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S Prusty

Publications and source records attributed to S Prusty.

At least 19 recordsLinked to original sources
PubMed2003

Hypertension-induced changes in monoamine receptors in the prefrontal cortex of rhesus monkeys.

Hypertension affects approximately 60 million people in the United States. Recent studies have demonstrated that hypertension may produce progressive changes in the CNS. The present study is focused on reports in the literature that hypertension may significantly alter neurotransmitter systems, particularly dopamine (DA) and norepinephrine (NE). To address this, DA and norepinephrine (NE) receptor binding was assessed in the prefrontal cortex (PFC) of 15 male rhesus monkeys using on-the-slide in vitro assays for the DA1, NE alpha1 and NE alpha2 receptors as well as for the DA and NE uptake transporters. Eight monkeys underwent surgical coarctation of the mid-thoracic aorta which produced sustained, untreated hypertension as defined by a systolic pressure above 150 mm Hg. Compared with normotensive controls, chronic, untreated hypertension produced a significant decrease in DA1 and NE alpha1 receptor binding and an increase in DA uptake (DAU) receptor binding in the prefrontal cortex. While the mechanisms by which untreated hypertension alters DA and NE receptors is not known, the use of this non-human primate model should provide the means to uncover neurobiological changes that occur with untreated hypertension.

Animals↗
PubMed2000

Intravascular circulation and distribution of human 51Cr-DBBF stroma-free hemoglobin, 51Cr-plasma, 51Cr-saline, 59FE-plasma, and 125I-albumin in the mouse.

Male B6C3HF1 mice were infused with human 51Cr-labeled DBBF (bis 3,5-dibromosalicyl fumarate) crosslinked stroma-free hemoglobin (SFH). In the first hour following SFH infusion, 11.2% of the infused radioactivity was found in the skin, 11.4% in muscle, 9.1% in the skeleton, and 5% in the liver. Twenty-four hours after infusion, 15.4% of the radioactivity was found in the skin, 10.3%, in the muscle, 16.6% in the skeleton, and 6.7% in the liver. The circulation and distribution of 51Cr-labeled DBBF-SFH were compared with levels of 51Cr labeled plasma, 51Cr in saline, 59Fe labeled plasma, and 125I albumin. The radioactivity in the blood was similar for 51Cr-DBBF-SFH, 51Cr-plasma, and 59Fe-plasma. During the 24-hour post-infusion period, extravascular distribution of the 51Cr-saline, 51Cr-plasma, and 125I albumin within the organs was similar to that of 51Cr-DBBF-SFH, with the highest levels being in skin, muscle, skeleton and liver, and no increase in the levels in the lung or spleen. The distribution of 59Fe compared to that of 51Cr-DBBF, 51Cr-plasma, 51Cr-saline, and 125I albumin can be explained by the fact that 59Fe is utilized in the production of new red blood cells.

Albumins↗
PubMed1999

Microinfarction as a result of hypertension in a primate model of cerebrovascular disease.

Ten adult cynomolgus monkeys were studied as a non-human primate model of hypertensive cerebrovascular disease. Seven were made hypertensive by surgical coarctation of the aorta and three served as unoperated controls. After survival periods of 8-30 months, the brains were serially sectioned and surveyed for neuropathological changes. The most conspicuous change was minute areas of microinfarction in the white and gray matter. The lesions were of irregular shape with an average maximum diameter of less than 0.5 mm. They were slightly larger in the gray than in the white matter and appeared to be of different ages. Their area of predilection was the white matter of the forebrain, with smaller numbers in the cerebral cortex and scattered lesions elsewhere in the forebrain, brain stem and cerebellum. These microinfarcts did not correspond to usually described lesions in the human brain in hypertension or in other animal models of hypertensive cerebrovascular disease. We suggest that they represent an early change in the natural history of hypertensive neuropathology.

Age Factors↗
PubMed1993

The effects of hypertension on cerebral atherosclerosis in the cynomolgus monkey.

