Biomedical subjects

J E Chimoskey

Publications and source records attributed to J E Chimoskey.

At least 19 recordsLinked to original sources

PubMed2006

The effect of pressure loading on the blood flow rate in human skin.

The effect of pressure on the blood flow in skin is of considerable clinical interest. Methods are described for the estimation of skin blood flow from the disappearance rate of an injection of 133Xe in saline. The flow rate may be monitored for a period long enough to establish the normal flow and the reduced flow resulting from a constant pressure load. Initial results indicate that the flow is reduced greatly by pressures up to 10 mmHg. This result is interpreted as a demonstration of an auto regulatory mechanism of skin blood flow. Above 30 mmHg the flow continues to decrease essentially to zero as systolic pressure is approached.

Journal Article↗

PubMed1992

Blood pressure response to acute changes in dietary sodium in young Zimbabwean men.

OBJECTIVE: The primary objective of this study was to determine the effect of acute alterations in sodium intake upon the blood pressure and hormone levels of young Zimbabwean men. DESIGN: Blood pressure, 24-h urinary electrolyte excretion and plasma concentrations of angiotensin II, aldosterone, and atrial natriuretic peptide were measured in normotensive black medical students. Three sets of measurements were taken: (1) during free access to sodium (baseline); (2) after 4 days on a low-sodium diet (10 mmol/day); and (3) after 4 days on a high-sodium diet (800 mmol/day). METHODS: Blood pressure was measured by random zero sphygmomanometry, hormone levels by radioimmunoassay, and urinary electrolytes by flame photometry. RESULTS: The low-sodium diet caused the range of pulse pressure to narrow, with a decrease in systolic blood pressure (SBP) and an increase in diastolic blood pressure (DBP). With the introduction of the high-sodium diet, SBP increased and DBP decreased. Mean arterial pressure did not change. At the same time, angiotensin II and aldosterone decreased. Plasma atrial natriuretic peptide did not change. A subgroup of the men on the high-sodium diet also received 100 mmol potassium/day. The increase in SBP associated with high sodium was significantly attenuated by the presence of added potassium. CONCLUSIONS: SBP of young black Zimbabwean men is lowered by dietary sodium restriction and rises with a large increase in dietary sodium for a short duration, but mean arterial pressure does not change due to the opposing decreases in DBP.

Adult↗

PubMed1990

Hemodynamic and behavioral effects of angiotensin II in conscious sheep.

Intracerebroventricular (ivt) angiotensin II (ANG II) at 0.4, 2, 10, and 50 ng.kg-1.min-1 increased arterial pressure in conscious sheep in a dose-related manner (26 mmHg, P less than 0.05, at 50 ng.kg-1.min-1). Total peripheral resistance (TPR) and right atrial pressure also increased. Heart rate, stroke volume, and cardiac output did not change. Pressor responses to ivt ANG II were not caused by leakage of ANG II into the periphery, because plasma concentrations of ANG II did not change from control (31 +/- 7 pg/ml) at the highest dose of ANG II infused. In contrast, intravenous (iv) ANG II, 10 and 50 ng.kg-1.min-1, increased arterial pressure 29 and 47 mmHg, respectively (P less than 0.05), and decreased heart rate. ANG II, 10 ng.kg-1.min-1 iv, increased plasma ANG II levels from 36 +/- 6 to 354 +/- 69 pg/ml (P less than 0.05). Intracarotid (ic) ANG II, 10 ng.kg-1.min-1, increased arterial pressure 31 mmHg (P less than 0.05) but did not alter heart rate. ANG II ivt caused a dose-related drinking response, with a positive correlation between the amount of water drunk during ivt ANG II infusion and the increase in arterial pressure. Infusions of ANG II at 50 ng.kg-1.min-1 ivt were associated with decreased plasma osmolality and potassium concentration and increased plasma vasopressin concentration.

Angiotensin II↗

PubMed1989

Plasma atrial natriuretic peptide in conscious rats with reduced renal mass.

