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Biomedical subjects

R G Carroll

Publications and source records attributed to R G Carroll.

96 records · Page 6Linked to original sources
PubMedDate not supplied

Chronic angiotensin II infusion decreases renal norepinephrine overflow in conscious dogs.

Sympathetic nerve activity and in particular renal sympathetic nerve activity were monitored in six conscious dogs subjected to 6 days of intravenous angiotensin (ANG II) infusion (20 ng/kg/min). This was accomplished by measurement of both arterial and renal venous plasma catecholamine concentration. During the initial 4 hours of ANG II infusion, mean arterial pressure (MAP) increased 35 +/- 8 mm Hg from a control value of 101 +/- 4 mm Hg. Although there were no significant changes in arterial plasma norepinephrine (NE) concentration at this time (control = 148 +/- 40 pg/ml), arterial plasma epinephrine (E) concentration increased threefold (control 42 +/- 15 pg/ml). After 24 hours of ANG II infusion, MAP remained elevated (132 +/- 5 mm Hg), but plasma E concentration returned to control levels. From Days 2 through 6 of ANG II infusion, MAP was elevated approximately 40 mm Hg, but there were no chronic increases in either arterial plasma E or NE concentrations. In contrast to arterial plasma catecholamine concentration, renal vein plasma NE concentration (control = 216 +/- 27 pg/ml) actually decreased during both the acute (122 +/- 12 pg/ml) and chronic (103 +/- 26 pg/ml) phases of ANG II infusion. Moreover, renal NE overflow (renal venous plasma NE concentration-arterial plasma NE concentration X effective renal plasma flow), an index of renal sympathetic nerve activity, was depressed during the chronic phase of ANG II hypertension. These results, therefore, do not support the contention that the sympathetic nervous system mediates the hypertension produced by elevated plasma levels of ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMedDate not supplied

Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation.

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.

Animals↗
PubMedDate not supplied

Clinical considerations concerning detection of venous air embolism.

Venous air embolism during neurosurgical procedures (detected by Doppler Ultrasound and aspiration via a right atrial catheter) was noted in 100 of 400 patients in the sitting position, 5 of 60 patients in the lateral position, 7 of 48 patients in the supine position, and 1 of 10 individuals monitored in the prone position. We confirmed venous air embolism in many of these cases by using serial technetium-macroaggregated albumin lung scans. Gravitational gradients from the venous portal of entrance to the right side of the heart were as small as 5.0 cm, with aspiration of 200 ml of air occurring. Doppler ultrasonic air bubble detection and aspiration through a previously inserted right atrial catheter are critical factors in the diagnosis and treatment of this condition.

Cardiac Catheterization↗
PubMedDate not supplied

Cerebral infarction: diagnosis and assessment of prognosis by using 123IMP-SPECT and CT.

A multicenter prospective study was performed in 49 patients with 77 regions of cerebral infarction. Each patient was evaluated in the acute (0-5 days) and subacute (6-17 days) phases by (1) clinical neurologic examination, (2) CT scans, and (3) N-isopropyl-p-123I-iodoamphetamine (123IMP) single-photon emission CT (SPECT) scans. The abilities of the scans to (1) detect a lesion and (2) predict the clinical outcome were assessed. For lesion detection, 123IMP-SPECT was superior to CT in the first 2 days, but the scans were equally effective 3-5 days after onset. In the subacute phase, IV contrast-enhanced CT was superior to 123IMP-SPECT and unenhanced CT. The clinical outcome was only mildly correlated with the results of the acute and subacute 123IMP-SPECT and the acute CT scans. Reduction in lesion size on the subacute scans did not correlate with clinical improvement. We conclude that the parameters measured by CT and 123IMP-SPECT in patients with acute cerebral infarction cannot reliably be used to predict clinical outcome. 124I contamination of 123IMP and the use of low-energy collimators may have decreased lesion detectability.

Adult↗
PubMedDate not supplied

Chronic potentiation of vasoconstrictor hypertension by adrenocorticotropic hormone.

The chronic effects of ACTH on mean arterial pressure (MAP) and related variables were studied in dogs with both chronic norepinephrine (NE)- and chronic aldosterone-induced hypertension. MAP was recorded continuously for 24 hours/day, and sodium intake was 71 mEq/day. ACTH was infused for 8 days at a rate that does not increase MAP in normotensive dogs and yet a rate that produces pronounced mineralocorticoid and glucocorticoid effects. Chronic ACTH infusion in dogs with NE hypertension caused natriuresis, kaliuresis, diuresis, hypernatremia, hypokalemia, and suppression of PRA; additionally, there was either no net change in water balance or net water balance was positive. However, in marked contrast to dogs without pre-existing hypertension, in dogs with NE hypertension ACTH produced a pronounced additional increase in MAP of 39 to 63 mm Hg. Although ACTH markedly potentiated NE hypertension, high infusion rates of aldosterone (+6 mm Hg) and cortisol (-7 mm Hg) had relatively weak effects on MAP; further, in dogs with NE hypertension, the increase in MAP associated with simultaneous infusions of high rates of cortisol and aldosterone was equal to only approximately half of that produced by ACTH. In dogs with aldosterone hypertension, the changes in salt and water balance produced by ACTH were comparable to those that occurred when ACTH was administered to dogs with NE hypertension. In dogs with aldosterone hypertension, however, ACTH did not produce kaliuresis, hypernatremia, or hypokalemia; moreover, ACTH did not exacerbate aldosterone hypertension. Thus, the data indicate that the hypertensive effects of ACTH are manifested in conditions of reduced renal excretory capacity such as exist when plasma levels of the potent sodium -retaining hormone NE are inappropriately elevated. Finally, the hypertensive effects of ACTH cannot be accounted for simply on the basis of enhanced mineralocorticoid and glucocorticoid activity.

Adrenocorticotropic Hormone↗