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Biomedical subjects

J L Blackshear

Publications and source records attributed to J L Blackshear.

At least 55 records · Page 3Linked to original sources
PubMed1991

Clinical utility of transesophageal echocardiography.

Routine transthoracic echocardiography fails to generate images of diagnostic quality in a significant number of patients who are obese, uncooperative, or unable to be properly positioned (eg, patients receiving ventilatory assistance), and in those with severe chronic obstructive pulmonary disease, chest wall deformities, or recent thoracic surgical procedures. In addition, posterior structures in the heart such as the left atrium, left atrial appendage, atrial septum, and mitral valve are seen with poorer resolution than structures closer to the anterior chest wall. Placement of a sonographic transducer in the esophagus immediately behind the heart circumvents these limitations. Newly developed probes are well tolerated by sedated conscious patients as well as by patients receiving ventilatory assistance in the intensive care unit and those under general anesthesia. Consequently, transesophageal echocardiography is now available for further enhancement of cardiac diagnosis in outpatients, for evaluating the hemodynamic status of critically ill patients in the intensive care unit, for intraoperative assessment of cardiac repairs, and for intraoperative cardiac monitoring in noncardiac surgical procedures. A series of case examples from our practice during a recent 1-year period illustrates the clinical utility of this technique in these settings.

Adult↗
PubMed1990

Streptokinase therapy for extensive venous thromboses in a patient with severe ulcerative colitis.

Thromboembolic disease is a known complication of patients with inflammatory bowel disease and often is associated with increased morbidity and mortality. In a patient with severe ulcerative colitis, extensive venous thromboses developed in three extremities. Despite active bleeding in the lower gastrointestinal tract, he was successfully managed preoperatively with infusions of streptokinase followed by full-dose heparinization. During the 48 hours he received streptokinase, his venous thromboses resolved dramatically. Within 2 weeks after admission, he underwent an uneventful proctocolectomy in conjunction with an ileoanal anastomosis.

Adult↗
PubMed1987

Medical approaches to prevention of restenosis after coronary angioplasty.

Although initial success rates for coronary angioplasty have improved, the rate of restenosis within 6 months of the procedure has persisted at 30 to 40%. The relation of restenosis to initial success, recurrence of symptoms and risk factors suggests that high grade or total lesions, long lesions, lesions in the proximal left anterior descending artery or in saphenous grafts, and the absence of intimal dissection after angioplasty are associated with an increased risk of restenosis. Unstable angina, male sex and diabetes are clinical factors associated with a greater risk of restenosis. Pathologic specimens suggest that plaque splitting and disruption are found acutely after angioplasty, but that restenosis occurs as an excessive reparative, proliferative response of smooth muscle cells leading to recurrent luminal narrowing. A prospective analysis of therapeutic interventions to prevent restenosis, such as administering antiplatelet and lipid-lowering agents, intensive diabetic therapy and administration of calcium antagonists, is proposed. Problems with timing of studies, design and sample size are considered. Current recommendations for anti-restenosis therapy include antiplatelet therapy before and after angioplasty, administration of heparin in some patients and intensive risk factor intervention for the 6 months after the procedure.

Angioplasty, Balloon↗
PubMed1987

Exaggerated renal vasodilator response to calcium entry blockade in first-degree relatives of essential hypertensive subjects.

