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R G Johnson

Publications and source records attributed to R G Johnson.

At least 109 records · Page 6Linked to original sources
PubMed1993

Blood and albumin cardioplegia preserve endothelium-dependent microvascular responses.

Alterations of vascular reactivity may be a cause of reduced myocardial perfusion after cardioplegic arrest. The effects of blood and albumin cardioplegia on endothelium-dependent coronary microvascular function and ultrastructure were examined after cardiopulmonary bypass, ischemic arrest, and reperfusion. During cardiopulmonary bypass, porcine hearts were arrested with either blood, albumin-crystalloid, or crystalloid cardioplegia for 1 hour, followed with reperfusion for 1 hour. Noninstrumented pigs were used as controls. Coronary microarterial vessels (90 to 190 microns in diameter) were studied in a pressurized, no-flow state with video microscopic imaging and electronic dimension analysis. Ischemic arrest with crystalloid cardioplegia markedly reduced endothelium-dependent relaxations to the adenine nucleotide adenosine diphosphate and the calcium ionophore A23187. Enhanced contractile responses were observed to the platelet-derived vasoactive substance serotonin and to the thromboxane A2 analogue U46619. Indomethacin corrected the enhanced contractile responses to serotonin, indicating the enhanced release of a constrictor prostanoid substance. Indomethacin had no effect on the impaired relaxations to adenosine diphosphate or A23187. Endothelium-dependent relaxations to adenosine diphosphate, serotonin, and A23187 were significantly preserved with either blood or albumin-crystalloid cardioplegia, whereas contractile responses to U46619 were normal. Endothelium-independent relaxation to nitroprusside was similar in all groups, indicating normal smooth muscle responsiveness. Electron microscopy revealed minimal alterations of vascular morphology of vessels in both crystalloid and blood cardioplegia groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1993

Cardiopulmonary bypass and pulmonary thromboxane generation.

Sporadic cases of inexplicable noncardiogenic pulmonary edema occur after operations requiring total cardiopulmonary bypass (CPB). Prostaglandins, such as thromboxane (Tx) A2, have been implicated in this form of pulmonary pathology in many clinical and experimental settings. Because Tx generation has been demonstrated in association with ischemia of solid organs, we postulated that total CPB, which decreases pulmonary tissue perfusion and oxygenation, would stimulate local Tx synthesis. Total CPB was examined in 7 sheep. The level of TxB2 (a stable metabolite of the active, unstable A2) was measured in the left and right atria before, during, and after 105 minutes of total CPB. Significant increases in TxB2 concentrations occurred in the left atrium compared with the right (p < 0.05) during CPB. Immediately after reperfusion, both the left atrial and right atrial TxB2 concentrations increased significantly over the baseline values (p < 0.05), but this increase and the atrial gradient were rapidly abolished with continued pulmonary perfusion. To determine the effect of extracorporeal circulation without significant (< 30%) alteration in pulmonary perfusion, we evaluated the effect of partial CPB in 5 sheep. Increased TxB2 concentrations were noted at 15 and 30 minutes after the onset of partial CPB (left atrium increased significantly over baseline; p < 0.05), but this elevation spontaneously diminished to insignificance after 15 and 30 additional minutes of extracorporeal circulation. These data establish that total CPB stimulates Tx generation in the lung, and although the effect of partial CPB is transient, that of total CPB is progressive and abolished by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effects of chronic cocaine administration on the serotonergic system in the rat brain.

Male Sprague-Dawley rats received injections of cocaine (20 mg/kg/dose, IP) every 12 h for 14 days and were sacrificed on the 15th day. The chronic cocaine treatment caused an increase in the levels of serotonin [5-hydroxytryptamine (5-HT)] and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the hippocampus. 5-HIAA levels in the frontal cortex were also increased, but 5-HT levels were unaltered by the chronic cocaine treatment. Similarly, striatal levels of 5-HT and 5-HIAA were unchanged by repeated administration of cocaine. Chronic cocaine administration did not alter the density of [3H]8-OH(DPAT), [3H]mesulergine, or [3H]ketanserin binding in the hippocampus, choroid plexus, and frontal cortex, respectively. Furthermore, repeated injection of cocaine did not alter serotonergic-mediated inhibition of adenylate cyclase activity. Thus, repeated administration of cocaine causes region-specific alterations in 5-HT levels but does not change the properties of the 5-HT1A, 5-HT1C, or 5-HT2 receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1993

Relaxation responses of the coronary microcirculation after cardiopulmonary bypass and ischemic arrest with cardioplegia: implications for the treatment of postoperative coronary spasm.

