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Biomedical subjects

J G Frazee

Publications and source records attributed to J G Frazee.

30 records · Page 2Linked to original sources
PubMed1985

Experimental chronic cerebrovascular spasm in the monkey: an assessment of the functional changes in the cerebral arteries and their protection by diltiazem.

The structure and function of cerebral arteries obtained from a monkey model of chronic cerebral vascular spasm 5 days after hemorrhage have been examined. Narrowing of the larger cerebral arteries demonstrated by angiography at all sites of measurement seems to be due primarily to an increased wall rigidity associated with cellular damage, the resultant inflammatory response and large, long-lasting spontaneous increases in muscle tone. Changes in agonist sensitivity were extremely variable. The reduction of contractility of the vessel wall to a mean of 30% of control diminished the consequence of any changes in active tone characteristics. Neurogenic control on the side of the lesion was remarkably depressed. When treated with diltiazem, beginning 1 day before induction of hemorrhage and continuing to the time of sacrifice, arterial diameter was reduced at only 1 of the 6 standard sites of measurement and then by only a small amount. Neurologic effects invariably seen in the untreated monkeys were prevented by diltiazem. Many of the changes in the artery wall, including structural alterations, were diminished by the drug. Abnormal spontaneous myogenic tone was present but was less in the diltiazem-treated group; however, nerve damage and its functional consequences were not prevented. It is concluded that diltiazem, presumably by preventing the accumulation of intracellular calcium within the cell, prevents the initial events in the evolution of chronic cerebrovasospasm or narrowing. This is probably achieved by a diminishing of the direct vasoconstrictor effects and the toxicity of putative spasmogens released from blood clots, nerves and the brain on the vascular smooth muscle, thus interrupting the sequence leading to pathologic change.

Animals↗
PubMed1985

Effect of diltiazem on experimental chronic cerebral vasospasm in the monkey.

The influence of diltiazem on chronic cerebral vasospasm was studied following subarachnoid hemorrhage (SAH) in a primate model. The model mimics the human experience including the production of neurological deficits. Six monkeys were pretreated with diltiazem (25 mg/kg twice daily) for 2 days prior to surgical production of an SAH and for 5 days after the hemorrhage. This group was compared with six untreated monkeys that also sustained an SAH. The mean diameter of cerebral arteries measured at six angiographic sites was 60.6% of the pre-SAH diameter for the untreated group and 99.7% for the diltiazem-treated group. These values are significantly different (p less than 0.0005). There was no neurological deficit in the pretreated animals. The mean diameter of the "most constricted vessel" in each experiment was 22% of the prehemorrhage diameter for the untreated and 84% for the treated group (p less than 0.0005). Arterial pressure was unaffected by the dosage regimen. These experiments with this primate model of chronic cerebral vasospasm demonstrate that vascular narrowing and neurological deficit can be markedly attenuated by diltiazem pretreatment.

Animals↗
PubMed1981

Intravenous nitroglycerin for the treatment of chronic cerebral vasoconstriction in the primate.

A primate model of chronic cerebral vasoconstriction is presented which closely approximates the human experience following subarachnoid hemorrhage. Treatment of the vasoconstriction with intravenous nitroglycerin produces a modest, but statistically significant, increase in the size of the most constricted vessels (11%, p less than 0.02) when compared with a control infusion of normal saline. The significance of these experiments is discussed.

Animals↗
PubMed1980

Bacterial intracranial aneurysms.

The treatment of 13 patients with bacterial intracranial aneurysms is reported. The incidence of bacterial intracranial aneurysms was 4% of all patients admitted with intracranial aneurysms and 3% of all patients admitted with bacterial endocarditis. Each patient had neurological signs or symptoms suggestive of intracranial disease prior to the diagnosis of an aneurysm. Alpha Streptococcus was the most common infecting organism. All patients were treated with specific, high-dose antibiotics, and five patients underwent surgery as well. There were no surgical deaths. Six of eight nonsurgically treated patients died. A review of the literature confirms a high mortality for patients treated with only antibiotics, and a low mortality for elective surgery. The authors conclude that 1) patients with bacterial endocarditis, who develop sudden severe headache, focal neurological signs or symptoms, or seizures, should undergo serial cerebral angiography every 7 to 10 days throughout their hospitalization; 2) if an aneurysm is identified it should be excised whenever possible; and 3) patients with proximal or multiple aneurysms should be considered for surgery.

Adult↗
PubMedDate not supplied

A primate model of chronic cerebral vasospasm.

