Biomedical subjects

P Coyle

Publications and source records attributed to P Coyle.

76 records · Page 5Linked to original sources

PubMedDate not supplied

Different susceptibilities to cerebral infarction in spontaneously hypertensive (SHR) and normotensive Sprague-Dawley rats.

Rapid occlusion of the middle cerebral artery (MCA) was undertaken in 5-6 week old rats to determine whether or not the young spontaneously hypertensive rat (SHR) or the normotensive Sprague-Dawley rat (SD) is protected against cerebral infarction by collateral circulation. Rats were killed 3 days after MCA occlusion and administration of Evans blue. As compared to SD, the SHR had elevated blood pressure prior to MCA occlusion, large cortical infarcts marked with Evans blue, and motor deficits contralateral to the occluded MCA. SHR did not develop an adequate collateral circulation, but SD were protected from infarction by it. Because the cerebral lesions were in young spontaneously hypertensive rats living prior to the established form of hypertension, the increased susceptibility to infarction was not secondary to it. Since normotensive rats usually do not infarct after sudden MCA occlusion, the infarction trait may be linked to the mechanism causing elevated blood pressure in spontaneously hypertensive rats.

Animals↗

PubMedDate not supplied

Blood flow through cerebral collateral vessels one month after middle cerebral artery occlusion.

Acute occlusion of a middle cerebral artery (MCA) reduces cerebral blood flow in normotensive Wistar-Kyoto rats (WKY) and in stroke-prone spontaneously hypertensive rats (SHRSP). The goal of this study was to determine whether MCA occlusion produces a sustained reduction in cerebral blood flow or whether collateral vessels restore blood flow to normal levels. We measured blood flow through cerebral collateral vessels to the territory of the occluded MCA and to homologous tissue of the other hemisphere in WKY 1 month after occlusion of the MCA. Cerebral blood flow, measured with microspheres, was restored to normal levels under control conditions in the territory of the occluded MCA. During vasodilatation produced by seizures, blood flow and vascular conductance were increased to similar levels in tissue distal to the site of MCA occlusion and in the homologous tissue of the other hemisphere. MCA occlusion did not produce infarction in any of the WKY. In contrast, 1 month after MCA occlusion in SHRSP, a large atrophic infarct was invariably present in the territory of the occluded MCA. The number of collateral vessels to the territory of the MCA do not differ in SHRSP and WKY. Internal diameter and orientation of the anastomotic vessels differ in SHRSP and WKY. We conclude that, after 1 month of MCA occlusion, changes in the collateral vessels supplying the territory of the occluded MCA in WKY were sufficient to restore blood flow to normal under control conditions and to virtually normal levels during vasodilatation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Spatial relations of dorsal anastomoses and lesion border after middle cerebral artery occlusion.

Occlusion of the middle cerebral artery invariably results in infarction of tissue in stroke-prone spontaneously hypertensive rats (SHRSP). To determine if the lesion border extends beyond the territory of the occluded middle cerebral artery or if the lesion enlarges with time after the occlusion, spatial relations of the lesion and the primary anastomosing collateral branches were investigated. Measurements were made 1 day (n = 8) or 21 days (n = 8) after occlusion in 5-8-week-old SHRSP brains marked by triphenyltetrazolium chloride (TTC) or tissue atrophy. After 1 day of occlusion, the border between TTC-marked and -unmarked tissue was parallel to, and without spatial displacement from, the medial border of infarcted tissue measured 21 days after the occlusion. Thus, the TTC border accurately localizes the medial border of ischemic tissue that progresses to atrophy. The lesion border was 1.16 +/- 0.04 mm downstream from the anastomoses, and the mean distance was not significantly different in frontal, parietal, or rostral occipital regions or between the 2 groups of rats. Thus, a small but significant amount of tissue between the anastomoses and the lesion border was protected against infarction after middle cerebral artery occlusion in SHRSP. After 21 days of occlusion, the dorsal anastomoses were enlarged, bilaterally symmetric in position but not size, and without displacement from the anastomoses in 1-Day rats. Large-diameter anastomoses were further from the lesion than small-diameter anastomoses in both groups of rats, thus indicating that protection is greater near large anastomoses than near small ones.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Altered insulin response to glucose in weight-losing cancer patients.

Cancer cachexia and the underlying metabolic disturbances are due in part to either altered insulin release and action. Glucose intolerance in cancer patients is frequently observed but the nature of the insulin response is not usually described. The aim of this study was to investigate the insulin response in fasted, weigh-losing cancer patients following an oral glucose load (75 g). All cancer patients (n = 35) showed glucose intolerance. Three types of response were identified; those with an increased insulin: glucose ratio (I:G) at 60 min, (average 12.3, n = 13), those with a normal I:G (average 7.2 n = 7) and those with a decrease I:G (average 4.2, n = 15). Fasting plasma glucose concentrations were normal in all groups prior to the glucose tolerance test. However, patients with the lowest I:G also had the lowest fasting plasma insulin concentrations, the lowest plasma albumin concentrations and the highest plasma triglyceride concentrations. Those patients with an abnormal insulin response (either high or low I:G) had significantly greater weight loss (16% for low I:G group, 13% for the high I:G) compared to the normal responders (8%). Plasma fatty acid concentrations were increased in all cancer patients and decreased appropriately after glucose administration, indicating that lipolysis remained sensitive to the action of insulin. It is concluded that weight loss in cancer is associated with glucose intolerance and an abnormal insulin response, and that this response is indicative of either insulin resistance (high I:G) or decreased pancreatic function (low I:G). These findings suggest a role for insulin replacement therapy in the latter group of patients.

Blood Glucose↗