Because an inherited renal factor may contribute to essential hypertension in humans, the study of family members is attractive. To assess the determinants of renal vascular tone, graded doses of either diltiazem (10-1000 micrograms/min) or acetylcholine (1-100 micrograms/min) were infused into the renal artery in 52 normotensive subjects, 16 with and 36 without a family history of hypertension when they were in balance on either a 10-mEq or 200-mEq sodium intake. Renal blood flow was measured with 133Xe. Restricted sodium intake potentiated renal vascular responses to diltiazem (p less than 0.01), suggesting a role for angiotensin as a determinant. In four subjects with no family history of hypertension on a 200-mEq sodium intake, angiotensin II in subpressor doses (1 ng/kg/min i.v.) induced renal vasoconstriction and enhanced the renal vasodilator action of diltiazem (p less than 0.001). In subjects with a family history of hypertension, the renal vascular response to diltiazem was enhanced (p less than 0.01) despite similar values of plasma renin activity, angiotensin II concentration, and sodium excretion. Because responses to acetylcholine were modified neither by sodium intake nor by family history, specificity for diltiazem was suggested. The intriguing possibility is raised that the enhanced renal vascular response to diltiazem reflects an abnormality in the control of renal vascular tone in the offspring of essential hypertensive subjects.

Acetylcholine↗
PubMed1986

Guanfacine as monotherapy for systemic hypertension.

Three clinical studies examined the effects of guanfacine as monotherapy. Study 1 was a double-blind, randomized, parallel trial with a placebo control with 26 patients with mild essential hypertension treated with 1-mg guanfacine or matching placebo daily at bedtime for 8 weeks. Pretreatment and posttreatment determinations of plasma volume, plasma aldosterone and blood pressure (BP) were made in all 26 patients. There were no significant differences between guanfacine and placebo with regard to changes in plasma volume or plasma aldosterone, but a significant decrease (p = 0.001) in both diastolic and mean BPs was seen with the active drug. No side effects were reported. From this study, it was concluded that guanfacine monotherapy is an effective and well-tolerated initial treatment for mild essential hypertension with no effect on either plasma volume or plasma aldosterone. Study 2 was a double-blind, randomized, parallel clinical study with placebo control with 42 patients with mild essential hypertension treated with either guanfacine (1 mg/day) or matching placebo at bedtime for 8 weeks. Pretreatment and posttreatment evaluations of serum cholesterol, triglycerides, low density lipoproteins, very low density lipoproteins and high density lipoproteins revealed no significant differences between the treatment and the placebo groups. A statistically significant (p less than 0.0001) decrease in diastolic BP was seen in the guanfacine group compared with those patients who received placebo. Guanfacine monotherapy was again shown to be an effective initial treatment for mild essential hypertension with no adverse influence on serum lipids.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Specific increase in sensitivity to serotonin of the canine hindlimb collateral arterial tree via the 5-hydroxytryptamine-2 receptor.

Evidence that platelet activation contributes to ischemia associated with atherosclerosis led us to examine the response of the limb collateral arterial tree to a platelet product, serotonin. In 23 anesthetized dogs we measured arterial diameter (angiography) and blood flow (133Xe transit) before or 2 weeks after superficial femoral artery ligation (SFAL). In normal hindlimbs blood flow increased after 5-hydroxytryptamine (5-HT) and there was a modest but measurable, dose dependent narrowing of 1- to 2-mm vessels, the major stem vessels for collateral blood flow. After SFAL, identical segments of these vessels responded to serotonin more: the slope relating dose and response became steeper (P less than 0.001), the threshold dose fell significantly (P less than 0.001), and calf blood flow fell. The vasodilator response to acetylcholine was reduced sharply after SFAL, but was still demonstrable. The 5-HT-2 serotonin antagonist, ketanserin, reversed serotonin induced spasm in the region served by collaterals (P less than 0.025). Responses to norepinephrine were not potentiated. A 5-HT-2 receptor dependent sensitization of collateral arterial vessels, and blunting of the normal vasodilator response, mediates a paradoxical decrease in perfusion induced by 5-HT in regions served by the collaterals.

Animals↗
PubMed1986

Serotonin and the renal blood supply: role of prostaglandins and the 5HT-2 receptor.

