Biomedical subjects
Publications and source records attributed to E C Rossi.
This article discusses anemia, the evaluation of symptoms, and the compensatory mechanisms that are brought into play by chronic anemia. The oxygen dissociation curve is described as is the effect of 2,3-DPG on hemoglobin-oxygen binding. Human tolerance to anemia is discussed and the article concludes with proposed transfusion strategies in chronic anemia.
The cost of delivering a unit of blood (whole blood or red cells) to a hospitalized patient was examined in 19 United States teaching hospitals. The average hospital acquisition cost was calculated by using the prices charged by regional blood centers for blood products. To this cost was added an estimate of costs incurred by hospitals for handling, testing, and administering blood. Across study sites, the average hospital cost per unit transfused was $155 and the average charge to the patient was $219. Acquisition cost, the price that hospitals pay for blood, was 37 percent of the total cost to the hospital; the other 63 percent of the hospital cost included costs for blood bank handling (13%), laboratory tests (43%), and blood administration (7%). Significant variations in blood transfusion cost were found within our sample. Most of the variability can be attributed to geographic location of the blood supply source, type of red cell product transfused, prices charged by blood transfusion services, and the frequency of laboratory tests. The results of this transfusion cost study may be helpful in determining the costs of health care delivery, especially when blood transfusions are indicated.
To determine the extent to which autologous blood that has been donated in advance ("predeposited") is used in patients undergoing elective surgery and to assess whether predonation decreases the use of homologous blood and the demand on the blood supply, we studied 4996 patients undergoing elective surgery at 18 tertiary care hospitals. Cross-matched blood was ordered for 1287 patients (26 percent), and of these, 590 (46 percent) were considered eligible for predepositing blood. Only 5 percent (32) of the eligible patients actually predeposited blood, indicating that predonation is not widely used. Of those who predeposited, only 13 percent (4 of 32) subsequently received homologous blood, as compared with 36 percent (199 of 558) of those who did not predeposit (P less than 0.01). Among the 199 patients who did not predeposit but required transfusion, we estimate that predonation could have avoided homologous transfusion in as many as 68 percent. If all eligible patients had predeposited autologous blood, they could have supplied as much as 72 percent of their own transfused red cells. The blood for as much as 10 percent of all red-cell transfusions could have been predonated by and transfused into the patients undergoing elective surgery. Greater use of predonation would not only reduce the demand on the blood supply by decreasing the need for homologous transfusion, but would probably also reduce the risk of hepatitis and other transfusion-associated illnesses.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Ketanserin, a serotonin antagonist, was used to control blood pressure during cardiopulmonary bypass in 12 patients having cardiac surgery. The drug was administered as a 10 mg bolus followed by a continuous infusion of either 40, 80, or 120 mg/hr to maintain mean arterial blood pressure below 70 mm Hg. There were 16 hypertensive episodes of which 15 (93.7%) were successfully controlled with ketanserin. Mean arterial pressure decreased significantly from an average of 72 +/- 3 to 52 +/- 9 mm Hg after 1 min. The effect that ketanserin had on platelets was also evaluated. Neither adverse nor salutary effects were seen in the platelet count, though a significant inhibition of serotonin-induced platelet aggregation was observed. Ketanserin proved effective for controlling hypertension during cardiopulmonary bypass but, despite inhibition of serotonin-induced platelet aggregation, it did not prevent thrombocytopenia.
Platelet activation was assessed in hospitalized third-trimester patients with preeclampsia (n = 11) or chronic hypertension with superimposed preeclampsia (n = 11) and in healthy outpatient pregnant controls (n = 10) by measuring plasma beta-thromboglobulin, platelet factor 4, the platelet aggregate ratio, and the amount of collagen required to produce half-maximal aggregation velocity (Kd). Only plasma beta-thromboglobulin levels differed significantly between patients with preeclampsia (50.1 +/- 37.9; p less than 0.05) or chronic hypertension with superimposed preeclampsia (47.6 +/- 16.3; p less than 0.01) and the control subjects (22.5 +/- 11.3). beta-Thromboglobulin values in patients with preeclampsia, but not chronic hypertension with superimposed preeclampsia, correlated directly with 24-hour urinary protein loss (r = 0.93, p less than 0.001) and serum creatinine levels (r = 0.62, p less than 0.05) and inversely with creatinine clearance (r = 0.60, p = 0.05). We conclude that (1) beta-thromboglobulin is elevated in patients with preeclampsia or chronic hypertension with superimposed preeclampsia, (2) the normal platelet aggregate ratio and the Kd indicate that the increase in beta-thromboglobulin is not due to an intrinsic change in platelet responsiveness, and (3) the elevation of beta-thromboglobulin in patients with either preeclampsia or chronic hypertension with superimposed preeclampsia appears to be secondary to platelet consumption in the microvasculature, although in patients with preeclampsia altered renal function may be contributory.