The effect of salt intake and reduction of renal mass (RRM) on plasma immunoreactive atrial natriuretic peptide (iANP) levels in conscious rats was studied. Rats were divided into RRM and sham-operated groups, and then further subdivided into groups infused with 1 or 6 mEq of sodium per day. Plasma urea nitrogen increased in the groups with RRM. Plasma sodium, sodium balance, and heart rate did not differ between the sham and RRM groups. Rats with RRM maintained on 1 mEq of sodium per day did not have an elevation of water intake, arterial pressure, or plasma iANP. Rats with RRM maintained on 6 mEq of sodium per day had significantly (P less than 0.05) elevated water intake, arterial pressure, and plasma iANP. Arterial pressure and plasma iANP were correlated (r = 0.800) for rats with RRM on either 1 or 6 mEq of sodium per day. Increased plasma iANP in the RRM group on 6 mEq per day was not caused by either RRM or high sodium alone; it was an effect of RRM plus high salt intake. The increase in plasma iANP in the RRM group may be caused by the increase in arterial pressure, possibly due to an increase in extracellular fluid volume. ANP may not be responsible for the sustained increase in fractional sodium excretion observed in RRM.

Animals↗

PubMed1989

Comparison of intracerebroventricular and intracarotid infusions of PGE2 in conscious sheep.

Conscious sheep chronically prepared with nonocclusive indwelling vascular and cerebroventricular catheters were used to compare hemodynamic, hematologic, hormonal, and behavioral responses of intracarotid (ic) prostaglandin E2 (PGE2) to intracerebroventricular (ivt) PGE2. PGE2 had less potent hemodynamic effects when infused ivt than when infused ic. Intracarotid PGE2, 100 ng.kg-1.min-1, increased arterial pressure and heart rate 31 mmHg and 26 beats/min, respectively (P less than 0.01), whereas ivt PGE2, 300 ng.kg-1.min-1, did not alter heart rate and increased arterial pressure 9 mmHg (P less than 0.01). Both ic and ivt PGE2 increased packed cell volume 3% (P less than 0.01). Neither ic nor ivt PGE2 caused changes in plasma concentrations of epinephrine or norepinephrine. Despite ivt PGE2S less potent hemodynamic effects, ivt administration of PGE2 decreased plasma osmolality 2 mosmol/kg (P less than 0.05) and sodium concentration 2 meq/l (P less than 0.01) and increased plasma vasopressin concentration 2.5-fold (P less than 0.05). Intracerebroventricular PGE2 also caused some physical and behavioral changes that were not observed during ic PGE2 administration or during ivt infusion of vehicle. These changes included pupillary constriction, vocalization, and coughing. We conclude that PGE2 given ivt may not reach the same sites in the brain as does ic PGE2 or that ivt PGE2 may reach the same sites in different concentrations.

Animals↗

PubMed1988

Alpha-human atrial natriuretic peptide is a coronary vasodilator in the Langendorff-perfused guinea pig heart.

The circulating form of atrial natriuretic peptide is now believed to be composed of 28 amino acids (1). Therefore, we studied the coronary vasoactivity of the 28 amino acid, alpha-human atrial natriuretic peptide (alpha-hANP) in five isolated guinea pig hearts Langendorff-perfused at constant pressure (46 mmHg) with Krebs-Henseleit solution. The reactivity of the coronary bed was assured in each heart with bolus injections of norepinephrine, adenosine, and the vasoconstrictor atrial natriuretic peptide, atriopeptin II (APII). APII was a coronary constrictor in each of these five hearts. Nineteen boluses of alpha-hANP were administered to the five hearts, spanning the range 1.6 to 64 nmol/g wet heart weight. alpha-hANP was vasodilator in all five hearts. The equation for the regression of y = flow, % increase, on x = dose, nmol/g, is y = 17.98 logx - 4.11. The correlation coefficient, r, is 0.83, and the coefficient of determination, r2, is 0.69. Analysis of variance of the regression of y on x yields an F statistic of 36.9, P less than 0.00001. These results indicate that coronary vasodilation is correlated with dose of alpha-hANP over much of the range 1.6-64 nmol/g.

Animals↗

PubMed1987

Central angiotensin II and PGE2 act independently to increase blood pressure in conscious sheep.

