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Biomedical subjects

J Grayson

Publications and source records attributed to J Grayson.

At least 37 records · Page 2Linked to original sources
PubMed1985

Transmural distribution of intramyocardial pressure measured by micropipette technique.

A technique is presented for measuring intramyocardial pressure (IMP) in beating hearts using the servo-nulling pressure transducer equipped with polyethylene micropipettes (ID less than 12 micron). The static and dynamic response characteristics of the system were tested in a pressurized, saline-filled container as well as in a pressurized, hollow, gelatin cylinder. The system was then used to measure IMP in vivo in the hearts of 12 dogs during stable cardiac performance and with aortic constriction. In vitro response characteristics were found to be satisfactory for accurate reproduction of cardiovascular waveforms. Peak systolic IMP was not found to exceed the simultaneously recorded left intraventricular pressure (LVP). Furthermore, the slope of the regression line relating the IMP to LVP during systole is linearly related (slope 0.98) to the depth of the micropipette tip in the ventricular wall, as normalized to total wall thickness. Diastolic IMP ranged between 1 +/- 1 (minimum during the cardiac cycle) and 4 +/- 2 mmHg (end diastolic) at associated LVP of 2 +/- 2 and 5 +/- 2 mmHg (mean +/- SD), respectively.

Animals↗
PubMed1983

T cell-replacing factor for glucocorticosteroid-induced immunoglobulin production. A unique steroid-dependent cytokine.

Glucocorticosteroids (GCS) added to otherwise unstimulated cultures of human peripheral blood mononuclear cells (PBMC) induce the synthesis and secretion of all classes of immunoglobulin. The magnitude of this response is similar to that seen with other polyclonal B cell activators such as pokeweed mitogen (PWM), and like that of PWM, the steroid effect is dependent on both T cells and monocytes. To determine the cellular target for GCS in these cultures, separated populations of T cells and non-T cells were preincubated with steroids and then recombined. No immunoglobulin was produced in any of these preincubation experiments. As a different approach to this question, supernatants were collected from various cell populations following stimulation with PWM, concanavalin A (Con A), phytohemagglutinin (PHA), alloantigens, or GCS. These supernatants were tested for their effects on GCS-induced Ig production by B cells. Supernatants from 3-d cultures of unstimulated, as well as GCS-treated, PBMC contained a T cell-replacing factor that permitted T-depleted PBMC to produce Ig upon steroid stimulation. This supernatant factor (TRF-S) could be produced in the absence of steroid stimulation, but both the factor and GCS were necessary for the induction of Ig synthesis. Production of the TRF-S required the presence of both T cells and adherent cells in culture and was found in the highest concentrations at 3-4 d of culture. Supernatants from cultures stimulated with PWM, PHA, Con A, and alloantigens did not contain detectable TRF-S activity, and TRF-S was unable to replace helper T cells for PWM-induced Ig production. TRF-S required the presence of adherent cells in the T cell-depleted responder population for its action. Further, it was effective in inducing Ig production along with GCS in the presence of a sufficient concentration of cyclosporin A to block all T cell helper activity for primary responses of PBMC to PWM or GCS. TRF-S was inactivated by trypsin treatment, heating to 56 degrees C, freezing, lyophilization, and storage at 4 degrees C for greater than 3 wk. Its molecular weight is probably 10,000 daltons or more, since TRF-S activity is not rapidly dialyzable. These experiments indicate that GCS-induced Ig production by human B cells does not require the presence of intact T cells in the cultures and therefore the steroids are not exerting their influence directly on T suppressor or T helper cells. Furthermore, they demonstrate a previously unrecognized cytokine that induces the differentiation of human B cells to Ig production in the presence of GCS.

B-Lymphocytes↗
PubMed1983

The effect of catecholamines on intestinal glucose and oxygen uptake in the dog.