To understand the pathophysiologic significance of abnormal serum prostacyclin (PGI2) binding activities in thrombotic thrombocytopenic purpura (TTP), we evaluated the PGI2 binding characteristics in three chronic TTP sera and 19 normal sera. PGI2 binding by serum was rapid and reversible. The binding activity in TTP sera (22.1 +/- SD, 4.4%) was significantly lower than that of normal sera (42.2 +/- 6.2%). Moreover, the antiaggregating activity and 6-keto-prostaglandin F1 alpha (6KPGF1 alpha) content in the gel filtrates representing the binding peak was proportionally lower in a TTP serum than normal serum. Although normal and TTP sera bound [14C]arachidonate with similar activity, and neither bound [3H]6KPGF1 alpha, there was a difference in prostaglandin E1 (PGE1) binding. Binding of [3H]PGE1 was subnormal in two TTP sera (W.J. and T.G.) and normal in the third (H.S.). Normal serum corrected the binding defects of TTP serum. Interestingly, the mixture of two TTP sera (W.J. and H.S.) mutually corrected their PGI2 binding defects. In addition, although in vivo plasma transfusions improved the PGI2 binding activity of W.J. and H.S., there existed a striking difference in the nature of their response. These observations indicate that there is at least two types of PGI2 binding defects in TTP. Our data indicate that TTP is associated with diminished serum binding of PGI2. This defect may reduce the availability of PGI2 to damaged vascular sites and decrease an important modulator of platelet thrombus formation at times of severe vascular insult.
The effects of intravenous nitroglycerin (NTG) upon the bleeding time, platelet aggregation response, and plasma 6-keto-PGF1 alpha concentration were measured in 17 patients about to undergo coronary bypass grafting. NTG produced a dose-related prolongation of the bleeding time that correlated with the accompanying decrease in systolic blood pressure. Platelet aggregation was not affected and measurements of 6-keto-PGF1 alpha failed to reveal detectable levels (less than 10 pg/ml) either before or after NTG infusion. This suggests that the prolonged bleeding time associated with NTG infusion may be due to vasodilation and increased venous capacitance, rather than altered vascular-platelet interaction.
Explore the source record for details and available documents.
The production of malondialdehyde (MDA) and thromboxane B2 (TxB2) by platelets following an arachidonic acid (AA) challenge was greater in nephrotic platelet rich plasma (PRP) than in normal PRP. The uptake of 14C-AA, and its subsequent conversion to 14C-TxB2 following a thrombin stimulus, was also greater in nephrotic than normal PRP. Normal plasma diminished the MDA production by nephrotic platelets. The addition of albumin to nephrotic PRP, or, the intravenous infusion of albumin in quantities sufficient to correct hypoalbuminemia also diminished the excessive production of prostaglandin metabolites by nephrotic platelets. The platelet aggregate ratio (PAR), which measures circulating platelet aggregates, was abnormal during the acute phase of nephrotic syndrome but reverted to normal following remission. These data indicate that hypoalbuminemia is associated with increased AA metabolism by platelets and suggest that platelet "hyperactivity" may contribute to the proclivity toward thrombosis observed in nephrotic syndrome.