Conscious adult female sheep chronically prepared with nonocclusive indwelling vascular and cerebroventricular catheters were used to determine whether centrally administered prostaglandin E2 (PGE2) increases blood pressure by activation of the brain renin angiotensin system or whether centrally administered angiotensin II (ANG II) increases blood pressure by stimulating prostaglandin synthesis in the brain. Intracerebroventricular (ivt) ANG II, 50 ng X kg-1 X min-1, increased arterial pressure 23 mmHg (P less than 0.01) 30 min after the start of infusion. Infusion of the ANG II antagonist [Sar1-Thr8]ANG II (sarthran), 1,000 ng X kg-1 X min-1 ivt, had no effect on arterial pressure when given by itself but reduced the ivt ANG II-induced pressor response to 5 mmHg (P less than 0.05) when the two peptides were infused at the same time. Intracerebroventricular infusion of sarthran did not alter the pressor responses to intracarotid (ic) PGE2 or to ivt PGE2. Blood pressure increased 21 mmHg (P less than 0.01) 30 min after the start of PGE2 infusion when PGE2 was given ic by itself, compared with 17 mmHg (P less than 0.01) when PGE2 was given ic at the same time as sarthran was given ivt. Blood pressure increased 14 mmHg (P less than 0.01) 30 min after the start of PGE2 infusion when PGE2 was given ivt by itself, compared with 16 mmHg (P less than 0.01) when PGE2 was given ivt at the same time as sarthran was given ivt. Pretreatment with the cyclooxygenase inhibitors indomethacin, 4 mg/kg sc, or flunixin meglumine, 3 mg/kg iv, did not alter the ivt ANG II-induced pressor response.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1985

Coronary vasoconstrictor effects of atriopeptin II.

Atrial natriuretic peptides lower arterial pressure, cardiac filling pressure, and cardiac output. In isolated, Langendorff-perfused guinea pig hearts, atriopeptin II, the 23-amino acid atrial natriuretic peptide, is also a potent coronary vasoconstrictor. The median effective dose for atriopeptin II in guinea pig hearts is 26 nanomoles, the threshold constrictor dose is 5 nanomoles, and flow nearly ceases at a dose of 100 nanomoles in perfused hearts at constant pressure. Similar concentrations of atriopeptin II also cause coronary vasoconstriction in rat and dog heart preparations. The disulfide bridge is necessary for vasoconstrictor activity; reduction of this bridge abolishes the activity, as it does the other biological activities of atrial natriuretic peptides.

Adenosine↗

PubMed1985

Atriopeptin II lowers cardiac output in conscious sheep.

Atrial natriuretic peptides cause natriuresis, kaliuresis, diuresis, and hypotension. They relax vascular smooth muscle in vitro, and they dilate renal vessels in vivo. Hence, we tested the hypothesis that they produce hypotension by lowering total peripheral resistance. The studies were performed in conscious chronically instrumented sheep standing quietly in their cages. Atriopeptin II (AP II) was infused into the right atrium for 30 min at 0.1 nmol X kg-1 X min-1. Atriopeptin II lowers arterial pressure (9%, P less than 0.05) by lowering cardiac output (18%, P less than 0.05), stroke volume (28%, P less than 0.05), and right atrial pressure (2.3 mmHg, P less than 0.05). Heart rate and total peripheral resistance increase (16 and 13%, respectively, P less than 0.05). Partial ganglionic blockade with trimethaphan camsylate during AP II infusion prevents the increases in heart rate and total peripheral resistance. The changes in right atrial pressure, stroke volume, and cardiac output persist, and arterial pressure falls further (27%, P less than 0.05). These hemodynamic data are consistent with direct AP II-induced relaxation of venous smooth muscle with reduction of venous return, right atrial pressure, stroke volume, cardiac output, and arterial pressure, followed by reflex activation of the sympathetic nervous system to increase heart rate and total peripheral resistance. Because partial ganglionic blockade alone and AP II alone cause similar reductions in right atrial pressure (2.1 and 2.3 mmHg, respectively) but AP II causes a greater fall in stroke volume (28 vs. 13%), it is possible that AP II also causes coronary vasoconstriction.

Animals↗

PubMed1985

Mechanism of tachycardia caused by intracarotid PGE2 in conscious ewes.