Coronary arteriolar spasm may occur following cardiopulmonary bypass and ischemic arrest, resulting in impaired cardiac function. Because myocardial perfusion is principally regulated by the microcirculation, the in vitro effects of various clinically used vasodilating drugs on porcine coronary microvessels less than 200 microns in diameter were examined following cardioplegic arrest and reperfusion. After 1 hour of ischemic arrest using either crystalloid or blood cardioplegia solutions followed by 1 hour of reperfusion, microvessels were studied in a pressurized (40 mmHg), no-flow state, and imaged with a video tracking device. Vessels were preconstricted by 30% to 60% of their resting diameter using acetylcholine, and various vasodilatory agents were applied extraluminally. Responses to the beta-adrenergic receptor agonist isoproterenol and the nitrovasodilator sodium nitroprusside were minimally altered by either cardioplegia solution as compared to control. In contrast, relaxation responses to both the calcium channel antagonist nifedipine and nitroglycerin were diminished after ischemic arrest and reperfusion. Relaxation responses were similar with crystalloid or blood cardioplegia for all drugs tested. Despite its somewhat attenuated response, nifedipine remained the most potent vasodilator of those studied. It is concluded that (1) following ischemic arrest with either crystalloid or blood cardioplegia solutions, responses to sodium nitroprusside and isoproterenol were minimally altered, while responses to nifedipine and nitroglycerin were attenuated; (2) relaxation responses of coronary arterioles were not significantly different with either blood or crystalloid cardioplegia; and (3) despite a slightly decreased response after cardioplegia, nifedipine was the most potent vasodilator of coronary arterioles, and may be the best choice for treating postoperative coronary arteriolar spasm.

Animals↗
PubMed1993

Mechanisms causing coronary microvascular dysfunction following crystalloid cardioplegia and reperfusion.

OBJECTIVE: The aim was to examine the mechanisms of coronary microvascular dysfunction during cardiopulmonary bypass and ischaemic arrest using a crystalloid cardioplegic solution. METHODS: Porcine hearts were arrested with cold hyperkalaemic (K+ = 25 mmol.litre-1) cardioplegic solution for 1 h during cardiopulmonary bypass and then reperfused for 1 h. Selected hearts were arrested but not reperfused. Coronary vessels of non-instrumented pigs were used as controls. In vitro vascular responses of subepicardial and subendocardial arterioles were examined in a pressurised (40 mm Hg) no flow state with video microscopy. RESULTS: Following 1 h of ischaemic cardioplegia, endothelium dependent relaxations of epicardial arterioles to the receptor mediated agent ADP and the non-receptor-mediated agent calcium ionophore A23187 were moderately reduced, and the contractile responses to KCl or the thromboxane A2 analogue U46619 were reduced compared to responses of vessels from control animals. After 1 h of reperfusion, U46619 caused contraction greater than control values, while contraction to KCl and endothelium dependent relaxations to ADP or A23187 were further reduced. Responses of endocardial microvessels to serotonin were slightly more affected by cardioplegia and reperfusion than were epicardial vessels, while the effect on responses of epicardial and endocardial vessels to bradykinin or A23187 were similar. Endothelium independent relaxation to sodium nitroprusside was not altered in any of the experimental groups. The addition of manganese superoxide dismutase to the cardioplegic solution markedly preserved endothelium dependent responses to ADP and A23187 and contractile response to U46619, compared to the responses of vessels from the plain crystalloid cardioplegia group, but had no effect on relaxation to sodium nitroprusside or on contraction to KCl. Five hours of normokalaemic hypothermia (5-10 degrees C) in Krebs buffer had minimal effect on vasodilator responses. Electron microscopy revealed preserved endothelial and smooth muscle cell structure, and focal mononuclear leucocyte-endothelium adherence following cardioplegic arrest and reperfusion. CONCLUSIONS: Ischaemic cardioplegia-reperfusion induced endothelium dependent and direct smooth muscle microvascular dysfunction is at least partially mediated by prolonged exposure of vessels to hyperkalaemia and to the generation of oxygen derived free radicals. Leucocytes probably mediate injury during reperfusion, while hypothermia has minimal effect on recovery of vasomotor function.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Risk of liver disease in HCV-seropositive kidney transplant recipients.