Serotonin (5HT) has been reported to increase, to decrease, or not to change renal blood flow. We postulated that prostaglandin release in response to 5HT acted as a confusing variable, and tested the hypothesis by comparing infusions of serotonin and angiotensin into one renal artery of 14 anesthetized dogs before and after indomethacin administration. Renal blood flow (Q, by EM flow-meter) responses to 5HT were routinely biphasic, an initial sharp decrease followed by a gradual increase which stabilized well above baseline at three to six minutes. Indomethacin, 1 to 2 mg/kg, did not alter the acute Q decrement induced by 5HT but abolished the increase in Q at three to six minutes (P less than 0.001). Instead, sustained vasoconstriction became apparent. Ketanserin reversed the sustained vasoconstrictor effect of 5HT in indomethacin-treated dogs, leading to striking, serotonin-induced vasodilatation. The latter vasodilatation in turn was inhibited by methysergide. Four independent elements, two promoting vasoconstriction and two vasodilatation, are suggested. One vasodilator response is abolished by prostaglandin synthetase inhibition and the other by methysergide, a complex 5HT receptor blocker. The sustained vasoconstrictor response is blocked by ketanserin, suggesting an action on the 5HT-2 receptor. The initial, transient vasoconstrictor response is resistant to the blockers employed. These complex interactions may account for the variability in reported responses of the renal blood supply to serotonin.

Angiotensin II↗
PubMed1986

Serotonin-induced visualization of the popliteal lymph node by angiography. A unique microvascular response to serotonin.

Regulation of the blood supply to lymph nodes is an important determinant of lymphocyte traffic but remains poorly understood. Infusion into the femoral artery of serotonin (5 HT), an agent that may produce either vasoconstriction or vasodilatation, induced striking arteriographic visualization of the popliteal lymph node in 19 of 20 dogs. Neither other vasodilator agents (acetylcholine, tolazoline, histamine, isoproterenol, sodium arachidonate, the prostaglandin analog CL115, 347) nor vasoconstrictor substances (norepinephrine, epinephrine, phenylephrine, and ergonovine maleate) produced the same effect. The timing of appearance and disappearance of the contrast medium during 5HT infusion suggests that an increase in capillary blood flow secondary to arteriolar dilatation in the lymph node is responsible for the augmented visualization. 5HT-induced visualization of the popliteal lymph node was not modified by pretreatment with either the specific 5HT-2 antagonist ketanserin or the nonspecific antagonist methysergide. The specificity of action of 5HT and its availability for release from circulating and noncirculating cellular elements suggest that it may be important in the regulation of lymph node circulation, and thereby, lymphocyte traffic. This approach may provide another means to enhance the visualization of lymph nodes.

Angiography↗
PubMed1986

Effects of oral potassium supplements on upper gastrointestinal mucosa: multicenter clinical comparison of three formulations and placebo.

In a carefully controlled multicenter investigation of the effects of oral potassium chloride (KCl) supplements on the gastrointestinal mucosa, 120 healthy men with no endoscopically apparent gastrointestinal lesions were confined to a research ward for 18 days. By random assignment, they were given 60 mEq/day (20 mEq TID) of KCl as either a microencapsulated gelatin capsule, a wax/polymer matrix tablet, or a powder-in-liquid formulation or a placebo capsule for two weeks. All subjects were given glycopyrrolate concomitantly to delay gastric emptying. After treatment was completed, endoscopic examinations of the esophagus, stomach, and duodenum were performed and evaluated by specialists blinded to the particular treatment given. Mild to moderate gastrointestinal irritation, characterized by erythema and edema, was found with similar frequency in all four treatment groups. Two of 30 subjects given the microencapsulated KCl had a single erosion each. Single or multiple erosions were also observed in 14/30 men given the wax/polymer matrix tablet, in 7/30 given the powder, and in 1/30 given placebo. One subject given the wax/polymer matrix tablet had a gastric ulcer. The incidence of gastrointestinal injury with the microencapsulated form was significantly less (P less than 0.01) than that with the wax/polymer matrix tablet and was not significantly different from that seen with either the powder or placebo.