Twenty-four patients who received no antiplatelet medications and underwent femorotibial bypass grafting (nine vein, 12 polytetrafluoroethylene [PTFE], and three composite PTFE-vein) had serial measurements taken of their platelet function and coagulation. The concentration of collagen required to produce half-maximal platelet aggregation (Kd), the platelet aggregation ratio, antithrombin III, factor VIII-related antigen, and fibrinolytic activity (platelet-rich plasma) was measured preoperatively and 3 and 7 days after surgery. Before surgery eight patients exhibited an increase of platelet reactivity to collagen. Following femorotibial bypass grafting, the mean preoperative Kd of 0.52 +/- 0.37 microgram/ml fell to 0.34 +/- 0.35 microgram/ml on the third postoperative day (P less than 0.001) and returned to 0.41 +/- 0.72 microgram/ml on day 7. Factor VIII-related antigen increased from a mean preoperative value of 248 +/- 29% of normal activity to a mean of 360 +/- 96% on postoperative day 3 (p less than 0.01) and further increased to 428 +/- 78% on day 7 (p less than 0.01). Fourteen patients had antithrombin III measurements taken, and their levels also fell on the third postoperative day (110 +/- 5.7% to 71 +/- 6.5%; p less than 0.001). No significant changes in fibrinolytic activity were noted. Persistent platelet reactivity was found in seven patients beyond the seventh postoperative day. After administration of 325 mg of aspirin, the abnormal platelet reactivity ceased. Increased platelet reactivity to collagen, factor VIII-related antigen, and a decrease in the antithrombin III level are indicative of a hypercoagulable state in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Tyramine and dopamine are taken up by rat platelets through the serotonin uptake mechanism while phenethylamine is not taken up. This indicates that an aromatic hydroxyl group is a structural requirement for the uptake of phenethylamine derivatives by rat platelets. Although none of these phenethylamine derivatives induce platelet shape change, they inhibit serotonin-induced shape change and serotonin uptake with the same relative potency (tyramine greater than phenethylamine greater than or equal to dopamine). This suggests that the receptors controlling serotonin uptake and serotonin-induced shape change have a common structural component that binds phenethylamine derivatives. However, the fact that phenethylamine derivatives activate the serotonin uptake mechanism but do not induce platelet shape change suggests that serotonin uptake and serotonin-induced shape change are mediated by two distinct activation sites of serotonin receptors.
Serial studies of platelets and factor VIII were performed in 16 patients enrolled in the Beta Blocker Heart Attack Trial. Eight patients received placebo, and eight were treated with propranolol, in doses ranging from 40 to 320 mg per day for periods of from 6 to 31 months. No differences in platelet-collagen affinity, factor VIII coagulant activity, factor VIII related antigen, or ristocetin cofactor activity were observed between treated and untreated patients. However, circulating platelet aggregates, which were initially increased in both groups, significantly declined in those receiving propranolol (p less than 0.05). This indicates that customarily used doses of propranolol affect platelet reactivity in vivo.
Twenty-eight consecutive patients with acute spinal cord injury were randomised to one of two regimens for the prevention of deep vein thrombosis (DVT): external pneumatic calf compression (EPCC, 15), or EPCC combined with aspirin, 300 mg bid, and dipyridamole, 75 mg tid (ASA/dip, 13). DVT, detected by the 125I-fibrinogen test and impedence plethysmography, was confirmed by contrast venography. The incidence of DVT in the total group was 33 per cent, significantly less than the 78 per cent observed in 37 untreated patients studied previously (p less than 0.001). DVT developed in six of 15 patients receiving only EPCC, and three of 12 on ASA/dip as well as EPCC (p less than 0.1). The untreated patients studied earlier had significantly increased circulating platelet aggregates, increased platelet affinity for collagen, and elevated factor VIII activities, which generally coincided with the development of DVT (usually 7-9 days after injury). Prophylaxis partially prevented these coagulation abnormalities and delayed the onset of thrombosis. While the differences in the haemostatic parameters between those not treated with ASA/dip and those receiving these agents were not statistically significant (except for the platelet-collagen affinity), there was a trend toward less elevated values in the drug-treated patients. We conclude that spinal cord injury patients are at extreme risk for DVT, and have abnormal platelet and factor VIII activities. Prophylaxis with EPCC significantly and safely reduces the risk of DVT in these patients.
Explore the source record for details and available documents.
Explore the source record for details and available documents.