OBJECTIVE: This study determined whether renal allograft recipients with antibodies to hepatitis C virus (HCV) at the time of transplantation experienced increased morbidity or mortality from hepatitis, liver disease, or hepatocellular carcinoma compared with patients without anti-HCV. SUMMARY BACKGROUND DATA: Chronic liver disease is a cause of significant morbidity and mortality after kidney transplantation and the contribution of HCV to this problem has not been determined. The recent characterization of the HCV genome has resulted in the development of screening tests for antibody to HCV, allowing the identification of end-stage renal disease patients with anti-HCV who are candidates for transplantation. The risk to these patients for the development of hepatic complications after subsequent transplantation is unknown. METHODS: Archived sera obtained from 163 kidney transplant recipients at the time of transplantation were tested for anti-HCV using the Abbott HCV 2.0 second-generation test system. Sera containing anti-HCV were further analyzed for reactivity against specific HCV recombinant proteins, including core, NS3 (c33c), and NS4 (c100-3), to determine whether a pattern could be identified in patients with hepatic complications. The follow-up of all patients was current (mean length of follow-up was 33 months) to identify patients with hepatic complications. All patients had previously been tested for HBSAg. RESULTS: Twenty-nine patients (18%) had anti-HCV and three (1.8%) had HBSAg. Forty-five patients (28% of total) had transient elevations of AST or ALT without subsequent evidence of liver disease. Three patients had a syndrome of acute hepatitis. Chronic liver disease developed in only six patients (3.6%) after transplantation. Four had anti-HCV only, one had HBSAg only, and one was positive for both. However, of the 29 patients with anti-HCV, chronic liver disease developed in 5 (17%), including 1 patient who was positive for HBSAg. No patient had hepatocellular carcinoma. CONCLUSIONS: Perturbations of liver function were common in the kidney transplant recipients studied, most were self-limited, and few were associated with evidence of viral hepatitis. The risk of developing

Adolescent↗
PubMed1993

Left ventricular diastolic chamber stiffness and intramyocardial coronary capacitance in isolated dog hearts.

BACKGROUND: Because the myocardium is perfused primarily during diastole, changes in diastolic properties of the left ventricle (LV) should influence the intramyocardial circulation. METHODS AND RESULTS: We examined the influence of LV diastolic properties on the magnitude and localization of intramyocardial coronary capacitance by analyzing the coronary pressure-venous flow relation in isolated, isovolumic dog heart preparations. After sudden occlusion of the left coronary artery during a long diastole, we measured precapacitance and postcapacitance resistances (RPRE and RPOST) and calculated intramyocardial coronary capacitance (CIM) from RPOST and the time constant of the coronary venous flow decay. Using this method, we characterized the effects of coronary vasodilation, LV diastolic volume, and LV diastolic chamber stiffness on the coronary circulation. The magnitude of CIM increased from 0.09 +/- 0.01 to 0.24 +/- 0.20 mL.mm Hg-1 x 100 g-1 (P < .01) after adenosine-induced vasodilation, whereas both RPOST and RPRE decreased significantly. The ratio of RPOST to RPRE+RPOST decreased from 0.35 +/- 0.02 to 0.23 +/- 0.02 (P < .01), suggesting redistribution of CIM to the distal portion of the coronary vascular tree. An increase in LV volume and wall stress was imposed to increase LV diastolic pressure from 2 +/- 0.1 to 25 +/- 1 mm Hg: this increased RPOST significantly but not RPRE and decreased the magnitude of CIM. The resistance ratio did not change significantly. Increased LV diastolic chamber stiffness induced by hypoxic perfusion (isovolumic LV diastolic pressure increased from 11 +/- 1 to 28 +/- 1 mm Hg) raised RPOST and decreased the magnitude of CIM from 0.32 +/- 0.12 to 0.17 +/- 0.04 mL.mm Hg-1 x 100 g-1 (P < .05). The resistance ratio increased significantly from 0.21 +/- 0.05 to 0.33 +/- 0.05 with increased LV diastolic chamber stiffness. Adjustment of LV diastolic volume to lower diastolic pressure to 10 +/- 1 mm Hg did not alter these changes significantly, suggesting that an intrinsic increase in myocardial stiffness played a major role in these changes. CONCLUSIONS: Extravascular compression by raised LV diastolic volume and/or increased LV diastolic chamber stiffness acted mainly on coronary vessels that determine intramyocardial capacitance and postcapacitance resistance.

