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Biomedical subjects

M Kobari

Publications and source records attributed to M Kobari.

151 records · Page 9Linked to original sources
PubMed1982

Effect of nimodipine, a calcium antagonist, on cerebral vasospasm after subarachnoid hemorrhage in cats.

Effect of a calcium antagonist, isopropyl-(2-methoxyethyl)-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5- pyridinedicarboxylate (nimodipine) on the cerebral vasospasm after experimental subarachnoid hemorrhage (SAH) was studied in ten adult cats. The vasospasm was induced by injecting of 0.2-0.3 ml fresh autologous whole blood into the cisterna magna. Diameter of pial vessels was continuously measured by means of the vidicon camera system developed in our laboratory. Intravenous administration of nimodipine (0.1 mg/kg) 20-30 min after SAH resulted in a complete disappearance of the spasm with the reduction of blood pressure. The dilatory response was more marked in the smaller arteries (less than 100 microns) than in the larger ones (greater than or equal to 100 microns). Administration of smaller dose of nimodipine (0.01 mg/kg) also produced dilation of the pial vessels, although the effect was less remarkable in the smaller arteries. These data suggest that nimodipine might be useful in the treatment of the cerebral vasospasm after SAH. The mechanism underlying the action of nimodipine was discussed.

Animals↗
PubMedDate not supplied

No intracerebral steal phenomenon in the ischemic brain following papaverine administration.

The steal phenomenon due to a vasodilator was investigated in 6 cats in which cerebral ischemia had been produced by left middle cerebral artery (MCA) occlusion. The photoelectric method was employed for continuous recording of the cerebral blood volume together with frequent determinations of the cerebral blood flow (CBF) through the ischemic cerebral tissue at the following four stages: before MCA occlusion, 2 hours after MCA occlusion before the injection of papaverine, after the injection of papaverine, and when the systemic arterial blood pressure (SABP) was adjusted non-pharmacologically to the control level using a "vasculator". The administration of the vasodilator produced conflicting results for the CBF changes in the ischemic area with a decrease in SABP as reported previously in the literature. However, when the SABP was corrected to the control level, the CBF in the ischemic region became increased in all 6 cases to above the control ischemic flow values. It is concluded that the decreased CBF in the ischemic tissue after vasodilator administration was not due to the steal phenomenon, but simply to a fall in SABP.

Animals↗
PubMedDate not supplied

Quantitative measurement of blood flow velocity in feline pial arteries during hemorrhagic hypotension and hypercapnia.

Due to methodologic difficulties, few investigations have been made on the blood flow velocity in the cerebral microcirculation. Using a newly developed video camera method, we simultaneously measured the blood flow velocity and diameter of pial arteries during hemorrhagic hypotension, after blood pressure recovery, and during CO2 inhalation in cats. When the mean arterial blood pressure was lowered from 129.7 +/- 6.6 to 71.5 +/- 4.1 mm Hg, the blood flow velocity inevitably decreased from 36.6 +/- 5.3 to 27.0 +/- 3.9 mm/sec (p less than 0.001). The calculated blood flow rate [pi X (diameter/2)2 X flow velocity] was preserved in cases with concomitant vasodilation. Conversely, the blood flow velocity increased from 25.3 +/- 5.1 to 31.0 +/- 5.4 mm/sec (p less than 0.001) after mean arterial blood pressure recovery from 67.1 +/- 3.7 to 129.8 +/- 5.8 mm Hg. The blood flow rate was again preserved in vessels with a vasoconstrictive response. Each pial artery apparently dilated or constricted in proportion to the decrease or increase in flow velocity during blood pressure changes, maintaining a constant cerebral blood flow. This indicated the importance of the pial arteries in the mechanisms of cerebral blood flow autoregulation. During 5% CO2 inhalation, the blood flow velocity increased markedly from 25.4 +/- 4.6 to 37.2 +/- 10.0 mm/sec (p less than 0.05), while the pial artery diameter (85.0 +/- 13.7 microns) increased by 9.6 +/- 1.5% (p less than 0.01). The increased flow velocity might be attributable to preferential dilatation of small arterioles or intraparenchymal vessels during hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Leukoaraiosis: correlation of MR and CT findings with blood flow, atrophy, and cognition.