Fourteen experiments have been completed to develop an improved primate model of chronic cerebral vasospasm. Results show that by placing a 0.4 mm needle through the intracranial internal carotid artery and percutaneously removing it the following day, cerebral vasospasm is regularly present five days later. There has been no mortality. The results of two monkeys followed with serial angiograms suggest that spasm first appears four days following the subarachnoid hemorrhage and lasts at least eleven days. The results of all experiments show that the most affected vessel in each experiment is reduced to 62% of control diameters. Vasospasm involves cerebral arteries both ipsilateral and contralateral to the site of hemorrhage and extends to the most distal vessels which can be measured. Finally, a neurological defect has been regularly demonstrated on the side contralateral to the site of hemorrhage.

Animals↗
PubMedDate not supplied

Functional arterial changes in chronic cerebrovasospasm in monkeys: an in vitro assessment of the contribution to arterial narrowing.

Cerebral arteries from monkeys with chronic cerebral vasospasm arising from experimental subarachnoid hemorrhage produced 5-6 days previously were examined for changes in their functional properties in an attempt to understand the basis of the narrowing. Hemorrhage was caused by puncture of the internal carotid artery just proximal to the circle of Willis. Segments taken close to the origins of the anterior and middle cerebral arteries consistently showed decreased distensibility. In addition, they exhibited large, prolonged, spontaneous increases in muscle tone. Other alterations observed include a marked reduction in the capacity of the vessel wall to contract, reduction in constrictor and dilator nerve influences on vascular tone, and some increased sensitivity to serotonin. Small pial arteries (150-200 micron o.d.) from the side of the injury showed large spontaneous irregular increases in tone. It is proposed that 5-6 days after experimental subarachnoid hemorrhage in monkeys the change most responsible for persistent narrowing in the larger arteries is an increased rigidity of the vessel wall. This is probably caused by an inflammatory response. In the smaller arteries, abnormal spontaneous contractile activity is a major factor in narrowing. This activity is not stretch-dependent. We suggest that the initial cause of the arterial narrowing after hemorrhage is the action of vasoactive substances released in the close vicinity of the arterial wall, which lead to tissue damage, abnormal tone, and an inflammatory response with fibrosis.

Animals↗
PubMedDate not supplied

Microvasculature in brain biopsy specimens from patients with Alzheimer's disease: an immunohistochemical and ultrastructural study.

Brain biopsy specimens from five patients with Alzheimer's disease obtained in the course of a trial of intracerebroventricular bethanechol were studied by immunohistochemical (antibody to A4 peptide) and ultrastructural techniques, with particular emphasis on the microvessels. In some cases, numbers of A4-immunoreactive lesions (senile plaques) correlated well with numbers of plaques demonstrable by silver stains. Prominent A4-immunoreactive amyloid angiopathy was seen in one patient. The patient with severe cerebral amyloid angiopathy (CAA) showed extensive arteriolar deposition of amyloid filaments with apparent destruction of the media but remarkably intact endothelium. A cell of origin for amyloid filaments was not apparent, although close proximity to smooth muscle cell remnants in the arteriolar media suggested this as one possible cell of origin. Frequent vessels showed medial or adventitial collagen deposition, even when the amount of amyloid was minimal or negligible. Thus relatively severe CAA can exist in the absence of overt endothelial injury, although related studies on this tissue indicate definite abnormalities of the blood-brain barrier. Conversely, destruction of smooth muscle cells and collagen deposition in vessel walls may be the cellular correlates of arteriolar weakening that can lead to CAA-related brain hemorrhage.

Alzheimer Disease↗
PubMedDate not supplied

Intraoperative digital subtraction neuroangiography: a diagnostic and therapeutic tool.

We report our experience with intraoperative digital subtraction neuroangiography to demonstrate its application as a diagnostic and therapeutic technique. Intraoperative neuroangiography was performed on 53 occasions in 43 patients using a portable imaging system. Thirty-two procedures were performed for diagnostic purposes after resection of arteriovenous malformations, clipping of aneurysms, or carotid endarterectomy. Unexpected problems were disclosed in seven cases and were surgically remedied immediately in four. In addition, angiography was used as a therapeutic tool in 21 cases to facilitate intraoperative embolization of a vascular lesion or to enable the angioplasty of a vessel inaccessible without direct surgical exposure. We found that by allowing a combined interventional neuroangiographic and neurosurgical approach, intraoperative angiography opened new avenues for treatment of intracranial vascular abnormalities.

Cerebral Angiography↗