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Biomedical subjects

J C Rose

Publications and source records attributed to J C Rose.

At least 127 records · Page 7Linked to original sources
PubMed1983

Subhourly variability of circulating norepinephrine and epinephrine in the pregnant ewe and fetal and newborn lamb.

Circulating norepinephrine and epinephrine were determined nine times over a 1-hour period in chronically instrumented ewes (n = 4), their fetuses (n = 4), and lambs (n = 4). In an apparent resting state, assessed by subjective and biophysical parameters, marked fluctuations were demonstrated in the mean norepinephrine and epinephrine values between animals and in the range of the concentrations of each individual animal. The significance of the fluctuations in resting plasma norepinephrine and epinephrine concentrations is discussed.

Animals↗
PubMed1983

Vasopressin is important for restoring cardiovascular homeostasis in fetal lambs subjected to hemorrhage.

To determine if the posterior pituitary hormone vasopressin is important for maintaining fetal cardiovascular homeostasis during hypovolemic stress, in seven chronically catheterized fetal lambs we induced hemorrhage of 20% of estimated blood volume in the presence and in the absence of a potent antagonist to the pressor effects of vasopressin. The study was a paired crossover design with at least 48 hours separating experiments in the same animal. Injection of the vasopressin antagonist did not alter basal fetal heart rate or arterial blood pressure, but hemorrhage of 2% of estimated fetal blood volume per minute for 10 minutes produced a greater fall in blood pressure (13 +/- 2 versus 10 +/- 2 torr, p less than 0.05) when the blocker was present than when it was absent. Arterial blood pressure remained below control levels longer following hemorrhage when the fetuses were pretreated with the antagonist (49.7 +/- 6 versus 26.6 +/- 6 minutes, p less than 0.01), and the integrated fall in arterial blood pressure with hemorrhage was greatest (283 +/- 53 versus 169 +/- 57 mm Hg . min p less than 0.01) when the blocker was used. The fall in heart rate following hemorrhage was similar with and without blocker pretreatment. These results indicate that vasopressin plays a physiologic role in blood pressure regulation in fetal lambs during periods of hypovolemia.

Animals↗
PubMed1983

A vasopressin antagonist blocks the norepinephrine and epinephrine responses to hemorrhage in the fetus.

In 8 chronically cannulated fetal lambs between 119 and 127 days gestation the resting plasma norepinephrine concentration was 528 +/- 77 pg X ml-1 and the resting plasma epinephrine concentration 159 +/- 42 pg X ml-1. Hemorrhage of 20% of estimated blood volume at 2% per min produced a 2.1-fold increase in plasma norepinephrine levels and a 3.4-fold increase in plasma epinephrine levels when the animals were pretreated with an injection of saline (1 ml). Plasma catecholamine levels returned toward control values following return of the shed blood. In contrast, hemorrhage of these animals following pretreatment with an antagonist of the pressor effect of vasopressin did not cause an increase in fetal plasma catecholamine levels. Thus, vasopressin may mediate the sympathetic responses to volume depletion in the fetus.

Animals↗
PubMed1983

Cardiovascular responses to leukotriene C4 in the rat.

Bolus injections of leukotriene C4, (LTC4; 0.1 to 10 micrograms/kg) were administered to anesthetized closed-chest rats i.v., before and min after administration of indomethacin (2 mg/kg). Systemic arterial pressure (SAP) and pulmonary arterial pressure (PAP) were monitored continuously. LTC4 produced dose-dependent changes in SAP and PAP. The characteristic SAP response to LTC4 (4 micrograms/kg) consisted of an initial transient rise (16 mm Hg), followed by a sustained decrease (18 mm Hg). LTC4 produced only a decrease in PAP (4 mm Hg). Cardiac output (CO) and heart rate (HR) were measured in the control period and during the maximum increase and decrease in SAP. Decreases in CO (32 ml/min) and HR (15 beats/min) occurred during the initial rise in SAP and further declined (36 ml/min and 21 beats/min, respectively) during the systemic hypotensive phase. Total peripheral resistance markedly increased during the transient rise in SAP (67%). Indomethacin potentiated the transient rise in SAP and attenuated systemic and pulmonary hypotensive responses induced by LTC4. Decreases in CO and HR induced by LTC4 were also attenuated by indomethacin, but total peripheral resistance was not significantly altered. These observations describe a characteristic hemodynamic response to LTC4 in the rat that reflects the composite actions of LTC4 as well as those of prostanoate compounds that may be synthesized and released after LTC4 administration.

