SUlMMARY1. In anaesthetized cats tetanic contraction of the hind-limb muscles, elicited by stimulating the ventral roots L 6-S 1, caused a rise of arterial -blood pressure, usually accompanied by small increases in heart rate and pulmonary ventilation: in decerebrate cats, all components of the response were much increased.2. With tetani of different strengths, obtained by stimulating with different intensities at the same frequency, the pressor response increased with increasing tension.3. When muscle contraction had been abolished by gallamine, or when dorsal roots L 6-S I had been sectioned, ventral root stimulation no longer caused a pressor response. The response is therefore a reflex, initiated in the exercising limb.4. The pressor response was not affected by section of all articular nerves to knee and ankle joints, or by section of the vagi. The stimulus therefore originates in the contracting muscles alone.5. The pressor response is potentiated by occluding the circulation through the working muscles. Reasons are discussed for concluding that the stimulus is chemical rather than mechanical, and that the 'metabolic receptors' for this exercise reflex are the free endings of group III and IV sensory nerve fibres located around the blood vessels.
1. Responses of sympathetic neurones to various afferent inputs have been analysed both in anaesthetized cats with intact neuraxis and in spinal cats. 2. In anaesthetized cats electrical stimulation of low threshold group III afferent fibres in skin and muscle nerves inhibited sympathetic neurones and gave depressor responses. The silent period following a sympathetic reflex discharge is most likely due to inhibition brought on by a particular subgroup within this afferent group. 3. High threshold group III and group IV afferent fibres excited sympathetic neurones and elicited pressor responses. 4. Sympathetic reflex arcs could be temporally facilitated during the somatic afferent induced inhibition, by group IV, and to a lesser extent by group III volleys. 5. Section of the spinal cord shortened the time course and lessened the degree of group III inhibition suggesting that suprasegmental pathways are involved in the long‐lasting depression following a reflex. 6. Baroreceptor afferent stimulation inhibited group III‐ and group IV‐ evoked reflexes even with some temporal facilitation in the pathway. 7. The special properties of the sympathetic reflex arcs and the relation of the results to other work on B.P. reflexes are discussed. It is suggested that the group III and IV muscle afferents have a chemoreceptor function and are responsible for mediation of the pressor reflex during muscle exercise.
SUMMARY Infarct, perfusion and blood pool scintigraphy were performed in 62 patients during hospitalization for acute myocardial infarction. The largest measured infarct or perfusion image defect and left ventricular ejection fraction were related to the late prognosis determined a mean of 16 months after the event.Breakpoint values for all scintigraphic variables could separate those who were asymptomatic on followup from those who died. The A search for simple and accurate indicators of prognosis after AMI has been prompted by the unreliability of clinical findings,18 the invasive nature of hemodynamic measurements, and the lack of reproducibility of enzymatic determinations of infarct size. 19 Recently, technetium-99m pyrophosphate (99mTc-PYP) infarct scintigrams and rest thallium-201 (207T1) myocardial perfusion scintigrams were shown to correlate well with pathologic measurements of acute infarct size in dogs20 21 and in humans. 22,23 Several investigators have reported promising results using scintigraphic variables as prognostic indicators of AMI. Rigo et al.24 and Schelbert et al.1' found that a normal scintigraphic left ventricular ejection fraction (LVEF) early after AMI predicted survival. The extent and intensity of the abnormality on infarct scintigraphy have also been correlated with morbidity and mortality after AMI.25 26 Recently, scintigraphic perfusion defect size measured early in patients in Killip class I and II was shown to be the best predictor of early and late mortality in patients with AMI.27In the current study, we sought to determine the value of scintigraphic indicators of infarct size and left ventricular function in predicting the late clinical course of patients after AMI. For this purpose, a quantitative analysis of 99mTc-PYP infarct scintigrams, 201T1 perfusion scintigrams, and equilibrium gated blood pool scintigrams was performed during the initial hospitalization in a population of patients admitted with AMI and was correlated with the clinical course of patients during follow-up after hospital discharge. Methods PatientsHistorical features, including the presence of prior infarction, and electrocardiographic, enzymatic and scintigraphic studies, were evaluated in 62 patients admitted to the coronary care unit with AMI. Fifty-one (82.3%) were males, mean age 69 years (range 52-81 years). The diagnosis of AMI was based on at least two of the following criteria: a history of typical, prolonged
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