Animals↗
PubMed1993

Research considerations: stress and perceived health status in the rural elderly.

1. Stress is recognized as a significant factor in the development of acute and chronic illnesses in adults. The rural aged experience high stress levels and poor-to-fair health. 2. Commonly reported stressful events and chronic strains in the rural elderly involve loss, isolation, decreased abilities to manage self-care activities, and financial concerns. 3. The older, single subjects in this study reported more stress and poorer health than younger, married subjects. 4. Nurses must develop strategies specifically designed to mediate the stress experienced by the rural aged.

Aged↗
PubMed1993

Altered pulmonary microvascular reactivity after total cardiopulmonary bypass.

Pulmonary vascular resistance is frequently elevated after cardiac operations in which cardiopulmonary bypass is used. In our study of the possible contribution of altered pulmonary microvascular reactivity to this condition, sheep were heparinized, cannulated via the aorta and right atrium, and placed on total cardiopulmonary bypass. After 90 minutes of total cardiopulmonary bypass and pulmonary arterial occlusion, the sheep were removed from cardiopulmonary bypass, and their lungs were perfused normally for 60 minutes. Noninstrumented animals were used as controls. To evaluate the effect of 90 minutes of extracorporeal circulation without reduced pulmonary perfusion, we studied additional sheep after they underwent right heart bypass with a pump-oxygenator. Pulmonary microarterial vessels (130 to 230 microns in diameter) from each group were examined in vitro in a pressurized (20 mm Hg), no-flow state with video microscopic imaging and electronic dimension analysis. After preconstriction of vessels with the thromboxane A2 analog U46619 by 30% to 40% of the baseline diameter, vasoactive drugs were applied extraluminally. Serotonin caused control microvessels to dilate. In the presence of the nitric oxide synthetase inhibitor NG-methyl-L-arginine, this was converted to a significant contractile response. Acetylcholine alone had minimal effect on control vessels. However, in the presence of the cyclooxygenase inhibitor indomethacin, acetylcholine caused a significant relaxation response. After total cardiopulmonary bypass and pulmonary reperfusion, pulmonary microvessels contracted significantly when exposed to acetylcholine and serotonin, compared with respective control responses. Both these contractile responses were inhibited in the presence of indomethacin. Endothelium-independent responses to sodium nitroprusside and U46619 and dilation responses to adenosine were not altered after cardiopulmonary bypass. Extracorporeal circulation with continued pulmonary arterial perfusion (right heart bypass group) had no effect on microvascular responses. In conclusion, total cardiopulmonary bypass with associated reduced pulmonary perfusion causes significant alterations of endothelium-dependent pulmonary microvascular responses because of the increased release of a constrictor prostanoid substance and possibly because of reduced release of endothelium-derived relaxing factor.

Acetylcholine↗
PubMed1992

An activator of protein kinase C inhibits gap junction communication between cultured bovine lens cells.

Currently little is known about the regulation of gap junction communication in the lens. We report here on the effects of the protein kinase C activator, 12-O-tetradecanoylphorbol-13-acetate (TPA), on cultured bovine lens cells which appeared to be epithelial in nature. Dramatically reduced intercellular transfer of the fluorescent dye Lucifer yellow was observed when the cultured lens cells were treated with octanol, a known inhibitor of gap junction communication. TPA (4 beta isomer) was also shown to reduce intercellular permeability within these cultures. In contrast, an inactive form of TPA, 4 alpha-TPA, did not decrease dye transfer. Permeability was evaluated in terms of both the number of cells receiving dye and the rate of decrease in fluorescence intensity in the injected cell. The maximum decreases in dye transfer occurred at 2 h of TPA treatment and dye transfer gradually increased to control levels over a time course of many hours. Incubation of cultures with 32Pi and immunoprecipitation using antibodies to the N- and C-terminal regions of connexin43 demonstrated a gap junction phosphoprotein of 43,000 Da. Phosphorylation of connexin43 increased during the first 2 h of TPA treatment. These results suggest that protein kinase C has a direct or indirect effect on gap junction communication in cultured lens cells.

Animals↗
PubMed1992

Inhibition of gap junction and adherens junction assembly by connexin and A-CAM antibodies.