Using the anaesthetized dog, continuous recording was made of the oxygen and glucose contents of the artery and the vein draining the upper jejunum. Flow was also measured and results expressed as differences in oxygen and glucose between the aorta and the jejunal vein (a-v), also as oxygen consumption and glucose uptake. Resting glucose uptake was greater than could be accounted for on the basis of oxidation. When adrenaline (1 microgram/kg. min) or noradrenaline (2 micrograms/kg. min) was infused intravenously, oxygen uptake rose by about 50% whereas glucose uptake rose by 300-500%; moreover, the rise in glucose uptake was apparent before the rise in oxygen uptake. The beta-blocking agent, propranolol (0 X 5 mg/kg. min) had no effect on oxygen uptake but caused a three-fold rise in glucose uptake. Subsequently infusion of adrenaline had no effect on oxygen uptake and no effect on glucose uptake. However, on stopping the infusion there was a marked drop in glucose uptake, which was not maintained. It is suggested that the effects of catecholamines may be due to altered arterial blood glucose levels and that the jejunum may play a role in glucose homeostasis which requires the action of beta receptors.

Animals↗
PubMed1983

Effect of cold exposure on various sites of core temperature measurements.

Rectal, esophageal, auditory canal, gastrointestinal tract, and sublingual temperature were recorded on five young Caucasian males who, in an environment of -32 degrees C and 11-km/h wind, sat during one 90-min exposure and walked on a treadmill at 2.9 km/h during another. The clothing permitted cooling of their torsos while giving adequate protection to their extremities. Control exposures involved subjects sitting in still air at 24-26 degrees C dressed only in thermal underwear. In the control environment all of the internal body temperatures measured gave comparable and consistent values; however, cold exposure affected the various sites differently. Esophageal temperatures fluctuated rapidly as a result of subjects swallowing cold saliva. Sublingual temperatures were below the lower limit of a clinical thermometer, possibly because of facial cooling. Auditory canal temperatures were low, perhaps also because of facial cooling. Rectal temperatures were high as were the gastrointestinal tract temperatures, due perhaps to local heat production in response to cold stimulation. Metabolic rate increased initially in the cold and again toward the end of the cold exposure.

Body Temperature↗
PubMed1981

Immunoglobulin production induced in vitro by glucocorticoid hormones: T cell-dependent stimulation of immunoglobulin production without B cell proliferation in cultures of human peripheral blood lymphocytes.

The direct effects of steroid hormones on the production of immunoglobulins and DNA synthesis by human T and B lymphocytes was evaluated in cultures of peripheral blood mononuclear cells. As detected by a reverse hemolytic plaque assay, the addition of 0.1 mM to 10 nM hydrocortisone to lymphocytes in culture in the absence of other stimulants or mitogens, resulted in the dramatic induction of immunoglobulin production with responses comparable to those seen in similar cultures stimulated with pokeweed mitogen. Steroid-stimulated immunoglobulin production was first seen after 48 h and peaked at 8-10 d of culture. The production of IgG, IgA, and IgM was induced following incubation with steroid. Glucocorticoids, but not estrogens or androgens, were capable of mediating this effect, and only compounds with affinity for the glucocorticoid receptor were active. The induction of immunoglobulin production was dependent on both T cells and monocytes; cultures depleted of either cell type did not produce immunoglobulin when stimulated with glucocorticoid hormones. Proliferation of B cells or T cells could not be detected by [3H]thymidine incorporation or total cell recovery from steroid-stimulated cultures, even though such cultures demonstrated marked increases in immunoglobulin production. The mechanism responsible for this functional maturation of B cells to become high rate immunoglobulin producing cells is as yet undefined, although it appears to involve more than merely steroid mediated inactivation of suppressor T cells.

Adult↗
PubMed1981

Ontogeny of humoral immune function in normal chickens: a comparison of immunoglobulin-secreting cells in bone marrow, spleen, lungs and intestine.