Administration, Oral↗
PubMed1985

Comparison of the response of the renal blood supply to acetylcholine and to a calcium channel blocking agent, diltiazem, in the dog.

Several vasodilators, including acetylcholine, are capable of inducing maximal renal vasodilatation when infused into the renal artery. Despite substantial interest in the renal vascular response to calcium channel blocking agents, there has been no systematic comparison of any of these agents to an index vasodilator, such as acetylcholine. We compared the renal vascular angiographic response to acetylcholine and diltiazem, infused into the renal artery in graded dosage, in 14 dogs. In eight of the dogs renal blood flow was measured with an electromagnetic flowmeter. At peak, the acetylcholine-induced increase in renal blood flow (155 +/- 25 to 309 +/- 55 ml/min) slightly exceeded that induced by diltiazem (143 +/- 13 to 257 +/- 58 ml/min). A close correlation was found between the maximal blood flow increase induced by acetylcholine and by diltiazem (R = .95). Dilatation of the intrarenal arterial tree evident on the renal arteriogram was substantially less striking with diltiazem than with acetylcholine in these eight dogs. To ascertain the possible contributing role of the surgery required for blood flow measurement, the two agents were assessed in six additional dogs without blood flow measurement. In these six dogs diltiazem and acetylcholine induced essentially identical degrees of renal arterial vasodilatation. It is concluded that diltiazem, the calcium channel blocking agent, produces near maximal renal vasodilatation at the arteriolar level and that responses of more proximal elements of the renal arterial tree, visible during renal arteriography, are sensitive to the conditions of the experiment.

Acetylcholine↗
PubMed1983

Identification of risk for renal insufficiency from nonsteroidal anti-inflammatory drugs.

Risk for renal insufficiency (RI) resulting from nonsteroidal anti-inflammatory drugs (NSAID) exists in cirrhosis with ascites, nephrotic syndrome, decompensated congestive heart failure, and chronic renal disease. We saw seven cases of NSAID RI that demonstrate important additional clinical risk factors. These include advanced age (mean, 76 years), use of diuretic drugs (6/7 patients), and evidence of renal vascular disease as suggested by long-standing hypertension, diabetes, or atherosclerotic cardiovascular disease (7/7 patients). Analysis of past case reports of NSAID RI also showed these features. Treatment of acute gouty arthritis was the most common precipitating event. Evolving NSAID RI was suggested by rising serum urea nitrogen, serum creatinine, and serum potassium levels, and body weight gain associated with low fractional excretion of sodium. We conclude that since NSAID RI is preventable and reversible, it is important to recognize and monitor the conditions of those patients at risk.

Acute Kidney Injury↗
PubMedDate not supplied

Beat-by-beat aortic valve area measurements indicate constant orifice area in aortic stenosis: analysis of Doppler data with varying RR intervals.

Gorlin formula calculation of aortic valve area suggests that orifice area increases in patients with aortic stenosis with rising cardiac output. Evidence that aortic orifice area varies was sought in patients with aortic stenosis by analyzing Doppler data beat by beat versus RR interval in 22 patients with spontaneous RR variability. Stroke volume increased in all patients from minimum to maximum RR interval by 129% +/- 19%. Over the same range of RR intervals, assessment of aortic valve area by (A) simultaneous inner and outer continuous wave Doppler signals, or (B) nonsimultaneous RR-matched pulsed wave Doppler from the left ventricular outflow tract and continuous wave Doppler from the aortic valve failed to suggest an increase in aortic valve area. A positive relationship between aortic valve area and RR interval was not consistently observed with the exception of seven out of eight patients with mild to moderate (pulsed wave Doppler/continuous wave Doppler time velocity integral ratio of 0.3 to 0.7) aortic stenosis (p less than 0.05). Beat-by-beat measurements of aortic valve orifice area using Doppler techniques do not suggest that the aortic stenosis orifice varies over a wide range of RR intervals and stroke volumes.

Aged↗