We examined the roles of the extracellular domains of a gap junction protein and a cell adhesion molecule in gap junction and adherens junction formation by altering cell interactions with antibody Fab fragments. Using immunoblotting and immunocytochemistry we demonstrated that Novikoff cells contained the gap junction protein, connexin43 (Cx43), and the cell adhesion molecule, A-CAM (N-cadherin). Cells were dissociated in EDTA, allowed to recover, and reaggregated for 60 min in media containing Fab fragments prepared from a number of antibodies. We observed no cell-cell dye transfer 4 min after microinjection in 90% of the cell pairs treated with Fab fragments of antibodies for the first or second extracellular domain of Cx43, the second extracellular domain of connexin32 (Cx32) or A-CAM. Cell-cell dye transfer was detected within 30 s in cell pairs treated with control Fab fragments (pre-immune serum, antibodies to the rat major histocompatibility complex or the amino or carboxyl termii of Cx43). We observed no gap junctions by freeze-fracture EM and no adherens junctions by thin section EM between cells treated with the Fab fragments that blocked cell-cell dye transfer. Gap junctions were found on approximately 50% of the cells in control samples using freeze-fracture EM. We demonstrated with reaggregated Novikoff cells that: (a) functional interactions of the extracellular domains of the connexins were necessary for the formation of gap junction channels; (b) cell interactions mediated by A-CAM were required for gap junction assembly; and (c) Fab fragments of antibodies for A-CAM or connexin extracellular domains blocked adherens junction formation.

Animals↗
PubMed1992

War in Croatia.

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Croatia↗
PubMed1992

Endothelial modulation of porcine coronary microcirculation perfused via immature collaterals.

Porcine hearts have relatively few native collateral vessels and lack the propensity to develop normal perfusion to the collateral-dependent myocardium. To examine microvascular responses in the collateral-dependent region, collateral vessels were stimulated in pigs by the Ameroid constrictor technique. After 4-7 wk, isolated microarterial vessels (90-170 microns ID) were studied in a pressurized (40 mmHg), no-flow state. Microvessels from noninstrumented pigs were used as controls for vascular studies. Although myocardium in the collateral-dependent region showed minimal evidence of infarction, percent systolic shortening was reduced at rest and after pacing compared with myocardium in the normally perfused region. Relaxations to the receptor-mediated endothelium-dependent agents ADP and bradykinin were impaired in collateral-dependent coronary microvessels. Relaxations to the calcium ionophore A23187, which acts through a non-receptor-mediated mechanism, were similar in control and Ameroid microvessels. Relaxations to the endothelium-independent agent sodium nitroprusside were markedly enhanced in microvessels from the collateral-dependent region compared with microvessels from control hearts. In conclusion, receptor-mediated endothelium-dependent relaxation is impaired and endothelium-independent relaxation to sodium nitroprusside is enhanced in microvessels from myocardium perfused by immature collateral vessels.

Animals↗
PubMed1992

Comparison of two transfusion strategies after elective operations for myocardial revascularization.

We performed a prospective, randomized trial of two different strategies for postoperative packed red blood cell replacement in 39 autologous blood donors undergoing elective myocardial revascularization. The "liberal" group received blood to achieve a hematocrit value of 32%, and the "conservative" group received transfusions for a hematocrit value less than 25%. Although the groups had significantly different mean hematocrit values from the fourth postoperative hour (28.7% versus 31.2%) through the fifth postoperative day (28.4% versus 31.3%), there were no significant differences in fluid requirement, hemodynamic parameters, or hospital complications. Significantly fewer units of packed cells were required in the conservatively transfused group (20 units/20 patients) compared with the liberally transfused group (37 units/18 patients) (p = 0.012). Exercise tests were performed on the fifth and sixth postoperative days, with a transfusion being given to the conservative group between tests. Although a significant improvement in exercise endurance occurred in the conservative group receiving a transfusion (p = 0.008), no significant difference in duration or degree of exercise was demonstrated between the two groups on either day. In comparing these two groups of profoundly anemic patients, we identified no adverse consequence associated with the greater degree of hemodilution and could identify no correlation between hematocrit value and exercise capacity. We conclude that although the limits of hemodilution are still poorly defined, postoperative blood transfusion in revascularized patients should be guided by clinical indications and not by specific hematocrit values.

Anemia↗
PubMed1992

Mechanical assistance of the left ventricle: acute effect on cardiac performance and coronary flow of different perfusion patterns.