BACKGROUND AND PURPOSE: There is substantial clinical, pathological, and experimental evidence that hypertension aggravates atherosclerosis of the extracranial vessels. The present study assesses the effects of hypertension on the development of cerebral atherosclerosis in nonhuman primates fed an atherogenic diet. METHODS: The extent and severity of cerebral atherosclerosis were evaluated morphologically, morphometrically, and biochemically in atherosclerotic monkeys with and without hypertension. Atherosclerosis was induced by feeding a hypercholesterolemic diet for 12 months; hypertension was produced by surgical coarctation of the thoracic aorta. RESULTS: At autopsy, gross atherosclerotic lesions of the major cerebral arteries were observed in 15 of 16 atherosclerotic monkeys with hypertension compared with 5 of 16 atherosclerotic animals without hypertension. In the hypertensive-atherosclerotic group, 38.5% of the vessels examined showed gross involvement compared with only 3.4% of the vessels involved in the atherosclerotic group (P < .001). The lesions in the atherosclerotic group were generally mild, whereas those in the hypertensive-atherosclerotic group were severe and resulted in significant luminal narrowing and occlusion of vessels (P < .001). The small branches of the cerebral arteries also showed severe disease with luminal obstruction in the hypertensive-atherosclerotic group. The extent and severity of cerebral atherosclerosis were significantly related to the severity of the hypertension (P < .05). CONCLUSIONS: Hypertension is an important factor in cerebral atherosclerosis because of its accelerating effect on the disease. Nonhuman primate models may be useful in clarifying the role of hypertension and atherosclerosis in cerebral vascular disease.

Animals↗
PubMed1992

Elevated expression of monocyte chemoattractant protein 1 by vascular smooth muscle cells in hypercholesterolemic primates.

Atherosclerosis is marked by an overt inflammatory infiltrate, with enhanced recruitment of monocytes/macrophages observed in both human and experimental atherosclerosis. We previously determined that monocyte chemoattractant protein 1 (MCP-1) accounts for virtually all of the chemotactic activity produced by vascular (aortic) smooth muscle cells in culture. We now report that arteries from a primate model of atherosclerosis with dietary-induced hypercholesterolemia exhibit increased levels of MCP-1 mRNA expression in vivo, whereas their normal counterparts demonstrate minimal MCP-1 expression. Furthermore, immunohistochemistry and in situ hybridization clearly indicate that the expression of MCP-1 protein and mRNA is in the smooth muscle cells of the medial layer of the artery and in monocyte-like and smooth muscle-like cells found in the overlying intimal lesion. These studies indicate that one of the responses to dietary hypercholesterolemia is the expression of MCP-1 by vascular smooth muscle cells. This expression, when augmented with other cellular and molecular factors, could significantly contribute to the recruitment of monocytes/macrophages to the vessel wall.

Animals↗
PubMed1992

Intravascular circulation and distribution of human 51Cr-DBBF stroma-free hemoglobin.

Male B6C3HF1 mice were infused with 51Cr-labeled DBBF (bis 3,5-dibromosalicyl fumarate) crosslinked stroma-free hemoglobin (SFH). The intravascular halftime (T50) of the DBBF-SFH, determined from plasma hemoglobin levels, was 0.5 hours in the first 10 minutes and 4.3 hours during the next 50 minutes. At 24 hours, less than 5% of the DBBF-SFH remained. Elution of 51Cr was reflected in a lower T50 determined from the radioactivity levels: during the first 10 minutes the T50 was 0.3 hours; in the next 50 minutes it was 1 hour. The radioactivity sequestered in each organ in the first hour following DBBF-SFH infusion was as follows: 11.2% of the infused radioactivity was in the skin, 11.4% in muscle, 9.1% in the skeleton, and 5% in the liver. After 24 hours, the percentages in skin, muscle, skeleton and liver were 15.4, 10.3, 16.6 and 6.7% respectively. The percentage of infused radioactivity in the gastrointestinal tract and kidney at 1 hour and 24 hours ranged from 3.5 to 5.5%. Less than 0.4% was found in the spleen and lung. At 24 hours, 25% of the radioactivity was recovered in urine and 3% in feces.

