Search PubMed⌕ Search

Biomedical subjects

D Boisvert

Publications and source records attributed to D Boisvert.

31 records · Page 2Linked to original sources
PubMed1984

Effect of reserpine-kanamycin treatment on chronic vasospasm after platelet-enriched subarachnoid hemorrhage in primates.

A model of chronic cerebral vasospasm (VSP) analogous to the clinical situation was established by inducing subarachnoid hemorrhage (SAH) in monkeys. Platelets harvested from 4 ml of blood were added to autologous blood in an attempt to accentuate any effect that vasoactive substances such as serotonin, contained in platelets, might have on producing cerebral VSP. Antiserotonin medications were administered in an attempt to reduce the frequency or severity of angiographically proven VSP. Animals were divided into small (1 ml/kg) and large (1.2 to 1.5 ml/kg) hemorrhage groups and later were randomized equally to receive either saline placebo or reserpine (0.013 mg/kg i.m.) and kanamycin (50 mg/kg p.o.) administered 3 hours after SAH and daily thereafter to Day 7. In both the small and the large hemorrhage groups of treated animals, there was a significant reduction in serotonin levels (P less than 0.01 and P less than 0.05, respectively) compared to base line levels. In the groups of nontreated monkeys with small and large hemorrhages, serotonin levels were not statistically different from control values. Despite reduction of serotonin levels to 19 and 26% of the control values in the small and large hemorrhage, treated groups, there was no apparent difference in the frequency or severity of angiographically proven VSP. This study found no evidence that reserpine and kanamycin have a beneficial effect on preventing VSP when treatment is begun after SAH.

Animals↗
PubMed1984

A randomized placebo-controlled double-blind trial of nimodipine after SAH in monkeys. Part 1: Clinical and radiological findings.

The authors have developed a method to induce chronic cerebral vasospasm after subarachnoid hemorrhage (SAH) in monkeys. With microsurgical techniques, 33 monkeys had a frontotemporal craniectomy and unilateral opening of the subarachnoid cisterns. Cerebrospinal fluid was drained and a fresh hematoma, obtained from an average of 7 ml of autologous blood, was carefully placed against the major arteries of the anterior circulation on one side. The 30 monkeys studied for 7 to 14 days after the SAH were allocated randomly to two treatment groups of 15: one group received placebo and the other nimodipine, 1 mg/kg every 8 hours. Indices monitored before and after SAH included neurological status, cerebral blood flow, computerized tomography, and angiographic vessel caliber. In the placebo group, delayed ischemic neurological deficit developed in one monkey 4 days after clot placement and was present at sacrifice on Day 14. No such deficit occurred in the nimodipine group. The effect of nimodipine on vessel caliber at this dosage was equivocal. Significant vasospasm (31% to 100% reduction in vessel caliber) developed in 87% (26 of 30) of the animals. Overall, vasospasm was slightly more common in the placebo group: in this group, on Days 7 and 14, the incidence of vasospasm was significantly higher (p less than 0.05) than in the nimodipine group. However, the average percentage reduction in vessel caliber of the maximally constricted vessel in each monkey was not significantly different between the two groups.

Animals↗
PubMed1984

A randomized placebo-controlled double-blind trial of nimodipine after SAH in monkeys. Part 2: Pathological findings.

Chronic cerebral vasospasm was induced in monkeys by placement of an autologous blood clot after the basal cisterns had been opened over the arteries of the circle of Willis on one side. The experimental protocol was detailed in Part 1 of this paper. Twenty of the 30 monkeys studied from both groups (one receiving placebo and the other nimodipine) underwent cerebral fixation (Day 14) at controlled pressure by intra-arterial perfusion. The arteries at the base of the brain were studied by light microscopy and scanning (SEM) and transmission electron microscopy (TEM). Cerebral angiography on Day 7 showed that vasospasm was significantly more common (p less than 0.0001) and more severe (p less than 0.01) on the clot side compared to the control or non-clot side. Vasospasm was less severe on Day 14, just before sacrifice. On SEM, 80% of the 20 middle cerebral artery (MCA) specimens that had been in spasm (Day 7) showed marked corrugation , and in some the endothelium had a fish-scale appearance. All of the 10 MCA's on the clot side examined by TEM that had been in spasm (Day 7) showed marked changes such as endothelial swelling, subendothelial proliferation, corrugation of the elastic lamina, and myonecrosis. With few exceptions, none of the basilar arteries or MCA's on the non-clot (control) side showed any abnormalities. The pathological findings of vessels in spasm were considered to be slightly less severe in the nimodipine group; however, the trial drug (1 mg/kg/8 hrs) did not prevent such abnormalities from occurring. The ultrastructural changes in the arterial walls of specimens from both placebo and nimodipine groups in vasospasm are described. Since dramatic changes are present in the vessel walls even after radiologically visible vasospasm has almost completely abated, we believe that vasospasm is due to long-lasting smooth-muscle constriction and not to vessel wall thickening caused by a cellular or subcellular infiltrate.