Hypodense periventricular white-matter lesions detected by CT (leukoaraiosis) and high-intensity T2 signals detected by MR imaging were correlated with measurements of local cerebral blood flow (LCBF), cerebral atrophy, and cognitive performance. Subjects studied included elderly volunteers who were neurologically normal (n = 6), patients with chronic cerebral infarctions and intact cognition (n = 2), patients with multiinfarct dementia (n = 14), and patients with Alzheimer dementia (n = 9). Leukoaraiosis correlated with periventricular high-intensity lesions detected by MR, LCBF reductions, cognitive impairments, and cerebral atrophy. Moderate to severe leukoaraiosis was associated with LCBF reductions in the cortex, basal ganglia, and frontal white matter. Periventricular MR lesions correlated with cerebral atrophy but not with cognitive impairments or reductions in LCBF. The exquisite sensitivity of MR revealed small lesions that did not correlate with LCBF reductions and cognitive impairments. Remote subcortical white-matter lesions detected by MR did not correlate with periventricular MR lesions, leukoaraiosis, LCBF, cerebral atrophy, or cognitive performance, indicating little clinical relevance. We concluded that diffuse cerebral hypoperfusion, particularly in combination with the poor collateral circulation of white matter surrounding the lateral ventricles, is responsible for leukoaraiosis.

Aged↗
PubMedDate not supplied

Conservative treatment in acute pancreatitis.

In the absence of causative therapy of acute pancreatitis the management of the disease focus on treatment and prevention of complications and symptoms. In mild acute pancreatitis intravenous fluid administration, analgetics and avoidance of oral fluid or food intake is sufficient in most cases. The treatment of severe pancreatitis involves identification of pancreatic and peripancreatic necroses, best demonstrated and evaluated by contrast-enhanced computerized tomography (CT). Infection of such necroses is the most common cause of death from acute pancreatitis. Recent data suggest that antibiotic prophylaxis is worthwhile and it should therefore always be instituted in the severe form of the disease. Careful monitoring of vital functions is mandatory and early treatment with assisted ventilation and renal dialysis is advised. Adequate volume replacement and nutritional support is important. The role of the gut in the development of infected necroses is becoming increasingly obvious. Also, the absence of food in the intestine may increase the intestinal barrier damage. Therefore, enteral nutrition is discussed as a logical step in pancreatitis treatment. However, the food should be delivered below the ligament of Treitz (below the area of the cholecystokinin (CCK) cells) as CCK stimulation probably worsen the course of the disease.

Acute Disease↗
PubMedDate not supplied

Surgery for chronic pancreatitis--extended pancreaticojejunostomy.

BACKGROUND/AIMS: The role of Frey's operation as extended pancreatic duct drainage operation was evaluated in patients with chronic pancreatitis. METHODOLOGY: 206 patients with chronic pancreatitis were surgically treated, evaluated and followed for a minimum period of 6 months, in order to ascertain the status of pancreatic function and pain relief for both pancreatic duct drainage operations, including Frey's operation, and pancreatectomy. RESULTS: Pain relief was established in 62 out of 86 patients (72.1%) undergoing pancreas duct drainage operation, in 51 out of 65 patients (78.5%) undergoing pancreatectomy. Fourteen out of 16 patients undergoing standard pancreaticojejunostomy with either persistent or alleviated pain had impacted calculi or pseudocysts in the pancreatic head and uncinate process preoperatively. Seventeen patients (16.3%) maintained normal glucose tolerance. Improvement was noted in 15 patients (14.4%) and in 27 patients the condition worsened (26.0%). The 10 years survival ratio in patients with diabetes mellitus preoperatively was 67.5% significantly lower than in patients without diabetes mellitus, 81.3% (p = 0.0029). Frey's operation was performed in 11 patients, providing satisfactory pain relief and preserving pancreatic exocrine and endocrine function. CONCLUSIONS: Frey's procedure should be considered as a new standard procedure in patients with pancreatic head complications and ductal dilatation in chronic pancreatitis.

Adult↗