Emergency shelters in Vancouver,Canada

The shelter experiences, employment history, income and social service needs utilization were examined among 124 emergency shelter users in Vancouver, British Columbia. Thirty-six (30.5%) reported this as their first experience with living in a shelter; the length of stay in the present shelter ranged from one to 90 days. Reasons for shelter use included: eviction from last place of residence, loss of job, or suffering from health problems rendering one unable to work. The highest unmet service needs were finding affordable housing and finding a job. This combination of scarcity of low-cost housing, health problems, and difficulty in finding employment have led to a situation where emergency shelters have become extended places of residence, a home to many.Sonia Acorn, RN, PhD is an Associate Professor at the School of Nursing, University of British Columbia, Vancouver, Canada.This research was funded by the Mr. and Mrs. P.A. Woodward's Foundation and the Vancouver Foundation.     

A comparison of perinatal mortality between ethnic Chinese and ethnic whites: Why the Chinese rate was lower

Objectives. To confirm the observation that has been occasionally reported in the literature that perinatal mortality rate is lower in ethnic Chinese than in ethnic whites, and to assess the reasons for this lower perinatal mortality rate.

Methods. Secondary‐analysis based on published data.

Results. This exercise demonstrates that the perinatal mortality rate was lower in ethnic Chinese than in ethnic whites. The birth weight distribution in ethnic Chinese was more favourable with reduced births at two extremes of the distribution, and the exposure to risk factors for perinatal death by their mothers was also lower.

Conclusion: Perinatal mortality rate is lower in ethnic Chinese than in ethnic whites, and the lower perinatal mortality rate in ethnic Chinese is probably caused by their favourable birth weight distribution and lower exposure to risk factors of perinatal death by their mothers.     

Inhibition of gastrointestinal motility by MPTP via adrenergic and dopaminergic mechanisms

The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was injected intraperitoneally in mice and caused an acute inhibition (of over 60%) of gastrointestinal motility, which was measured by the transit of charcoal. This inhibition was not related to conversion of MPTP to MPP⁺. Administration of the -adrenergic blocker propranolol significantly reduced, but did not completely block, the effect of MPTP. The dopaminergic blocker haloperidol also partly reversed the effects of MPTP. When these blockers were administered together, the action of MPTP was fully blocked. The results indicate that the toxin acted by releasing catecholamines (presumably norepinephrine and dopamine), thereby inhibiting motility.Supported by a grant from the Joint Research Fund of the Hebrew University and Hadassah.     

Acute systemic and antiischemic effects of epanolol in patients with coronary artery disease

Summary Antiischemic effects of ₁-blocking agents are based on intrinsic negative inotropic and chronotropic properties. Partial ₁-agonistic activity, although useful in preserving cardiac function, may counteract such antischemic properties by modulating the intrinsic negative cardiac effects of beta-blockade. To investigate the acute hemodynamic and antiischemic profile of epanolol, a cardioselective ₁-antagonist and partial agonist, 20 patients with left coronary artery disease underwent two incremental atrial pacing tests, 45 minutes before (APST I) and 15 minutes after (APST II) 4 mg intravenous epanolol, administered over 5 minutes. Additional measurements were carried out at 1, 3, 5, 10, and 15 minutes after epanolol, at basal and fixed heart rates. Epanolol immediately reduced heart rate with a maximum of 10% at 15 minutes and decreased contractility (Vmax) by 7% (both p<.05), whereas cardiac output fell temporarily by 9% (p<.05). Other hemodynamic parameters did not change, except for a significant 11% reduction in myocardial oxygen demand. Despite comparable pacing conditions, both the double product and contractility decreased significantly less during APST II, resulting in a 17% lower myocardial oxygen consumption (p<.05). Myocardial ischemia was markedly reduced, indicated by normalization of lactate metabolism [lactate extraction 16±7% vs. –7±8% (APST I)], less ST depression (21%), and modulation of LV end-diastolic pressure postpacing (all p<.05 vs. APST I), whereas angina was absent or less in 14 patients. None of the patients reported an adverse effect. Thus, under resting conditions intravenous epanolol induces moderate, short-lasting negative chronotropic and inotropic effects, but does not alter cardiac pump function or vascular resistance, reflecting its additional ₁-agonistic properties. Alternatively, during pacing it still reduces ischemia through negative inotropic effects and diminishes myocardial oxygen demand, reflecting its ₁-antagonistic profile.     

Long-term follow-up of consequences of percutaneous endoscopic gastrostomy (PEG) tubes in nursing home patients

PEG (percutaneous endoscopic gastrostomy) tubes are frequently placed in nursing home patients. The aim of this study was to assess retrospectively the long-term changes in functional and nutritional statuses, tube-related complications, and factors influencing survival in 46 nursing home residents, mean age 73.6 years (range 19–96). Functional status was evaluated by a standard rehabilitation medicine scale. Nutritional status was evaluated by serum albumin and cholesterol concentrations and by weight. PEG-related complications requiring hospitalization or emergency room or clinic evaluations were noted. Additionally, changes in resuscitation status were noted. The predominant indication for PEG placement was dementia (52%). At PEG placement, 48% of patients had total functional impairment. Regardless of the severity of impairment, no patient's functional status improved after PEG. Nutritional status did not improve significantly. Mortality approached 50% and 60% at 12 and 18 months, respectively, and was significantly related to age, resuscitation status, and serum albumin concentration. All patients under 40 years of age at PEG survived, in contrast to 41.3% of patients over 40 years of age (P<0.001). Sixty-three percent of patients who were full code at PEG placement survived, in contrast to 10% of no code patients (P<0.001). Albumin 3.5 g/dl at PEG or thereafter was associated with improved survival (P<0.001) as compared to albumin <3.5 g/dl. PEG-related complications occurred in 34.7% of patients, and the first occurred four months after PEG. We conclude that realistic expectations of what PEG can accomplish be a factor in the decision to place a PEG tube in nursing home patients.     

