[Development tendencies in nuclear medicine].
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Evidence is presented supporting the hypothesis that the positive inotropic effect after an abrupt increase in systolic pressure (Anrep effect) is the recovery from subendocardial ischemia induced by the increase and subsequently corrected by vascular autoregulation of the coronary bed. Major evidence consists of data obtained from an isolated heart preparation showing that the Anrep effect can be abolished with coronary vasodilation, and that with an abrupt increase in systolic pressure there is a significant reduction in the distribution of coronary flow to subendocardial layers of the ventricle. Furthermore, the intracardiac electrocardiogram shows S-T segment and T wave changes after an abrupt increase in ventricular pressure similar to that noted after coronary constriction. Major implications are that normally there may be ischemia of the subendocardial layers tending to reduce myocardial contractility which may account, in part, for the positive inotropic effect of various coronary vasodilators; that with an abrupt increase in ventricular pressure the subendocardium is rendered temporarily ischemic, placing the heart in jeopardy from arrhythmias until this is corrected; and that end-diastolic pressure and the intracardiac electrocardiogram may provide a means of evaluating the adequacy of circulation to subendocardial layers in diseased ventricles when systolic pressure is abruptly increased.
Studies were performed to define the mechanisms involved in the redistribution of renal cortical blood flow to inner cortical nephrons which occurs during hemorrhagic hypotension in the dog. The radioactive microsphere method was utilized to measure regional blood flow in the renal cortex. Renal nerve stimulation decreased renal blood flow 40% but had no effect on the fractional distribution of cortical blood flow. Pretreatment with phenoxybenzamine, phentolamine, propranolol, or atropine did not alter the redistribution of cortical flow during hemorrhage. A reduction in renal perfusion pressure by aortic constriction caused a qualitatively similar alteration in regional blood flow distribution as occurred during hemorrhage. When perfusion pressure was kept constant in one kidney by aortic constriction followed by hemorrhage, no redistribution occurred in the kidney with a constant perfusion pressure while the contralateral kidney with the normal perfusion pressure before hemorrhage had a marked increase in the fractional distribution of cortical flow to inner cortical nephrons. Additionally, retransfusion had no effect on the fractional distribution of flow in the kidney in which perfusion pressure was maintained at the same level as during hemorrhage while in the contralateral kidney in which pressure increased to normal there was a redistribution of flow to outer cortical nephrons. These studies indicate that the redistribution of renal cortical blood flow which occurs during hemorrhage is not related to changes in adrenergic activity but rather to the intrarenal alterations which attend a diminution in perfusion pressure.
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1. In pregnant rabbits near term, cardiac output and its distribution were measured by injection of isotope-labelled microspheres into the left ventricle. Hypoxaemia (mean P(a,O2) 35 mm Hg) caused a reduction in placental and renal flows, while myometrial flow was unchanged and coronary and cerebral blood flows increased.2. In the lateral (ovarian) end of the uterine horn foetal and placental weight and absolute maternal placental blood flow were greater than in intermediate or medial positions. Placental flow (per 100 g placental tissue) was most in the most lateral placenta and decreased in the intermediate positions, especially when there were many placentas in the same horn.3. Abortions and runts (more than 2 S.D. below the mean weight for their age) occurred most often in the medial end of the uterine horn, while oversize foetuses (more than 2 S.D. above the mean weight) usually occupied the most lateral position.4. Ovarian blood flow (460 ml./100 g. min) was relatively large (e.g. compared with renal flow, 275 ml./100 g.min).
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Bone metastases that develop in patients with advanced prostate cancer often cause deep, unremitting pain. Palliative options for the control of this pain include analgesic support, cytotoxic chemotherapy and external-beam radiotherapy. In addition to external irradiation, interest in intravenously injected radioisotopes that are preferentially localized to bone has been mounting. Metastron (an isotope of strontium) imitates the biodistribution of calcium in vivo and is avidly taken up into bony metastases where it has a biological half-life of just over 50 days. The biological half-life in undiseased bone is far shorter, approximately 14 days. Various studies have been conducted to evaluate the role of Metastron in metastatic prostate cancer. An optimum dose has yet to be finalized, but it is clear that the change of haematological toxicity becomes more significant at much larger doses. In the large, randomized Trans Canada study in which Metastron or placebo was given to patients as an adjunct to local field irradiation, those patients treated with Metastron had a significantly reduced intake of analgesics. Furthermore, progression of pain, as measured either by sites of new pain or by the requirement for further palliative radiotherapy, demonstrated statistically significant differences in favour of Metastron. There is thus increasing evidence of a useful role for Metastron in the treatment of prostate cancer metastatic to bone.
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