Search PubMed⌕ Search

Biomedical subjects

D F Adams

Publications and source records attributed to D F Adams.

At least 127 records · Page 7Linked to original sources

Angiographic abnormalities associated with alterations in regional myocardial blood flow in coronary artery disease.

To evaluate the association between alterations in myocardial blood flow and angiographic findings, myocardial blood flow was compared in 26 patients with asymergy, 15 patients with a similar extent of coronary artery disease but without asynergy, and 10 patients without coronary artery disease or obvious myocardial or valvular disease. Myocardial blood flow was measured at rest with an Anger camera and PDP-11/20 computer after the intracoronary injection of 133xenon. In comparison with the normal subjects, whole heart blood flow was significantly reduced in patients with asynergy. In addition, myocardial blood flow in regions of anteroapical asynergy was reduced (85-7 +/- 7-0 ml/min per 100 g3 in controls to 65-4 +/- 4-5, P less than 0-05) and a similar reduction was noted in regions of posterolateral asymergy (91-5 +/- 8-8 in controls to 66-8 +/- 5-0, P less than 0-05). In general, regional myocardial blood flow was reduced distal to left anterior descending or left circumflex stenosis of less than 50 per cent, with a trend toward further reduction distal to less than 75 per cent stenosis. In these same patients, the presence of anteroapical or posterolateral asynergy resulted in a similar trend to even greater reduction of flow. The effect of collaterals was variable: 7 of 8 patients without asynergy but with less than 75 per cent left anterior descending stenosis and collateral circulation to the lower left anterior descending quadrant had minimally reduced flows. However, in the 17 patients with anteroapical asynergy, regional myocardial blood flow was very similar in the 9 patients with collaterals compared with the 8 patients without them. This study suggests that the degree of coronary artery stenosis and presence of asynergy are both important in evaluating alterations in myocardial blood flow in coronary artery disease, while the role of collaterals remains uncertain.

Adult↗

Renal blood flow and its response to angiotensin II. An interaction between oral contraceptive agents, sodium intake, and the renin-angiotensin system in healthy young women.

A variety of estrogen- and progestin-containing oral contraceptive agents reduced renal blood flow (RBF) significantly in 23 healthy, nonhypertensive young women, to a mean of 75 +/- 3.3% of the value expected for their age and dietary sodium intake (P less than 0.001). There was also significant activation of the renin-angiotensin system: renin substrate was increased approximately 3-fold in association with a striking increase in the circulating renin activity and angiotensin II levels in relation to sodium intake and excretion. Two observations suggest that the RBF reduction was directly mediated by angiotensin II. A correlation was demonstrable between circulating angiotensin II and RBF (P less than 0.01), and renal vascular responsiveness to angiotensin II infused into the renal artery was reduced significantly (P less than 0.001). Moreover, the oral contraceptive agents modified the basic relationship between sodium balance and vascular responsiveness to angiotensin II, suggesting that the agents acted through some mechanism other than alteration in the state of sodium balance. These observations provide further evidence for an important role of angiotensin II as a determinant of RBF. Renal vasoconstriction may contribute to the genesis of a number of complications, such as sodium retention and hypertension, associated with oral contraceptive use.

Adult↗

beta-adrenergic blockade in essential hypertension: reduced renin release despite renal vasoconstriction.

The acute effects of small doses of intravenous propranolol on renin release and on circulatory dynamics were studied at the time of renal arteriography in 12 persons with essential hypertension. All of the subjects had a normal peripheral renin response to chronic sodium depletion and all had normal renal function. Seven subjects received a 10-mEq sodium diet. At the time of arteriography, arterial blood pressure, pulse rate, cardiac output, renal blood flow, and arterial and renal venous renin activity were measured before and 6-20 minutes after the intravenous administration of propranolol (9-18 mjg/kg). Average renin secretion rate in the salt-depleted subjects fell from 367 +/- 80 (SEM) U/ml per 100 g/min to 122 +/- 51 U/ml per 100 g (P=0.03) and renal plasma flow fell from 189 to 155 ml/min per 100 g (P = 0.018). We also found that in the salt-loaded subjects, renal plasma flow fell from 213 to 184 ml/min per 100 g (P = 0.025), whereas renin secretion did not change significantly in either group. We conclude that propranolol rapidly blocks renin release despite circulatory changes which ordinarily constitute a stimulus for renin secretion, i.e., renal vasoconstriction and reduced renal blood flow.

