The Lived Experience of Novice Helpers as First Responders in a Shared War Reality.

Purpose: This study sought to explore the lived experience of trained social work students as first responders in a shared war reality. Method: Data were gathered from three focus groups conducted with social work students following their professional intervention during a period of protracted warfare. Results: The main theme depicts a movement from an experience of uncertainty to certainty, as the students shifted from being subjects under threat to being object-helpers on duty. Discussion: The findings highlight the interactive nature of individual and environmental aspects of resilience as a dynamic process in the face of adversity. Practical implications are discussed in the context of first responders' resilience in a shared war reality. Conclusion: First responders must experience certainty in order to function effectively. To provide more support to novice helpers, a first responders training program should be implemented as part of the mandatory curriculum of social work studies.

Organ-localized hypothalamic-stimulated vasculature changes in the cat.

Stimulation of specific lateral hypothalamic targets in a cat model induces vascular and/or cardiac changes. Evidence is presented that these may consist of discretely localized sympathetically mediated changes taking place in just one or two organs. Moreover, following stimulation of either one of two adjacent lateral hypothalamus sites, pressor effects are induced that superficially look similar, but prove to be mediated by different pathways. To investigate possible synapsing at sympathetic ganglia, e.g. in superior cervical or stellate ganglia, 50 micrograms atropine methyl nitrate, a ganglionic blocker, was applied directly to the ganglia. This was shown to potentiate the pressor effects, in some cases when applied to the superior cervical ganglia, in others to stellate ganglia, presumably by blockade of a ganglionic attenuating mechanism. The contributions made by different sympathetic nerves to the lateral hypothalamus-induced pressor effect were analysed. Stimulation of one of the lateral hypothalamus sites (TAR.I) in eight cats induced a pressor effect that was abolished by severing a nerve branch, from the superior cervical ganglia laterally, shown to innervate neck muscle vasculature. In another group of nine cats stimulation of TAR.II induced a pressor effect abolished by cutting a branch from the superior cervical ganglia medially, shown to be destined to the vasculature of pharyngeal muscles and possibly lower respiratory tract. The hypothesis that central control via the sympathetic nervous system is responsible for differential organ specific regulation of blood flow to individual organs is discussed.

Depressor effects of muscarinic and non-muscarinic mediation induced by lateral hypothalamic stimulation in the cat.

Transient sympathetically-mediated depressor effects were induced by stimulation of a small locus in the lateral hypothalamic peri-fornical region, medial to the fields of Forel. The ganglionic blocking agent, atropine methyl nitrate (ATMN), was used to show that muscarinic as well as non-muscarinic sympathetic ganglion receptor neurotransmission was involved. Evidence is presented that stimulation of this LH site co-activates a number of mechanisms and that depending on which of these are activated, the ganglionic blocking agent ATMN may either block, reverse or potentiate the depressor effect.

Sympatho-inhibitory mechanisms acting at sympathetic ganglia to attenuate hypothalamic-induced pressor effect in the cat.

Pressor and tachycardic effects induced in the cat by stimulation of a lateral hypothalamic (LH) site, are shown to be mediated by sympathetic ganglia nicotinic receptor, and potentiated under atropine methyl nitrate sympathetic ganglia blockage. It is postulated that a sympatho-inhibitory pathway muscarinic ganglionic mechanism, co-activated by the LH stimulation, attenuates the pressor and tachycardic effects, the potentiation presumably being a manifestation of blockage of that mechanism.

A pharmacological analysis of autonomic pathways mediating myocardial disturbances originating in a lateral hypothalamic area of the cat.

A study was made of the mechanisms mediating autonomic changes resulting from stimulation of a site in the lateral hypothalamic area (LHA). This site, when stimulated, induced angina-like ECG disturbances similar to those observed in some cases of brain traumas. These ECG changes were often associated with other autonomic changes, such as pressor response, tachycardia (in some cases bradycardia), nictitating membrane (NM) contraction and pupillary dilatation. Most symptoms were sympathetic: they were largely abolished by spinal cord section between C1 and C2, but were not affected by vagotomy, except that bradycardia was converted to tachycardia. Adrenal catecholamines were not involved since adrenal vein ligation was without effect. Hexamethonium (5-10 mg/kg) prevented pressor response and tachycardia in most cats but only partly protected against ECG changes and NM contractions. Atropine methyl nitrate (0.2 mg/kg) abolished the remaining ECG abnormalities and NM tension. The beta-receptor antagonists, propranolol and practolol (50 micrograms/kg) completely prevented the ECG changes induced either by isoprenaline or LHA stimulation. It is concluded that the symptoms induced by LHA stimulation result from noradrenaline release in the target organs.

Angina-like cardiac disturbances of hypothalamic etiology in cat, monkey, and man.

Angina-like phenomena of CNS etiology were studied. Data were collected and analyzed from clinical cases of cerebral hematoma, concussion, and tumors in which cardiological disturbances were observed consequent to compressive brain lesions or surgical brain manipulations. The cases in which the disturbances were largely angina-like and without ectopic beats or arrhythmias were chosen for study. The brain region most significantly related to this phenomenon seemed to be the hypothalamus. Experiments conducted in cats and monkeys showed that stimulation of specific sites in the hypothalamus resulted in angina-like manifestations with no other cardiac changes. These data support our working hypothesis that a cerebrally induced syndrome that is conspicuously angina-like must be related to hypothalamic involvement. In the awake monkey hypothalamic stimulation caused angina-like ECG changes and behavior suggestive of referred pain. In some cases, repetitions of the stimulations or irritations in all of the species resulted in permanent pathological myocardial changes, mostly bleeding into the myocardium. In some animals there were minute hemorrhagic necroses that were subepicardial in distribution. It is significant that the most severe or permanent pathological changes were found in cases in which the angina-like ECG alterations were persistent. There were also cases, however, with persistent angina-like ECG changes that showed no such pathology.