Animals↗
PubMed1984

Effects of photoradiation therapy on normal rat brain.

Laser photoradiation of the brain via an optical fiber positioned 5 mm above a burr hole was performed after the injection of hematoporphyrin derivative (HpD) in 33 normal rats and 6 rats with an intracerebral glioma. Normal rats received HpD, 5 or 10 mg/kg of body weight, followed by laser exposure at various doses or were exposed to a fixed laser dose after the administration of HpD, 2.5 to 20 mg/kg. One control group received neither HpD nor laser energy, and another was exposed to laser energy only. The 6 rats bearing an intracranial 9L glioma were treated with HpD, 5 mg/kg, followed by laser exposure at various high doses. The temperature in the cortex or tumor was measured with a probe during laser exposure. The rats were killed 72 hours after photoradiation, and the extent of necrosis of cerebral tissue was measured microscopically. In the normal rats, the extent of brain damage correlated with increases in the dose of both the laser and the HpD. In all 6 glioma-bearing rats, the high laser doses produced some focal necrosis in the tumors but also damaged adjacent normal brain tissue. We conclude that damage to normal brain tissue may be a significant complication of high dose photoradiation therapy for intracranial tumors.

Animals↗
PubMed1982

Psychophysiological disorders in anxious patients: hypertension and hypotension.

Anxious patients have a higher incidence than the general population for cardiovascular disorders and sudden death. Several studies have emphasized abnormal pulse rate, abnormal heart response conditioning, high incidence of arrhythmia, and abnormal blood pressure. Essential hypertension has been studied in relation to stress, and chronic hypotension ('low blood pressure syndrome') has been clinically recognized for decades, but rarely systematically studied. We investigated these abnormal blood pressures in anxious patients, during controlled trials with 80 patients having generalized anxiety disorder as defined in DSM III, for at least 6 months duration, and of moderate to severe intensity. They were randomly assigned to placebo, or bromazepam, 18 mg/day. Blood pressure, pulse, and several other measurements were taken on a weekly basis for 2 months (washout phase--1 week, treatment phase--4 weeks, and withdrawal phase--3 weeks). One third of these patients had an abnormal blood pressure (hypertension or hypotension) while untreated, and this is statistically significant when compared to a matched control group of nonanxious patients. Bromazepam improved several patients having either hypertension or chronic hypotension. These findings are relevant for long-term treatment of anxious patients, since cardiovascular psychosomatic complications are a major health problem.

Adolescent↗
PubMed1982

Chronic cerebral vasospasm after large subarachnoid hemorrhage in monkeys.

The authors have developed a model of chronic cerebral vasospasm analogous to the clinical situation, by inducing a large subarachnoid hemorrhage (SAH) in monkeys. With this model, the size of the SAH apparent on the first computerized tomography (CT) scan was correlated with the incidence and severity of cerebral vasospasm that developed. Indices monitored for up to 21 days after SAH included cranial CT scan, cerebral blood flow, vessel caliber, and neurological status. The 18 monkeys studied for 48 hours or more were divided into two groups according to the size of the SAH on CT scan. Vasospasm was more common in the group with large SAH. In this group, on Days 0, 7, and 14, the incidence of vasospasm was significantly higher than at other times (p less than 0.001, p less than 0.01, and p less than 0.05, respectively), and the percentage reduction in vessel caliber was significantly greater than in the group with small/medium SAH (Day 7, p less than 0.02; Days 0 and 14, p less than 0.05). Delayed neurological deficit developed in two monkeys with large SHA. Apathy was noted from Day 17 to Day 21 in one, and unsteadiness and drowsiness were noted on Days 4 and 5 in the other. Overall, the incidence, degree, and time course of vasospasm reflected the size of the hemorrhage.

Animals↗