Adult↗

Blockade and stimulation of renal, adrenal, and vascular angiotensin II receptors with 1-Sar, 8-Ala angiotensin II in normal man.

We have assessed the capacity of an analogue of angiotensin II (A II), 1-Sar, 8-Ala A II (P113) in normal man to stimulate and block responses to A II in four systems: blood pressure was monitored directly from an arterial catheter, and renal blood flow was measured with 133Xe and arterial renin and aldosterone concentrations by radioimmunoassay. The 31 normal subjects were in balance on a daily intake of 200 meg sodium and 100 meq potassium to suppress endogenous renin. P113 administered intravenously induced a dose-related renal blood flow reduction, with a threshold dose of 0.1 mug/kg/min. This dose also induced a small but significant increase in arterial blood pressure and plasma aldosterone as well as a reduction in plasma renin activity. In contrast to its effect on the renal vasculature, no tendency to a progressive response in the latter three parameters was noted as the P113 dose was increased 30-fold, to 3.0 mug/kg/min. P113 also reduced the clearance of para-aminohippurate, creatinine, sodium, and potassium, a pattern similar to that induced by A II. P113 at 0.1 mug/kg/min reduced significantly the blood pressure and renal vascular and aldosterone responses to graded doses of A II. Higher P113 doses totally obliterated all three responses to A II infused at 10 ng/kg/min, a dose that provides arterial A II concentrations in the range found in angiotensin-mediated hypertension. When A II was infused first, to induce a pressor, renal vascular, and aldosterone response, P113 induced a dose-related reversal of the response in each system. In conclusion, P113 is a partial agonist in normal man, inducing an angiotensin-like response in settings in which endogenous A II is not playing a tonic role, and displaying dominant antagonist activity in settings in which A II is active. Moreover, the studies suggest that the receptors mediating the responses to A II are different in the renal vasculature and other systemic vascular beds. The adrenal receptor must also differ. This agent should be useful in dissecting the role of A II in diseases characterized by hypertension or abnormalities of renal and adrenal function.

Adrenal Glands↗

Computed tomography of the normal and infarcted myocardium.

After intravenous administration of contrast agent, in vitro cardiac scanning showed a significant difference between the attenuation coefficients of the intracavitary blood pool and the myocardial wall, permitting clear delineation of the ventricular cavity. A substantial alteration in hematocrit permitted similar visualization of the intracavitary blood pool-myocardial wall interface. The attenuation coefficient of infarcted myocardium differed sufficiently from that of normal myocardium to render computed tomographic distinction feasible. In three hour old infarctions, the differences between normal and ischemic or infarcted tissue were enhanced by prior administration of contrast agent. These differences in attenuation coefficient indicate that a properly gated CT scanner could be utilized as a noninvasive approach to evaluating suspected or known myocardial infarction and other aspects of cardiac structure and function both in man and in experimental animals.

Animals↗

Comparison of observer performance with 16 mm cinefluorography and 70 mm camera fluorography in coronary arteriography.

Clinical 16 mm cinefluorography and 70 mm camera fluorography were compared in 30 unselected patients undergoing coronary arteriography. Accuracy in detecting coronary arterial stenosis and collateral vessels and in assessing the degree of stenosis was similar with the two techniques. With both methods, there were significant inter- and intraobserver differences in estimating the degree of stenosis. These differences indicate that coronary arteriography is only a semiquantitative method for making decisions about treatment, prognosis and follow-up of patients. The use of more than one observer increases the likelihood that stenotic lesions will be detected. Interobserver variation in detecting collateral circulation is small.