A reverse haemolytic plaque was employed to study the ontogeny of immunoglobulin (Ig) secreting cells of either IgG, IgA, or IgM class in normal chickens. After hatching, IgM-secreting cells were detectable in the spleen by 3 days of age whereas IgG- and IgA-secreting cells were first noted at 6 days. Adult levels of Ig-secreting cells of all three classes were attained by 31 days of age in bone marrow and two separate lymphoid populations (lamina propria and intraepithelial lymphocytes). By contrast, adult levels of Ig-secreting cells were not obtained in either the spleen or the lungs until after 50 days of age. In the case of the spleen, the delay in attainment of adult levels of total Ig-secreting cells reflected the smaller spleen size in immature birds, whereas the percentages of cells secreting Ig of each class were in the adult range by 31 days. By contrast, the numbers of cells recovered from the lungs of 50-day-old chickens were near the adult range, while the percentages of cells secreting either IgG, IgA, or IgM were much fewer than those seen in the lungs of adult chickens. These data indicate that the lungs of normal chickens are populated more slowly with Ig-secreting cells than either the bone marrow, spleen, or intestine. At all ages studied, greater numbers of Ig-secreting cells, particularly of the IgG and IgM classes, were recovered from the bone marrow and spleen as compared to the lungs and intestine. Since only a portion of the total bone marrow population was studied, these data include that the bone marrow may be a major site of Ig-secreting cells in chickens beginning shortly after hatching.

Aging↗
PubMed1980

The effect of adrenaline and noradrenaline on coronary vascular reserve in the dog.

1. Experiments were performed on dogs, anaesthetized with pentobarbitone sodium to measure the oxygen utilization of anterior ventricular wall. The anterior interventricular vein was used for venous blood collection and flow measurement. 2. Oxygen contents of arterial blood and coronary vein were measured. 3. Intravenous (femoral vein) adrenaline infusions raised arterial blood pressure and caused an initial fall in oxygen extraction from control values of 67-45%. Noradrenaline caused an initial fall from 67 to 51%. With both, the oxygen extraction began to rise during the infusion and continued, reaching maximum levels, (mean -82%) 10 min after start of infusion. The range of maximum values for oxygen extraction ratio after noradrenaline was 76-95%. 4. An inverse linear relation was established between blood pressure and oxygen extraction; whereas a direct linear relationship was established between coronary venous blood flow and mean arterial pressure. 5. When a change in blood pressure was prevented, the oxygen extraction ratio rose. 6. In all experiments, whether extraction rose or fell, the oxygen consumption rose. 7. It is suggested that oxygen extraction is a controlled variable and, with coronary blood flow, contributes quantitatively to coronary vascular reserve. 8. The tension-time index was not directly related to oxygen consumption in these experiments. Oxygen consumption rose in response to catecholamines by about the same amount even when mean arterial blood pressure was controlled. It is suggested that cardiac adjustments to altered afterload may also involve alterations in mechanical efficiency.

Animals↗
PubMed1980

Function of the coronary arterial collateral network in healthy myocardium: studies of peripheral coronary pressure in the dog.

Coronary collateral arterial network function was studied in normal dog myocardium using measurements of peripheral coronary pressure (pressure measured distal to a ligature in a branch of the anterior descending coronary artery). Free communication between all parts of the anastomotic network was demonstrated. Adrenaline infusion raised systolic and diastolic levels of peripheral coronary pressure both when the systemic blood pressure was allowed to rise and in experiments where rise in systemic arterial pressure was prevented by haemorrhage. It is suggested that myocardial contraction pressurizes the subendocardial network thus facilitating perfusion of postnetwork vessels. This effect prolongs the time during which coronary vessels affected by rising intramyocardial pressure in systole can be perfused during the cardiac cycle. Additional evidence is presented to indicate the existence of a critical closing pressure in the coronary circulation at about 1.7 kPa (12.8 mmHg).

Animals↗
PubMed1980

Critical closing and critical opening phenomena in the coronary vasculature of the dog.

