Summary: Local cerebral hemodynamics and oxygen metabolism were measured by positron emission tomog raphy (PET) with the oxygen-15 C50) steady-state method in baboons, immediately before (TO), 1 (Tl), and 3-4 (T2) h after permanent middle cerebral artery occlu sion (MCAO). At Tl, there was a marked fall in both cerebral blood flow (CBF) and the CBF/cerebral blood volume (CBV) ratio in the occluded territory; these changes were sustained at T2, indicating stable reduction in cerebral perfusion pressure and lack of spontaneous reperfusion within this time range. Compared with pre occlusion conditions, the oxygen extraction fraction (OEF) in the occluded territory was elevated at both Tl and T2, indicative of a persistent oligemia/ischemia for up to 3 h after MCAO. At T2, however, this OEF increase had lessened, concomitantly with a decline in cerebral metabolic rate of oxygen (CMR02). This impairment of Positron emission tomography (PET) studies in humans have provided a unique insight into the metabolic and hemodynamic events which charac terize the evolution of acutely ischemic tissue, es pecially in relation to its function and viability (Baron et aI., 1981(Baron et aI., , 1983 Lenzi et aI., 1982; Wise et aI., 1983;Powers and Raichle, 1985; Hakim et aI.,

Testing vasoreactivity with CO2 or Diamox is a common diagnostic procedure for the study of haemodynamics in stroke patients. CO2 reactivity (CO2R) was tested in 5 baboons six hours after permanent occlusion of the left middle cerebral artery (MCA) in order to attain new insights into interpretation of vasoreactivity tests. Using the microsphere method, cerebral blood flow (CBF) was determined in the various vascular territories as well as in the centre of the ischemia, the penumbra and the remaining MCA-tissue. CBF decreased significantly in the affected MCA in all animals and in addition in the contralateral cerebellum in one animal (p < 0.05). In addition, the left anterior cerebral artery (ACA) demonstrated a similar decrease. During hypercapnia CBF increased in all areas with the exception of the left, occluded MCA territory. Thus CO2 enhanced the difference between ischaemic and non-ischaemic tissue (i.e., tissue with diaschisis). Mean CO2 R was 3.37 ml/100 g/min/mmHg in the right MCA, 0.16 in the left. While the left ACA demonstrated a decreased perfusion during normocapnia in a similar range to the MCA territory, only CO2R was able to identify precisely the territory of the occluded vessel. CO2 R was zero or negative in the ischaemic core, close to zero in the penumbra and profoundly decreased in the remaining MCA tissue. The overall CO2 R of the MCA was almost zero, suggesting vasoparalysis in response to hypercapnia in the core and penumbra and exhausted CO2 R even in non-infarcted, non-penumbral tissue. One animal displayed a negative CO2 R equivalent to an intracerebral steal-phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)

The nocturnal production of melatonin synthesis has been associated with circadian mechanisms of the organization of sleep. It is well known that the synthesis of melatonin is under the control of pineal beta 1-adrenoreceptors. In this study the effect of ten weeks treatment with the beta-adrenoreceptor (beta-AR) blockers propranolol and ridazolol on melatonin synthesis and on sleep quality was examined in 42 patients suffering from essential hypertension. Before and after 6 and 10 weeks of beta-AR-blocker administration urinary sulfatoxymelatonin excretion rates were measured and sleep factors were evaluated by using a standardized sleep inventory consisting of self-rating sleepiness scales. After 6 and 10 weeks of treatment, a significant about 50 percent reduction of sulfatoxymelatonin was measured. No relationship between these reductions and changes in sleep factors was found. The results indicate that a reduced nightly amplitude of melatonin has minor significance for the organization of physiological sleep. Furthermore, it is suggested that pineal mechanisms beside the beta 1-adrenergic receptor transduction system serve to maintain the melatonin signal to a considerable extent during a chronic beta 1-AR blockade.

Intracranial pressure (ICP) was recorded by epidural transducer and cisterna magna catheter, and regional cerebral blood flow (rCBF) using the intraarterial Xenon 133-technique were measured in baboons with normal and during increased ICP provoked by an inflatable balloon positioned subdurally. Arterial blood pressure was altered by controlled infusion of Sodium-nitroprusside (SNP), Nitroglycerine (NG) or Trimetaphan (TMP) with the aim of reducing blood pressure by about 20%. During exflated balloon SNP provoked an increase of ICP which was more prominent than with NG and TMP. During increased ICP (due to inflation of the balloon) again SNP led to a higher further increase of ICP than both NG and TMP. rCBF rose during the state of normal ICP when SNP was infused. This was not observed with infusion of NG or TMP. When ICP was increased again by inflation of the balloon all 3 substances reduced rCBF, indicating damage to the autoregulation. CO2-reactivity as measured by induced hyperventilation with reduction of arterial CO2-tension was affected by all 3 substances thus indicating impairment of vasoconstriction during increase of ICP and simultaneous decrease of blood pressure. However, this impairment of physiological vasoconstriction was more prominent with SNP than with NG and TMP. The results indicate that all 3 substances should be used with care to reduce blood pressure during surgery or under intensive care condition, particularly in patients with increased ICP.