Adult↗

Congenital renal arteriovenous malformation: angiography in its diagnosis.

Two patients with renal arteriovenous malformations are presented along with the distinct changes shown by urography, arteriography, and pharmacoangiography. The relevant roentgen signs in such patients include multiple small cobblestone-like identations caused by well-formed vascular channels projecting into the collecting structures, no angiographic or urographic evidence of a mass displacing the intrarenal vessels or collecting structures, normal sized arteries and veins leading to and from the malformation, and a decrease in size of the malformation after intra-arterial infusion of epinephrine. These patients may have flank pain or hematuria later in life or may remain asymptomatic. A complete urographic and angiographic examination will help to determine the appropriate therapy. Corrective surgery is usually reserved for symptomatic patients and, when indicated, require only surgical ligation of the vessels feeding and draining the malformation.

Adult↗

Renal vascular tone in essential and secondary hypertension: hemodynamic and angiographic responses to vasodilators.

The renal vascular response to graded doses of acetylcholine, dopamine and phentolamine, assessed by xenon washout and selective arteriography was used to define the relative contribution of fixed and reversible vascular abnormalities to increased renal vascular resistance in patients with essential or secondary hypertension. The increase in blood flow induced by acetylcholine and dopamine was blunted strikingly in patients with advanced nephrosclerosis, chronic pyelonephritis and polycystic kidney disease and was normal in the kidney contralateral to a significant renal artery stenosis. Conversely, the response to both was potentiated in 9 of 13 (69%) patients with mild essential hypertension. Equivalent potentiation of the response to acetylcholine was induced in normal subjects by increasing renal vascular tone pharmacologically with angiotensin. Phentolamine infused into the renal artery also increased renal blood flow significantly in 6 of 9 (67%) patients with mild essential hypertension, but in none of 15 normal subjects, over a dose reange that paralleled that for alpha-adrenergic blockade. Changes in the selective renal arteriogram were in excellent accord: potentiated response to acetylcholine, phentolamine or dopamine was associated with reversal of the small vessel abnormalities visualized in the arteriogram. The reduced blood flow response in advanced nephrosclerosis or parenchymal disease was associated with a reduced angiographic change during dilator infusion. The results suggest a quantitatively important, functional renal vascular abnormality--perhaps mediated by the sympathetic nervous system--in many patients with mild essential hypertension. Conversely the renal vascular abnormality associated with advanced nephrosclerosis or renal parenchymal disease is largely fixed and is probably due to organic changes.

Acetylcholine↗

Coronary vascular patterns during occlusion arteriography.

The arteriograms from 18 studies in which the catheter accidentally occluded the right coronary artery were analyzed and compared with successful studies in 25 patients with normal coronary arteries and 20 patients with coronary artery stenosis. The occlusion arteriograms showed distinct early filling of the anterior cardiac veins and occasionally retrograde filling of the left circumflex artery. Although there were no serious complications due to occlusion arteriography in our patients, the potential for producing ventricular tachycardia, ventricular fibrillation or cardiac arrest must be borne in mind. Angiographers should be aware of these filling patterns in order to recognize them as artifacts of the technique and not as manifestations of disease.

Angiography↗

Acute renal failure in McArdle's disease and myoglobinuric states.

Reversible acute oliguric renal failure associated with skeletal muscle abnormalities due to either McArdle's disease or myoglobinuria developed in two patients. Renal angiographic and hemodynamic data revealed a preferential diffuse reduction in cortical perfusion. Arteriography showed absence of a cortical nephrogram and attenuation of the distal interlobar and arcuate arteries. Contrast medium was delayed in passage through the edematous kidney. These changes are distinct from those of chronic renal failure due to parenchymal disease. The renal arteriogram can be a useful adjunct in the differential diagnosis of acute renal failure of obscure origin.

Acute Kidney Injury↗