Animals↗
PubMed1988

Occurrence of stroke in a nonhuman primate model of cerebrovascular disease.

A relation between hypertension, atherosclerosis, and stroke is well documented in humans. We report a similar relation in two hypertensive cynomolgus monkeys with severe cerebral atherosclerosis. In our primate model hypertension is induced by surgical coarctation of the aorta. These monkeys, when fed an atherogenic diet, develop severe cerebrovascular atherosclerosis. In this setting two monkeys developed spontaneous cerebral hemispheric strokes that occurred during treatment of hypertension. Since the strokes were topographically related to severe atherosclerotic narrowing of cerebral arteries and occurred without evidence of either thrombosis or embolization, they are presumed to be related to disturbances of blood flow. In both humans and animals cerebral perfusion is autoregulated to a constant flow over a wide range of mean arterial blood pressures. In hypertension both the upper and lower limits of autoregulation are increased. With treatment of hypertension readaptation to more normal levels is reported to be inconsistent and slow to develop. It is therefore postulated that the strokes in these two monkeys were due to hypoperfusion as a result of the combination of pharmacologic reduction in blood pressure and severe occlusive atherosclerosis.

Animals↗
PubMed1977

Role of hypertension in ischemic heart disease and cerebral vascular disease in the cynomolgus monkey with coarctation of the aorta.

The role of hypertension in cardiovascular disease was studied in the hypertensive coarcted monkey during the feeding of an atherogenic and nonatherogenic diet. During the 15-month period of observation, half of the hypertensive coarcted monkeys developed cardiovascular disease which included heart failure, ischemic heart disease, stroke, and sudden death. There were no cardiovascular complications in the control normotensive monkeys except for one cholesterol-fed animal. The incidence of ischemic heart disease and sudden cardiac death was higher in monkeys with both hypertension and hypercholesterolemia than in those with hypertension or hypercholesterolemia alone. Postmortem studies revealed that the former monkeys had both hypertensive and atherosclerotic heart disease, whereas the monkeys with hypertension or hypercholesterolemia had either hypertensive or atherosclerotic heart disease. Hypertensive heart disease was characterized not only by hypertrophy of the left ventricle but also by focal myocardial degeneration and fibrosis and by focal thickening and narrowing of the small coronary arteries, particularly the sinus node artery and the atrioventricular node artery. The finding of transmural myocardial infarction in two monkeys with patient coronary arteries suggests a possible role of coronary artery spasm in ischemic heart disease in hypertension. The cerebral vascular complications of hypertension included hypertensive encephalopathy, transient "ischemic" attacks, and hemorrhagic stroke. The complications were associated with severe hypertension and with hypertensive vascular disease or hypertensive and atherosclerotic vascular disease of the cerebral arteries.

Animals↗
PubMed1975

Aortic regurgitation from infective endocarditis in Fallot's tetralogy and pulmonary atresia.

Three cases of aortic regurgitation acquired as the result of bacterial endocarditis complicating Fallot's tetralogy and pulmonary atresia have been described. One also had mitral regurgitation from a 'jet lesion' of the anterior cusp of the mitral valve. Surgical treatment of all abnormalities with aortic valve repair or replacement was undertaken in each patient and was successful in two. Difficulties in diagnosis and surgical treatment are discussed.

Adult↗
PubMed1975

Adult cyanotic congenital heart disease.

The surgical treatment of cyanotic heart disease in the adult poses some technical difficulties in correcting severe anatomical deformities and compromised physiological states over a wide range of conditions. Various abnormalities and their surgical management have been reviewed. Forty-six patients over the age of 18 years have been operated with 10 operative deaths. Of the survivors, 63% have had excellent clinical result; 69.5% of the total group had an excellent or good result following surgery. It is concluded that the age of the patient is not a bar to the complete repair of these deformities, and all cases of adult cyanotic heart disease should be investigated with a view to surgical correction.

Adolescent↗