Mechanical circulatory assistance by ventricular assist devices provides an opportunity to influence the aortic pressure pattern, which may affect ventricular loading and coronary perfusion. The effect of synchronous, pulsatile coronary perfusion of an assist device-supported left ventricle has not been studied. To analyze the effect of different perfusion patterns on left ventricular performance and on coronary flow, independent of pressure and volume loading, we used three different modes of aortic perfusion in an isometric, contracting, isolated canine heart model. The effect of nonpulsatile, counter-pulsatile, and copulsatile coronary perfusion was analyzed in four subgroups to simulate different, clinically relevant situations (using two different ventricular end-diastolic volumes [normal and high] and two mean perfusion pressures [normal and critically low]). Our experiments demonstrated that total coronary flow is optimized by making the perfusion pressure pulsatile and by synchronously timing the pump systole with ventricular diastole (counterpulsation). Under identical conditions of preload and mean perfusion pressure, coronary flow and left ventricular contractility were decreased during non-pulsatile and copulsatile aortic perfusion when compared with counterpulsatile flow. There were no significant differences between the nonpulsatile and copulsatile modes. We conclude from these data that a nonejecting, but contracting, left ventricle will have improved systolic function and coronary blood flow if the coronary perfusion pressure is synchronized in a counterpulsatile manner. This is a significant implication for mechanical left ventricular assist devices when used to promote myocardial recovery.

Animals↗
PubMed1992

Pnemostasis of injured lung in rabbits with gelatin-resorcinol formaldehyde-glutaraldehyde tissue adhesive.

Peripheral bronchopulmonary fistulas, or parenchymal air leaks, may occasionally be resistant to conventional suture or stapling techniques. In such instances, the tissue is poor and the associated morbidity of a persistent leak will be the greatest. We tested a previously described tissue adhesive compounded from gelatin resorcinol and polymerized at the time of application with a glutaraldehyde-formaldehyde mixture. We evaluated the ability of the adhesive to seal incisional air leaks acutely in the lungs of rabbits under conditions of positive intratracheal pressure and persistent ventilation. We also tested the efficacy of the glue at intervals after compounding to assess the shelf life of this nonproprietary formula. We established a technique for application of this adhesive and demonstrated its ability to decrease consistently the magnitude of air leaks, while generally providing complete pneumostasis in the presence of clinically relevant positive pressure ventilation. We conclude that this material can be prepared months in advance of its occasional use as an effective means of dealing with parenchymal air leaks encountered at operation.

Animals↗
PubMed1991

Hepatitis C virus infection in post-transfusion hepatitis. An analysis with first- and second-generation assays.

BACKGROUND: The causes of post-transfusion non-A, non-B hepatitis are still not fully defined, nor is it clear how accurate the tests are that are used to screen blood donors for hepatitis C virus (HCV) and to diagnose post-transfusion hepatitis caused by infected blood. METHODS: We used two first-generation enzyme-linked immunoassays (EIAs) and one second-generation immunoassay to test for anti-HCV antibodies in serum samples collected between 1976 and 1979 in the Transfusion-Transmitted Viruses Study (from 1247 patients who underwent transfusion and 1235 matched control subjects who did not receive transfusions). We tested serum collected before and after infection from the patients in whom non-A, non-B hepatitis developed, serum from their blood donors, and serum from 41 of the control subjects who had hepatitis unrelated to transfusion. RESULTS: Of the 115 patients in whom post-transfusion non-A, non-B hepatitis developed, the initial serum samples of 111 were anti-HCV-negative; after hepatitis developed in these 111 patients, the first-generation EIAs detected anti-HCV in 51 (46 percent), and the second-generation assay detected anti-HCV in an additional 16 (14 percent), for a total of 60 percent. Of 40 controls, 37 were anti-HCV-negative initially, and none seroconverted after hepatitis developed. If the 3 percent rate of non-A, non-B, non-C hepatitis among the controls (37 of 1235) was applied to the 1247 transfusion recipients, only 74 of the 111 cases of hepatitis were attributable to the transfusion. Thus, 91 percent (67 of 74) of the cases of post-transfusion hepatitis were caused by HCV. Of the 99 donors, 60 were HCV-positive (9 on second-generation tests only) and 39 were not. CONCLUSIONS: Nearly all cases of non-A, non-B post-transfusion hepatitis are caused by HCV. Screening with a second-generation assay improves the rate of detection of HCV infection in patients with post-transfusion hepatitis and in blood donors. The use of this test showed a 3.6 percent risk of non-A, non-B, non-C hepatitis, which was not significantly different from the rate in the controls (3.0 percent).

Blood Donors↗