Conscious adult ewes prepared with nonocclusive indwelling vascular catheters were used to determine the mechanism by which heart rate increases during central administration of prostaglandin E2 (PGE2). Heart rate increased 14 bpm during steady-state intracarotid infusion of PGE2, 10 ng/kg/min (P less than 0.05). Intravenous atropine methyl bromide, 1 mg/kg, increased heart rate 26 bpm (P less than 0.05) 5 min after injection. Heart rate remained elevated 30 min after injection. The heart rate response to PGE2 plus atropine was greater than the heart rate response to either atropine or PGE2 alone (P less than 0.05). Propranolol, 1 mg/kg bolus plus intravenous infusion, 0.025 mg/kg/min, did not change resting heart rate. Propranolol attenuated but did not abolish the increase in heart rate caused by intracarotid PGE2. Although heart rate increased in response to PGE2 after administration of either propranolol or atropine alone, the combination of propranolol and atropine prevented any further increase in heart rate during subsequent PGE2 infusion. The increase in heart rate when all three drugs were given together was not different from the increase observed during atropine alone. Thus, both beta-adrenergic activation and muscarinic deactivation contribute to the PGE2-induced tachycardia.

Acetylcholine↗

PubMed1984

Cardiac atria of BIO 14.6 hamsters are deficient in natriuretic factor.

The hearts of 220-day-old hamsters of the BIO 14.6 strain are deficient in atrial natriuretic factor; saline extracts of atria produce one-third the natriuretic and diuretic effects of extracts of atria from age-matched normal hamsters. BIO 14.6 hamsters are known to develop congestive heart failure with edema when they are about 200 days old, and the venous congestion and edema are preventable by parabiosis with normal hamsters. The humoral mediator, the deficiency of which causes venous congestion and edema in BIO 14.6 hamsters, may be atrial natriuretic factor.

Animals↗

PubMed1984

Mechanisms of central prostaglandin E2 hypertension in conscious dogs, sheep, and calves.

Intracarotid prostaglandin E2 (PGE2) infusions (10 ng X kg-1 X min-1) increased arterial pressure in conscious dogs, sheep, and calves. Total and regional peripheral resistances (renal, superior mesenteric, and iliac) increased in conscious calves. Arterial pH and CO2 tension did not change, implying no activation of the chemoreflex. The arterial baro-reflex was reset upward during intracarotid PGE2 infusion; arterial pressure increased with little heart rate change, but baroreflex sensitivity was unchanged. In contrast, equipotent intracarotid angiotensin II infusions (10 ng X kg-1 X min-1) both reset the baroreflex upward and decreased baroreflex sensitivity. Pretreatment with alpha-, but not beta-, adrenoceptor blocking agents attenuated the intracarotid PGE2 pressor effect. Increasing PGE2 infusions (10-200 ng X kg-1 X min-1) caused dose-related arterial pressure increases; plasma renin activity was increased only at the largest infusion rate. Pretreatment with captopril, an inhibitor of the angiotensin-converting enzyme, attenuated the PGE2 pressor effect. During barbiturate-halothane and chlorolose-urethan anesthesia, no pressor effect was observed during intracarotid PGE2. We conclude that intracarotid PGE2 acts centrally to augment sympathetic vasomotor outflow. The central action of PGE2 is not affected by activation of the arterial chemoreflex or alteration of baroreflex sensitivity and has a small renin-angiotensin component.

Anesthesia↗

PubMed1983

PGE2 does not act at carotid sinus to raise arterial pressure in conscious sheep.

Conscious chronically instrumented adult female sheep were used to determine whether direct action of prostaglandin E2 (PGE2) on the carotid sinus baroreceptors contributes to the pressor response observed during infusion of PGE2 into the common carotid artery (CCA). During infusion of PGE2 into the CCA caudal to an intact carotid sinus, into the CCA caudal to a denervated carotid sinus, and into the external carotid artery, mean arterial pressure (MAP) rose 17, 22, and 17 mmHg, respectively (P less than 0.01). Heart rate (HR) rose 6, 6, and 8 beats/min, respectively (P less than 0.05). Cardiac output (CO) was also measured by indicator dilution using indocyanine green. In these experiments with infusion of PGE2 into the external carotid artery, MAP rose 15 mmHg (P less than 0.01), HR increased 6 beats/min (P less than 0.05), CO did not change, and total peripheral resistance (TPR) increased 23% (P less than 0.01). With infusion of PGE2 past a denervated carotid sinus, MAP rose 20 mmHg (P less than 0.01), HR rose 4 beats/min (P less than 0.05), CO did not change, and TPR increased 29% (P less than 0.01). There were no statistically significant differences in MAP or HR responses when PGE2 was infused past an intact carotid sinus, past a denervated carotid sinus, or beyond the carotid sinus. There is no evidence that direct action of PGE2 on carotid sinus baroreceptors either augments or inhibits the observed pressor effect of intracarotid PGE2. Intracarotid PGE2 acts rostral to the carotid sinus to increase MAP, HR, and TPR in conscious sheep.