Adrenergic,purinergic, and endothelial mediators and modulators of norepinephrine-induced mesenteric autoregulatory escape

We evaluated the effects of potential factors in autoregulatory escape from norepinephrine-induced vasoconstriction in rat anterior mesenteric artery. We determined mesenteric artery blood flow velocity with a pulsed Doppler, sonic flowmeter, and systemic arterial blood pressure with a transducer. A 4-min norepinephrine infusion (0.125–1.0 × 10^–8 M/min) intravenously evoked a dose-dependent, initial vasoconstriction that was followed by rapid escape of blood flow toward or above the control value during sustained norepinephrine administration. Neonatal capsaicin treatment enhanced vasoconstrictor responses to norepinephrine but failed to affect escape parameters. Propranolol decreased norepinephrine-induced escape dose dependently. Adenosine deaminase attenuated escape, and the combination of this enzyme plus propranolol nearly abolished escape from norepinephrine-induced vasoconstriction. Methylene blue also diminished autoregulatory escape. These findings suggest that norepinephrine-induced autoregulatory escape involves simultaneous -adrenoceptor, purinergic, and endothelial mediation. Norepinephrine-evoked mesenteric vasoconstriction appears to involve predominantly ₂-adrenoceptors and is modulated by peptidergic sensory nerves and adenosine.NIH grant number supporting these studies: USPHS # DK37050.     

Nitric oxide mediates inhibitory nerve effects in human esophagus and lower esophageal sphincter

The effect of inhibition of nitric oxide synthase on nonadrenergic, noncholinergic nerve-mediated responses in circular smooth muscle of the human esophageal body and lower esophageal sphincter (LES) was examinedin vitro. Tissues were obtained from 10 patients (eight esophageal resection for cancer, two transplant donors). Muscle strips from the LES developed significant spontaneous tension (11.6 ± 2.1 mN/mm²,N=6) and relaxed in response to electrical stimulation. The nitric oxide synthase inhibitor,N -nitro-l-arginine (NNA), at 10^–5 M, inhibited the relaxation, but had no significant effect on the spontaneous tension (13.0 ± 2.6 mN/mm²,P=0.07). Esophageal body strips developed little spontaneous tension, demonstrated an off contraction following the cessation of the electrical stimulus, and when contracted with 10^–5 M carbachol, relaxed during electrical stimulation. NNA (10^–5 M) inhibited the off contraction and the relaxation seen after carbachol and unmasked a prominent intrastimulus contraction. This intrastimulus contraction was enhanced by eserine and inhibited by atropine and tetrodotoxin. NNA showed similar potency in the esophageal body and LES and its effects were reversed byl-arginine, but notd-arginine. The results indicate that nitric oxide is an important mediator for nonadrenergic, noncholinergic nerve effects in the human esophagus and lower esophageal sphincter.This research was supported in part by an ICI Pharma/Medical Research Council of Canada Research Fellowship grant awarded to H.G. Preiksaitis and a Medical Research Council Program Grant PG8.     

Observations on the arterial baroreflex in neurally mediated vasodepressor syncope

The arterial baroreflex was studied in subjects who had recently had an episode of vasodepressor syncope. This was determined using 2–3 mcg/kg intravenous boluses of phenylephrine and assessing the bradycardic response. The values were measured in ms/mmHg and expressed as the angular coefficient of the regression line between the increase in R—R interval on the electrocardiograph and the systolic arterial pressure. In subjects examined immediately after the vasodepressor syncope episode the bradycardic response was much more marked than in controls (p < 0.01) and in the subjects themselves 6 months after the episode, provided that they were symptom-free (p < 0.01). It is concluded that in vasodepressor syncope there is a phase in which the baroreflex is highly sensitive and that this is due not to a lowering of the stimulation threshold but to a gain in the efferent arc, which explains a vagotonic response.     

Intraoperative measurement of javid shunt flow with transit-time ultrasound

Transit-time ultrasound methods were used to measure blood flow in 37 patients undergoing carotid endarterectomy. Internal carotid flow before (ICF^bef) and after (ICF^aft) endarterectomy was measured with a 6 mm perivascular probe, and Javid shunt flow (SF) was measured with a clamp-on probe. For the entire group ICF^bef averaged 117±67 ml/min and ICF^aft was 173±67 ml/min. Shunt flow averaged 123±51 ml/min. The differences between ICF^bet and ICF^aft and between SF and ICF^aft were significant (ANOVA,p<0.01) but the difference between ICF^bef and SF was not. The relationship between ICF^bef and SF appeared to define two groups of patients. Those in whom SF was greater than ICF^bef (SF > ICF^bef) had more stenosis evident on preoperative arteriograms (64.7%±14.55% maximum single diameter stenosis) and a greater average increase in ICF (151%±159%) than those with SF ICF^bef (43.3%±20.9% stenosis and 34%±54% increase in ICF), suggesting that the relationship between SF and ICF^bef defines groups with different hemodynamic responses. The similarity between SF and ICF^bef indicates that Javid shunt flow offers adequate protection from cerebral ischemia. A practical benefit of the shunt clamp-on flow probe is the ability afforded to recognize shunt occlusions.Presented at the Twelfth Annual Meeting of the Southern California Vascular Surgical Society, Coronado, Calif., September 17–19, 1993.