Yasuyuki Morotomi

Cerebral infarction following bilateral carotid artery ligation in normotensive and spontaneously hypertensive rats: a pathological study.

A pathological examination was performed on normotensive rats (NTR) and spontaneously hypertensive rats (SHR) following bilateral common carotid artery ligation. After ligation, diffuse and extensive cerebral infarcts in the carotid artery territory occurred frequently in SHR, while NTR occasionally had wellcircumscribed small infarcts. The posterior communicating arteries, which are the major anastomotic channels connecting the carotid and vertebrobasilar systems, did not show any anomalies and were well developed in SHR and NTR. Vascular changes secondary to hypertension, such as fibrinoid necrosis or thickening of the wall, were not observed in SHR. Because of the paucity of structural difference of the blood vessels, the more diffuse and extensive cerebral infarcts in SHR after carotid occlusion were attributed to the hemodynamic difference rather than the morphological difference between the two groups. The results of the present experiment suggest that hypertension per se, i.e., hemodynamic factors, may be operative for the development of cerebral infarction.

Effects of Bilateral Carotid Artery Ligation on Brain Lactate and Pyruvate Concentrations in Normotensive and Spontaneously Hypertensive Rats

Brain lactate, pyruvate, and arterial acid-base balance were measured in normotensive rats (NTR) and spontaneously hypertensive rats (SHR) 60 minutes after bilateral carotid artery ligation. Brain lactate and lactate-pyruvate ratios were significantly increased in both SHR and NTR following carotid occlusion, although lactate increase in the former was six and one-half times greater than in the latter. These findings suggest that bilateral carotid occlusion in SHR may cause more severe circulatory changes which result in increased anaerobic metabolism. Furthermore, higher brain lactate was concomitant with lower arterial carbon dioxide tension. The mechanism of spontaneous hyperventilation following cerebral ischemia was discussed.

Suppressive effect of captopril on platelet aggregation in essential hypertension

Effects of captopril on platelet aggregation were studied in 12 essential hypertensive subjects. At the same time, the effects of captopril and angiotensin II on platelet aggregation in vitro were examined in 20 volunteers. A 50-mg oral dose of captopril was administered daily to hypertensive subjects for 2 weeks; the dose was then increased to 100 mg daily for the next 2 weeks. Values of platelet aggregation induced by ADP, epinephrine, collagen, and arachidonic acid before captopril treatment were 71.9 ± 4.5, 77.3 ± 4.2, 72.4 ± 4.1, and 70.8 ± 4.3% (mean ± SE), respectively. Two weeks after daily administration of 50 mg captopril, these values were 56.7 ± 4.5, 50.8 ± 7.6, 64.0 ± 4.6, and 60.9 ± 3.9%, respectively, with significant reduction of platelet aggregation (p < 0.001, p < 0.01, p < 0.01. and p < 0.005, respectively). Daily administration of 100 mg captopril also had a significant suppressive effect on platelet aggregation. Changes of platelet count and serum lipids were not significant. In vitro, captopril and angiotensin II added to plateletrich plasma had no effect on platelet aggregation. These results show that the suppressive effect of captopril on platelet aggregation is a secondary action in vivo.

Reduced regional cerebral blood flow in aged noninsulin-dependent diabetic patients with no history of cerebrovascular disease: Evaluation by N-lsopropyl-123I-p-iodoamphetamine with single-photon emission computed tomography

Regional cerebral blood flow was measured using N-isopropyl-123I-iodoamphetamine with single-photon emission computed tomography (CT) in 16 aged patients with noninsulin-dependent diabetes mellitus (NIDDM, average age 72.8 years, average fasting plasma glucose 7.7 mmol/L), and 12 nondiabetic subjects (71.6 years, 5.3 mmol/L). None had any history of a cerebrovascular accident. Systolic blood pressure (SBP), total cholesterol, and triglyceride levels did not differ between groups. Areas of hypoperfusion were observed in 14 diabetic patients (12 patients had multiple lesions) and in 6 nondiabetic subjects (3 had multiple lesions). Areas where radioactivity was greater than or equal to 65% of the maximum count of the slice was defined as a region with normal cerebral blood flow (region of interest A, ROI-A), and areas where the count was greater than or equal to 45% were defined as brain tissue regions other than ventricles (ROI-B). The average ROI-A/B ratio of 16 slices was used as a semiquantitative indicator of normal cerebral blood flow throughout the entire brain. Mean ROI-A/B ratio was 49.6 +/- 1.7% in the diabetic group, significantly lower than the 57.9 +/- 1.6% at the nondiabetic group (p less than 0.005). The ratio was inversely correlated with SBP (r = -0.61, p less than 0.05), total cholesterol (r = -0.51, p less than 0.05), and atherogenic index (r = -0.64, p less than 0.01), and was positively correlated with high-density lipoprotein (HDL) cholesterol (r = 0.51, p less than 0.05) in the diabetic, but not the nondiabetic group. These observations suggest that the age-related reduction in cerebral blood flow may be accelerated by a combination of hyperglycemia plus other risk factors for atherosclerosis.