Animals↗

PubMed1983

Hemodynamics of high afterload left heart failure for assist device testing.

The hemodynamic responses to increased afterload of the left ventricle were studied in conscious calves during exercise. The calves were chronically instrumented to measure (or derive) heart rate, stroke volume, cardiac output, iliac, superior mesenteric and renal flows and resistances, mean carotid, aortic, right atrial, pulmonary artery, and left atrial pressures, the systemic and pulmonary pressure gradients, and total systemic and total pulmonary resistances. The calves were also instrumented to produce reversible partial constriction of the ascending aorta and common carotid arteries and for cooling of the cervical vagus nerves. The hemodynamic responses to increased afterload were characterized during treadmill exercise at 2 mph. These responses were compared to the hemodynamic responses to bilateral carotid artery occlusion with and without vagal cooling.

Animals↗

PubMed1983

Cardiac and sinoaortic reflexes during aortic constriction in awake calves.

The hemodynamic responses to increased afterload of the left ventricle were studied in conscious calves before and during cooling of the cervical vagus nerves bilaterally. The calves were chronically instrumented to measure (or derive) heart rate, stroke volume, cardiac output, iliac, superior mesenteric and renal flows and resistances, mean aortic, right atrial, pulmonary artery, and left atrial pressures, the systemic and pulmonary pressure gradients, and total systemic and total pulmonary resistances. The calves were also instrumented to produce reversible partial constriction of the ascending aorta and for cooling of the cervical vagus nerves. The hemodynamic responses to increased afterload were characterized before and during bilateral cervical vagus nerve cooling to 6-7 degrees C. Aortic constriction causes stroke volume, cardiac output and aortic pulse pressure to decrease. Left atrial pressure and total peripheral resistance increase. Mean aortic pressure is constant during aortic constriction alone, despite a continued decrease in pulse pressure, due to a balance between sinoaortic reflexes which attempt to increase arterial pressure in response to the decreased pulse pressure and cardiopulmonary reflexes which attempt to decrease arterial pressure in response to the increased left atrial and cardiopulmonary pressures. Vagal cooling removes cardiopulmonary reflex modulation of the sinoaortic reflexes. During aortic constriction and vagal cooling, the carotid sinus reflex, acting alone, causes large increases in renal and total peripheral resistance and mean aortic pressure.

Animals↗

PubMed1982

In vitro evaluation of U.S. and U.S.S.R. artificial hearts.

This report summarizes the results of the in vitro evaluation of Soviet and American artificial hearts. The devices were tested at the All-Union Institute of Transplantation and Artificial Organs, Moscow, U.S.S.R., and Baylor College of Medicine, Houston, Texas, U.S.A. These studies were designed to standardize procedures to allow comparison of artificial ventricles of different designs. Also, these studies might provide a means for evaluation of other characteristics such as hemolysis, durability, and reliability. Static and dynamic tests were performed, varying preload, afterload, rate, and systolic and diastolic time intervals. All designs demonstrated comparable function curves with capability of taking over the pressure and volume work of the natural heart.

Blood Flow Velocity↗

PubMed1978

Endothelial cell culture on dacron fabrics of different configurations.

The growth of tissue-cultured aortic endothelial cells from the calf using 12 different configurations of Dacron polyester (U.S. Catheter and Instrument Co.) as substrates was studied. Scanning electron microscopy showed maximum cell coverage on tightly knit configurations, whereas loose knits and velours did not support cell growth.

Animals↗

PubMed1978

Comparison of tissue-cultured bovine endothelial cells from aorta and saphenous vein.

Endothelial cells were harvested from bovine aorta and saphenous vein with collagenase and cultured in McCoy's 5a medium (modified GIBCO) supplemented with 10% fetal bovine serum. The cells were subcultured through 17 passages over 4 to 5 months. The growth properties in culture of the two cell types were compared. Morphological comparisons included phase microscopy and scanning and transmission electron microscopy. Comparisons with cultured aortic smooth-muscle cells were made using phase and scanning electron microscopy. No differences were found between cultured endothelial cells from aorta and saphenous vein. Differences in growth patterns in culture clearly distinguished both endothelial cell types from smooth-muscle cells. The presence of Weibel-Palade bodies identified the cells from both sources as endothelial.

Animals↗