Biomedical subjects

L N Cothran

Publications and source records attributed to L N Cothran.

10 recordsLinked to original sources

PubMed1994

Atrial natriuretic peptide-like (ANP-LIR) and ANP prohormone immunoreactive astrocytes and neurons of human cerebral cortex.

Atrial natriuretic peptide (ANP) represents a family of related peptides originally isolated from cardiac atria that have potent natriuretic, diuretic, and vasorelaxant properties. ANP has previously been localized in neurons of the rat brain in regions subserving cardiovascular functions and fluid/electrolyte balance and has been localized in astroglia of the canine brain. To determine whether ANP is present in astrocytes of the human brain and to validate the canine model for future studies, human brain tissue was obtained from autopsy cases with no brain damage or neurological or vascular disease. Human brains were obtained less than 3 h postmortem, and anterior cingulate and striate cortices were dissected following perfusion or immersion fixation. Immunohistochemical processing utilized antibodies against the processed form of ANP (ANP IV, ANP104-128) and against rat proANP (amino terminus) and the avidin-biotin-peroxidase technique. Isolated, strongly ANP-immunoreactive protoplasmic astrocytes were observed in all layers of the cingulate and striate cortex gray matter. ANP-positive fibrous astrocytes were observed in the white matter. Additionally, distinctive immunopositive astrocytes were found both within and immediately subjacent to the glia limitans. Antibody against the prohormone stained only protoplasmic astrocytes and sublimitans astrocytes and processes. In addition to the astroglia, ANP was detected in scattered multipolar neurons in the cerebral gray matter. These results provide additional evidence for diversity of peptide localization in astrocytes and suggest roles for ANP in the local regulation of cerebral blood flow, blood-brain barrier permeability, or cerebrospinal fluid volume.

Adult↗

PubMed1993

Distensibility of small pulmonary blood vessels.

Although vasomotor activity in small pulmonary vessels has been studied extensively in the past, using the concept of resistance to flow, information on the distensibility of these vessels is very sparse. In an attempt to reduce this deficit, we adapted a theoretical method developed for small systemic vessels, to estimate distensibility of pulmonary resistance vessels in experimental animals and man. Pressure-flow data from 11 dogs and 10 human subjects (5 control subjects and 5 patients with long-standing left heart failure) were used to calculate distensibility of small pulmonary vessels. The conductance, G, was calculated from these data as the ratio of blood flow to driving pressure. The slope of the relationship between the logarithm of G1/4 and the average distending pressure (ADP) provides a graphic picture of circumferential extensibility, E, defined as percent change in radius for an infinitesimal change in ADP. Results indicate that: (1) the value of E in dogs was 1.85 +/- .40 mmHg-1 for the control state, which decreased to 1.45 +/- .43 mmHg-1 during norepinephrine administration; however, the decrease in the value was not statistically significant (p = 0.53); (2) the value of E in control human subjects was 3.38 +/- .47 mmHg-1 and the value of E in patients with left heart failure was -0.64 +/- 0.39 mmHg-1; the difference was significant (P = .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Clinical relevance of distal arterial compliance.

AIM: To calculate the compliance of resistance vessels. METHODS: Pressure-flow data (plethysmographic and sphygmomanometric) were obtained non-invasively from six normal and six hypertensive subjects, and the results were compared with similar data obtained previously from large blood vessels. The parameter used to represent compliance was extensibility (E), defined as the percentage change in radius for a given change in pressure. RESULTS: The hand vessels of hypertensive subjects (E = 0.126 +/- 0.034/mmHg) were significantly stiffer (P < 0.02) than those of the normotensive subjects (E = 0.272 +/- 0.047/mmHg); and the values of E for the resistance vessels were larger than those for the large arteries.

Arteries↗

PubMed1990

Effect of hypertension on elasticity and geometry of aortic tissue from dogs.

Inflation-extension experiments were carried out on segments of the descending thoracic aortas from 4 normotensive and 4 hypertensive dogs rendered hypertensive using either unilateral or bilateral renal artery constriction. Intravascular pressures up to 200 mm Hg and axial forces up to 200 g were used. The external diameter of the segment and the distance between two longitudinally spaced gage marks were recorded photographically at each pressure-force level combination. Dimensions in the underformed configuration were measured at the end of the inflation-extension experiment. Data were analyzed for changes in geometry and force-deformation response. Results indicate that: 1. Under sustained hypertension the wall thickness in the underformed configuration increases with a concurrent reduction in the in-situ longitudinal extension ratio. 2. This dual tissue response accomplishes substantial reductions in the circumferential and longitudinal stresses from the levels that would be reached at equivalent pressures in the absence of these geometric changes. 3. At comparable intravascular pressures the extensibility in the circumferential direction is slightly greater for the hypertensive aortas as compared to normals. However, the stress-extension ratio relationship in the circumferential direction is similar in the two groups. 4. The stress-extension ratio relationship in the longitudinal direction indicates that the hypertensive aorta is stiffer than its normotensive counterpart.

Animals↗

PubMed1988

Absence of increase in left ventricular mass in dogs with bilateral renovascular hypertension.