Direct measurements of coronary venous outflow in a right-heart bypass preparation were used to study the critical closing (CC) and critical opening (CO) phenomena in the anesthetized dog heart. Arterial pressure was lowered rapidly by hemorrhage, and CC pressure was the pressure at which coronary flow stopped completely. Shed blood was returned immediately or after 3 min of ischemia. The pressure at which coronary flow resumed (CO pressure) was measured. Coronary flow stopped at a mean aortic pressure of 14.3 mmHg. Vasodilator drugs and ischemic lowered CC pressure to 10.5 and 10.2 mmHg, respectively. Aortic pressure of 47.3 mmHg was needed to resume coronary flow following perfusion arrest. A brief period of ischemia did not significantly change the CO pressure. These results confirm the presence of CC phenomenon in dog heart and show that CC pressure can be altered by ischemia or vasodilators. It is suggested that the high value of CO pressure may be responsible for myocardial injury associated with ischemic cardiac arrest during open-heart surgery.

Animals↗
PubMed1978

Effect of a local cold stress on peripheral temperatures of Inuit, Oriental, and Caucasian subjects.

Male subjects comprised of six Inuit from Igloolik, N.W.T., and five Orientals and six Caucasians from Toronto, Ont., volunteered for tests to determine the effect of localized cold stress on peripheral temperatures. In each subject, skin temperatures of the right index finger, the arm, and the cheek, as well as blood pressure and heart rate, were measured before, during, and after foot immersion in water of 10 degrees C temperature for 10 min. There was an immediate decrease in finger temperature on foot immersion in all three subject groups; however, the Inuit finger temperatures recovered very quickly to control values, the Caucasian finger temperatures began to increase after decreasing for 7.5 min, and the Oriental finger temperatures decreased continuously during the foot immersion and remained cool even 10 min after the removal of the cold stimulus. The cold stimulus did not affect the cheek or arm temperatures of any of the groups. In all subjects, systolic and diastolic blood pressures and heart rates increased on foot immersion, gradually returning towards normal values. No intergroup differences were seen in these parameters.

Adult↗
PubMed1976

Effect of alterations in ambient temperature on blood flow in the skin.

The effect of changing ambient temperature on skin temperature was recorded in human subjects; also, its effect on blood flow was measured using venous occlusion and optical plethysmography. When cold stimulus was removed in stages using a heating cabinet, it was found that a biphasic flow response occurred in the fingers with each step change in temperature. There was a rapid transient rise followed by a decline to an equilibrium flow level. The transient rise occurred even when the temperature rose from 37 to 40 degrees C, although at this level the equilibrium remained unchanged. It is suggested that the transient rise was due to stimulation of Hensel's dynamic warmth receptors, whereas the rise in equilibrium temperature was due to removal of cold stimulus, which at low ambient temperatures maintains reflex vasoconstriction through activation of static cold receptors. Upper arm skin responded to removal of cold stimulus by a fall in temperature. Immersion of a different limb in cold water produced vasoconstriction in fingers but vasodilatation in the upper arm skin. It is suggested that this may be due to neurogenic vasodilatation, though the present work gives no indication as to pathways.

Adult↗
PubMed1975

The action of nitroglycerine and dipyridamole in normal and ischaemic dog heart.

1 Network and post-network resistances were measured together with heat clearance and heat production in the myocardium. 2 Nitroglycerine dilated all resistance vessels but was twice as effective on network as compared with post-network vessels. 3 Dipyridamole dilated network and post-network vessels equally. 4 Nitroglycerine had no effect on heat clearance or heat production in ischaemic myocardium. 5 Dipyridamole increased heat clearance in normal but not in ischaemic myocardium. 6 Dipyridamole depressed heat production in normal and ischaemic myocardium. 7 That the clinical effectiveness of nitroglycerine does not depend entirely on its coronary vasodilator properties is confirmed. 8 It is suggested that the action of dipyridamole in depressing myocardial heat production may be due to an action on the efficiency of oxygen utilization during cardiac contraction.

Animals↗