Effect of carotid artery ligation on regional cerebral blood flow in normotensive and spontaneously hypertensive rats.

Regional cerebral blood flow (rCBF) was measured in normotensive rats (NTR) and spontaneously hypertensive rats (SHR), in a lightly anesthetized state and with control of Pacos by artificial ventilation. Without carotid artery ligation, NTR and SHR showed almost identical rCBF values and distribution, despite s gnificantly elevated levels of blood pressure in SHR. Bilateral carotid artery ligation, however, caused much more pronounced decreases of rCBF (ischemia) in SHR than NTR, in regions supplied by the carotid artery. The reduction of rCBF in SHR was rather homogenous and symmetrical. Mechanisms causing the differences between NTR and SHR are discussed.

Male siblings with Takayasu's arteritis suggest genetic etiology

SummaryTakayasus arteritis is a nonspecific arteritis involving the aorta and its major branches. The disease mainly affects young females and familial incidence is uncommon. In this paper, two rare cases of male siblings with Takayasus arteritis and the results of their HLA typing are described. The HLA haplotype of the two cases was completely identical—A2-B40-Cwl and A24(9)-Bw59-Cwl, DR2, and DR4. It is reported that BW52(5) is strongly associated with the disease. However, in our cases, Bw52(5) was not found, while DR2 and DR4, which have been reported in association with several autoimmune disease, were detected. Accordingly, in these cases, genetic factors might be associated with the pathogenesis of the disease through an autoimmune mechanism.

Posterior tibial somatosensory evoked potentials in Duchenne-type progressive muscular dystrophy

Posterior tibial somatosensory evoked potentials were recorded from 10 patients with Duchenne-type progressive muscular dystrophy (DMD). The results of the patients were compared with age-matched controls. The ratio of height to latency (H/P38 and H/N22-P38) decreased significantly in DMD, which indicated central conduction disturbances in DMD.

Brain metabolism and arterial acid-base balance following bilateral carotid occlusion in normotensive and experimental hypertensive rats.

The effects of bilateral common carotid artery occlusion on brain metabolism and arterial acid-base balance were studied in normotensive and experimental renovascular hypertensive rats. One hour after carotid occlusion in hypertensive rats, supratentorial lactate increased to 383% and lactate-pyruvate ratio to 280% of the controls, while adenosine triphosphate (ATP) decreased to 69%. These metabolic changes were thought to be due to cerebral ischemia. Arterial pCO2 was lowered and the pH was raised in the hypertensive animals due to cerebral ischemia induced hyperventilation. In the normotensive rats, carotid occlusion had minimal effects on cerebral metabolism and arterial acid-base balance. These results suggest that hypertensive rats are more susceptible to cerebral ischemia caused by carotid occlusion than normotensive rats. Increased cerebrovascular resistance in hypertension is discussed as a causal factor in cerebral ischemia.

Brain metabolism following bilateral carotid occlusion in 2 different models of experimental hypertensive rats.

Brain metabolites and arterial acid-base measurements were made one hr after bilateral carotid artery occlusion in 2 different models of hypertensive rats. Animals used included renovascular hypertensive rats (RHR) with an altered renin-angiotensin system and desoxycorticosterone hypertensive rats (DHR) with low plasma renin activity (PRA). The mean value for supratentorial lactate of 7.41 mM/kg in RHR was significantly higher than in DHR (3.90 mM/kg) or in control normotensive rats (3.10–2.56 mM/kg). Concomitantly, the lactate/pyruvate ratio tended to increase and ATP to decrease in RHR only. In these same rats (RHR) infratentorial lactate was also increased. The results suggest that bilateral carotid occlusion leads to anaerobic metabolism of the brain in RHR but not in DHR, suggesting that the renin-angiotensin system may play some role in the susceptibility to cerebral ischemia following carotid occlusion in the hypertensive rats.

HAEMODYNAMIC AND HORMONAL EFFECTS OF PRAZOSIN ON HEAD-UP TILT IN ESSENTIAL HYPERTENSIVE PATIENTS: COMPARISON WITH THOSE OF PROPRANOLOL

1. To evaluate the haemodynamic and hormonal effects of prazosin, head‐up tilt was performed in 10 essential hypertensive patients, and these effects of prazosin on the tilt were compared with those of propranolol. The tilts were performed in control phase and the last days of treatment for two weeks with propranolol (90 mg/day) or prazosin (3–6 mg/day).