially corrected by pentylenetetrazol through a facilitatory influence on the brain stem interpreted to be independent of its convulsant action. These experiments demonstrate correction of pathological breathing by two chemically unrelated agents which share the ability to increase central excitatory state.

Animals↗
PubMed1981

Emetic action of xylazine on the chemoreceptor trigger zone for vomiting in cats.

Xylazine is an effective sedative analgesic that induces vomiting in the cat. A consistently effective intramuscular emetic dose of xylazine was established in normal cats in this laboratory. Animals in which the area postrema of the medulla oblongata had been chronically destroyed did not exhibit emesis in response to the standard test dose of xylazine but continued to show sedation. By contrast, sham-operated cats responded normally. Refractoriness to deslanoside, a known specific emetic drug, was used as functional proof for successful ablation of area postrema, and the lesions were also validated histologically. We conclude that xylazine exerts its emetic action on the chemoreceptor trigger zone of the area postrema. It is suggested that this action may be mediated by an opiate type of molecular receptors.

Animals↗
PubMed1980

Central respiratory and circulatory effects of Gymnodinium breve toxin in anaesthetized cats.

1 In cats anaesthetized with pentobarbitone, observations were made on respiration, spontaneous and evoked diaphragmatic electromyograms, blood pressure, heart rate, indirectly-induced contractions of the anterior tibialis muscle and nictitating membrane, and electrical excitability of the inspiratory centre in the medulla oblongata.2Gymnodinium breve toxin (GBTX) was administered intravenously, intra-arterially to the brain, and intracerebroventricularly. Physiological effects were recorded while alveolar P(CO) (2) was controlled at a constant level except when changes in gas tension were made in order to measure CO(2)-ventilatory responsiveness.3 Adequate doses of GBTX given intravenously by bolus injection elicited a non-tachyphylactic reflex response triad of apnoea, hypotension and bradycardia mediated by the vagus nerves independently of arterial baroreceptor and chemoreceptor innervation.4 After vagotomy, additional amounts of GBTX (i.v.) resulted in apneustic breathing, hypertension and tachycardia. The cardiovascular effects were abolished by ganglionic blockade with hexamethonium.5 Smaller doses of GBTX were required intra-arterially and intracerebroventricularly than by the intravenous route of injection to produce respiratory irregularity and cardiovascular hyperactivity.6 Evoked motor responses, electrical excitability of the medulla oblongata and CO(2)-ventilatory responsiveness were largely spared even though GBTX caused marked disturbances in respiratory rhythmicity and cardiovascular functions.7 It is concluded that GBTX acts reflexly on vagally innervated receptors to evoke a Bezold-Jarisch effect but that the toxin further acts centrally to cause irregular breathholding and hypertension with tachycardia, leading ultimately to respiratory and circulatory failure.

Anesthesia↗
PubMed1980

Central respiratory and circulatory depression caused by intravascular saxitoxin.

1 In cats anaesthetized with pentobarbitone and vagotomized, observations were made on the phrenic nerve action potential and the diaphragm electromyogram (EMG) at constant end-tidal Pco(2). Arterial blood pressure was stabilized by intravenous infusions of noradrenaline.2 Intravenous administration of saxitoxin (STX) initially abolished respiratory activity in the EMG and caused a slowing of oscillation in the central phrenic neurogram. Additional STX produced apneustic phrenic discharges followed by a progressive loss of nerve action potentials.3 The inspiratory centre in the medulla oblongata was stimulated electrically to evoke a sustained phrenic nerve discharge. STX, given intravenously, resulted in the elimination of spontaneous nerve activity without interfering with the evoked response.4 The cephalic intravascular infusion of STX into a carotid or vertebral artery depressed spontaneous respiratory activity while sparing EMG activity evoked by electrical stimulation of the intact phrenic nerve.5 Spontaneous respiratory discharge in the phrenic nerve was eliminated by smaller doses of STX administered intra-arterially than were required intravenously. In addition, onset of and recovery from neural silence occurred faster following intra-arterial injection of STX.6 Depressant effects on arterial blood pressure coincided with those on respiration when STX was given intra-arterially.7 An electrophysiological assay on frog sartorius muscle was used to measure STX in the cerebrospinal fluid. Levels of STX detected were proportional to amounts of the toxin infused intra-arterially.8 It is concluded that STX exchanges rapidly between blood and brain to bring about central depression and this adds to its peripheral paralytic actions.

Animals↗
PubMed1978

Dynamics of respiratory VT response to isocapnic pHa forcing in chemodenervated cats.

Arterial blood pH (pHa) was continuously monitored in decerebrate or pentobarbital-anesthetized cats with a rapidly responding hydrogen ion sensor inserted into the aorta. Alveolar carbon dioxide partial pressure and pHa were controlled independently during infusions of 1 N NaHCO3 or 0.5 N HCl into the inferior vena cava. Shifts in pHa up to 0.3 unit were effected isocapnically within 2.5-20 s over a working pHa range of 6.9-7.7. Before carotid sinus neurotomy, average onset latency of the tidal volume (VT) response to acid and alkaline pHa shifts was less than 5 S and the average VT response half time was less than 8.5 s regardless of whether the vagus nerves had been interrupted. After carotid sinus neurotomy, the deltaVT onset latency was approximately doubled, whereas the response half time was prolonged about eightfold on the average. Subsequent vagotomy tended further to increase the responding time lag. Nevertheless, the minimum response latency after peripheral chemodenervation was less than the deltapHa forcing rise time. It is concluded that the central chemoreceptors promptly sense pH change in the arterial blood and that neural processes adjust the time course of the respiratory response through the VT controller.

Animals↗