Using sonomicrometric and indwelling pressure transducers, 16 healthy, normotensive dogs were prepared for semicontinuous monitoring of left ventricular (LV) mass, volumes, pressures, flows and wall tension (W Ten), aortic pressure (AP), total peripheral resistance (TPR), and indices of myocardial contractility. After a period of control measurements, bilateral renal artery constriction (2K-2C) was produced in 5 dogs and monitoring continued for 3 weeks or more. Mean arterial pressure (MAP) and LV end-systolic pressure (LVESP) was significantly higher (P less than 0.01) in the 2K-2C dogs compared to controls. There was no significant difference in LV mass, W Ten, or dP/dt, although TPR was 65% higher in the 2K-2C dogs. Comparable data from five dogs with single kidney hypertension (1K-1C), after 3 weeks, showed an elevated MAP and LVESP similar to the 2K-2C dogs. This group also showed a significant increase in LV mass and dP/dt (P less than 0.01), while the TPR was significantly decreased. The data suggest that the mechanism of hypertension development in the 2K-2C dog is different from that of the 1K-1C dog, and that there is evidence of increase in neuroadrenergic activity (viz, myocardial contractility) associated with the development of LV hypertrophy. The role of W Ten in the hypertrophic process was less clear from these data. Further study of these models may provide insight into the relative roles of the neuroadrenergic and volume-vasoconstriction components in the pathogenesis of hypertension and changes in LV mass.

Animals↗

PubMed1988

A theoretical method for estimating small vessel distensibility in humans.

A simple theoretical approach is presented for estimating vascular distensibility of small blood vessels from noninvasively obtained pressure-flow data in the hand and forearm of human subjects. To the extent that Poiseuille's law applies to blood flow in these vascular beds, conductance (the reciprocal of vascular resistance) can be calculated from these data as the ratio of blood flow to mean arterial pressure. The fourth root of the conductance is proportional to the radius of the vascular bed. The slope of the relation between the logarithm of the radius of the vascular bed and the transmural pressure is proportional to the vascular extensibility (E), which, in turn, for small deformations and constant vascular length, is proportional to the distensibility of small blood vessel. Data obtained from the hands of six hypertensive subjects were compared with that obtained from six normotensive subjects, all with their vascular beds in a maximally dilated state. Also compared were data obtained from four normal subjects with their vascular beds in the resting state and when the beds were maximally dilated. The results indicate that 1) in the hypertensive subjects, the small blood vessels of the maximally dilated vascular bed of the hand are significantly (p less than 0.02) less distensible (E = 0.126 +/- 0.034/mm Hg) than those in the normotensive subjects (E = 0.272 +/- 0.047/mm Hg) and 2) the small blood vessels of the normal forearm at resting levels of vasomotor tone are more distensible (E = 1.00 +/- 0.38/mm Hg) than in the maximally dilated state (E = 0.51 +/- 0.08/mm Hg).

Adult↗

PubMed1986

Noninvasive determination of small vessel distensibility in man.

The present study describes and illustrates a noninvasive method for computing extensibility of the 'resistance vessels', from an experimentally obtained resistance vs transmural pressure plot, in a maximally dilated vascular bed of man. Limb blood flow was measured plethysmographically following 10 min of arterial occlusion, and blood pressure was measured by the arm cuff method. A ratio of two resistance values taken 30 mm Hg apart was used to compute percent change in radius and the extensibility, E. The computed values of E were 0.71 mm Hg-1 for normal hand and 0.13, 0.22 and 0.69 for the hypertensive forearm, hand and finger respectively. These results indicate that the method may prove useful in the understanding and management of diseases such as hypertension or other small vessel diseases.

Capillaries↗

PubMed1986

Estimation of left ventricular mass in conscious dogs.

The short-axis area-length method for the estimation of left ventricular mass (LVM) and volume was validated in 24 formaldehyde-fixed canine hearts, using the truncated ellipsoid model. Estimates of the short-axis muscle area were highly correlated with directly measured values (R = 0.92; P less than 0.001). Similarly, LVM calculated using the area-length method showed good correlation with the actual weight of the left ventricle (LVW) (R = 0.85; P less than 0.001). When the regression equation was used, retrospectively, to correct the LVM estimates, the correlation between the actual LVW and the calculated LVM was markedly improved (R = 0.96; P less than 0.001). In awake dogs instrumented for measuring transverse and long axis ventricular dimensions using sonomicrometry, short-axis two-dimensional echocardiograms were used to convert the sonar external transverse dimensions to true diameters. The combined use of the corrected diameters and the regression equation to calculate LVM in the intact dog resulted in values that were highly correlated with the actual LVW (R = 0.95; P less than 0.001). Application of this technique for monitoring LVM in awake instrumented dogs demonstrated the method to be reproducible from day to day and to be sensitive enough to detect serial changes in mass such as during the development of left ventricular hypertrophy.

Animals↗

PubMed1986

Massive sequestration of human sickle cells after transfusion to a baboon.

A baboon was exchange-transfused with sickle cell anemia patients' blood. The animal died suddenly, and postmortem examination showed widespread red cell sequestration, particularly in the spleen and liver. The clinical and pathological findings were similar to those in children with sickle cell anemia who die of acute splenic sequestration syndrome. A control animal, exchange-transfused with normal human blood, tolerated the procedure without difficulties for a period of 4 days, when a delayed transfusion reaction occurred. Thus the baboon can be used as a model for the abnormal circulatory behavior of sickle cells and for the sickle cell sequestration syndrome.

Anemia, Sickle Cell↗

PubMed1980

Brain ischemia hypertension.

Hypertension was produced in anesthetized and conscious dogs when cerebral perfusion was reduced. It lasted up to 19 days in chronic studies, was not abolished by carotid sinus denervation nor with beta receptor blockade, but was absent after removal of brachiocephalic artery constriction (BCAC). The cardiovascular features of this "neurogenic hypertension" are presented.

Animals↗