Validity of Maori ethnicity statistics.
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Abstracting and Indexing↗
Biomedical subjects
R S Hoskins
Publications and source records attributed to R S Hoskins.
The general practice contract scheme: was it targeted?
OBJECT: to determine whether the contracted general practices were situated in areas of greatest health need. METHOD: the health and equity index was used to determine the level of health need of the geographical location of the contracted practices. RESULTS: the health and equity index for the urban contracted practices showed a high level of health need. In the rural practices, the census area unit in which the practices were located showed a high level of health need, however when surrounding census area units were considered, they were located in areas of average health need. CONCLUSION: the general practice contract scheme was well targeted.
Delivery of Health Care↗
Neighbourhood of domicile and hospital admissions in Auckland: is there a relationship?
The relationship between the health and equity index of socioeconomic status/need and hospital admission rates has been investigated. The index is based on an area's population characteristics, and has previously been used for determining service provision and to describe an area's health need. This study demonstrates a strong positive correlation (r = 0.88, 95% confidence intervals 0.75 to 0.94) between the index and standardised hospital admission rates in the Auckland urban area. This association validates the index as a proxy for morbidity, in as much as hospital admission rates measure morbidity, and supports suggestions for its use to alter interregional and intraregional resource allocation.
Adolescent↗
Selective vagal postganglionic innervation of the sinoatrial and atrioventricular nodes in the non-human primate.
The distribution of parasympathetic postganglionic nerves to the atrioventricular (AVN) and sinoatrial nodal (SAN) regions was investigated in the non-human primate heart. Eight male monkeys (Macaca fascicularis) weighing 5.5-7.0 kg. were anesthetized (alpha-chloralose, 50 mg/kg and urethane, 500 mg/kg) and instrumented to measure arterial pressure, electrocardiogram, atrial and ventricular electrograms. The cervical vagi were electrically stimulated (20 Hz, 4 V, 2 ms) before and after selective denervation (D) of the AVN and/or SAN. Vagal stimulation was repeated during atrial pacing to assess parasympathetic modulation of AVN conduction. Ablation of parasympathetic pathways to the AVN, accomplished by the disruption of the epicardial fat and surface muscle layer at the junction of the inferior vena cava and inferior left atrium eliminated (P less than 0.01) the dromotropic effects of vagal stimulation without affecting the heart rate response (right vagus, before D, paced: atrial rate 218.0 +/- 6.3, ventricular rate 67.1 +/- 23.7; after D: atrial rate 210.3 +/- 6.4, ventricular rate 210.3 +/- 6.4 beats/min, means +/- S.D.). In sharp contrast, surgical dissection of the fat pad overlying the right pulmonary vein-superior vena cava junction significantly (P greater than 0.01) attenuated negative chronotropic effects of vagal stimulation (left vagus, before D the R-R interval increased by 832.7 +/- 146.4 ms, 209.5% increase; after D 37.4 +/- 18.0 ms, 8.8% increase). These data demonstrate discrete vagal efferent pathways innervate both the SAN and AVN regions of the non-human primate heart.
Animals↗
Time-series analysis of heart rate variability during submaximal exercise. Evidence for reduced cardiac vagal tone in animals susceptible to ventricular fibrillation.
Periodic fluctuations in the R-R interval have been used as noninvasive measures of cardiac autonomic tone. For example, a reduced heart rate variability has been shown to correlate with an increased mortality in patients recovering from myocardial infarction. The effects that physiologic perturbations such as exercise have on this heart rate variability have not been investigated. Therefore, heart rate variability was measured throughout a submaximal exercise test in 36 mongrel dogs with healed anterior myocardial infarctions. The amplitude of the respiratory component (0.24-1.04 Hz) was determined by time-series analysis techniques and was used as an index of cardiac vagal tone. On a subsequent day, a 2-minute coronary occlusion was initiated during the last minute of exercise. Twenty-two animals developed ventricular fibrillation (susceptible), whereas 14 animals did not (resistant). Exercise elicited a significantly greater increase in heart rate (resistant, 205.4 +/- 7.1; susceptible, 227.0 +/- 5.4 beats/min) in susceptible animals, which was accompanied by a greater reduction in the cardiac vagal tone index (resistant, 2.7 +/- 0.3; susceptible, 1.1 +/- 0.2 ln msec2) as compared with resistant animals. Conversely, atropine sulfate (50 micrograms/kg) given during exercise elicited a greater heart rate increase in the resistant dogs (heart rate change: resistant, 54.2 +/- 7.0; susceptible, 18.7 +/- 4.4 beats/min). Taken together, these data suggest that exercise elicited a greater reduction in cardiac vagal tone in animals known to be susceptible to ventricular fibrillation.
Adrenergic beta-Antagonists↗
Prevention of ventricular fibrillation with magnesium sulfate.
Mongrel dogs with healed myocardial infarctions were given a 2 min coronary occlusion during an exercise test. The exercise plus ischemia test induced ventricular fibrillation in nine animals. One week later, the test was repeated after pretreatment with magnesium sulfate (100 mg/kg i.v.). Magnesium prevented ventricular fibrillation in seven of the nine animals without adverse side effects. Thus, magnesium may be useful in the management of ventricular fibrillation during ischemia.
Animals↗
Cocaine-induced ventricular fibrillation: protection afforded by the calcium antagonist verapamil.
There is increasing evidence that the use of cocaine can trigger lethal cardiac events, including ventricular fibrillation. The mechanism responsible for these lethal cardiac arrhythmias remains to be determined. Therefore, 13 mongrel dogs were instrumented so that heart rate, left ventricular pressure (LVP), and d(LVP)/dt could be measured. After a 3- to 4-wk recovery period, the left circumflex coronary artery was occluded for 2 min, beginning with the last minute of an exercise stress test and continuing for 1 min after the cessation of exercise. None of the dogs developed cardiac arrhythmias during the control exercise plus ischemia test. On a subsequent day, the test was repeated after the injection of cocaine HCl (1.0 mg/kg). Cocaine significantly (P less than 0.01) elevated heart rate, systolic LVP, and d(LVP)/dt, and it elicited cardiac arrhythmias in 12 of the 13 animals during the exercise plus test. In fact, 11 animals developed ventricular fibrillation. Verapamil, a calcium channel antagonist (250 micrograms/kg), attenuated the hemodynamic effects of cocaine and prevented the development of ventricular arrhythmias. These data suggest that cocaine can induce ventricular fibrillation during myocardial ischemia and that these lethal arrhythmias may be prevented by a calcium channel antagonist.
Animals↗