Animals↗
PubMed1983

Plasma cortisol response to feeding in African green vervets.

The timing of a single daily meal of monkey chow in African green vervets exerts a synchronizing influence on plasma cortisol concentrations with an initial increase after feeding followed by a decrease to minimal levels five hours after feeding.

Animals↗
PubMed1982

Effects of gestation on glucose tolerance and plasma insulin in cynomolgus monkeys (Macaca fascicularis).

Gestational alterations in carbohydrate metabolism in a group of cynomolgus monkeys were characterized by a decrease in fasting plasma glucose and by an increase in peak plasma insulin response subsequent to a glucose challenge. These changes are prominent as early as the first trimester of pregnancy. Glucose clearance rates and fasting plasma insulin did not show significant changes during gestation or post partum. Peak plasma insulin remained elevated in lactating animals studied 4 to 10 weeks post partum.

Animals↗
PubMed1982

Effect of TMB-8 on the pulmonary vasoconstrictor action of prostaglandin F2 alpha and the thromboxane mimic, U 46619.

1 TMB-8 (8-(N,N-diethylamino)octyl-3,4,5 trimethoxybenzoate HCl), an intracellular calcium antagonist, had no direct action on the pulmonary vasculature of the perfused canine lung lobe preparation. 2 The pulmonary pressor response to the thromboxane mimic, U46619, was not affected by TMB-8. 3 The vasopressor response to prostaglandin F2 alpha (PGF 2 alpha) was significantly attenuated but not completely blocked by TMB-8. 4 We conclude that the pulmonary pressor response to PGF 2 alpha is dependent on both intracellular and extracellular calcium pools for contraction and that U46619 facilitates either solely extracellular calcium influx or mobilizes an intracellular calcium pool not inhibited by TMB-8.

Animals↗
PubMed1982

Developmental aspects of pituitary and adrenal responses to arterial hypotension in neonatal, weanling, and adult sheep.

We have studied neuroendocrine and heart rate responses to arterial hypotension in unanesthetized, chronically cannulated neonatal (less than 10 days old), weanling (3- to 4-wk-old), and adult sheep. Nitroprusside-induced arterial hypotension in the absence of hypovolemia promptly increased plasma ACTH, vasopressin (AVP), and cortisol levels in all three groups. The integrated adenohypophyseal and neurohypophyseal responses to a standard hypotensive stimulus were similar at the three ages, suggesting that the functional development of the systems subserving these responses is complete by the immediate postnatal period. The integrated cortisol/ACTH ratio was greatest in the youngest animals, suggesting that enhanced adrenal responsiveness to ACTH exists in neonatal as well as in late-gestation fetal lambs. The reflex tachycardia accompanying the arterial hypotension in the weanling and adult sheep was absent in the neonates.

Adrenal Glands↗
PubMed1982

In vivo evidence for increased adrenal sensitivity to adrenocorticotropin-(1-24) in the lamb fetus late in gestation.

Plasma concentrations of immunoreactive ACTH and cortisol were monitored daily in chronically cannulated sheep fetuses during the last 3 weeks of gestation. A prepartum increase in fetal plasma cortisol occurred without a concomitant rise in fetal plasma ACTH. When fetal lambs were injected with various doses of ACTH-(1-24) and the plasma cortisol responses were integrated over time, the resulting changes in the log dose-response curves indicate that fetal adrenal sensitivity increases late in gestation. Thus, the marked rise in fetal plasma cortisol before birth can be explained, at least in part, by an increase in fetal adrenal sensitivity to ACTH.

Adrenal Glands↗