Biomedical subjects

C Tong

Publications and source records attributed to C Tong.

At least 55 records · Page 3Linked to original sources

PubMed1995

Postoperative analgesia from intrathecal neostigmine in sheep.

Spinal neostigmine produces analgesia in chronically prepared rats, but not in sheep. However, since pain itself activates bulbospinal inhibitory pathways, neostigmine may be more effective in the postoperative period. We examined in sheep the antinociceptive effect of intrathecal neostigmine in the acute postoperative period and determined the muscarinic receptor subtype activated by neostigmine. A cervical intrathecal catheter was inserted via a laminotomy in 14 sheep that then received, in random order 1 mg of spinal neostigmine or saline on postoperative Day 1 and the other injection on postoperative Day 2. Three additional sheep received, on separate days, intrathecal neostigmine alone or with the muscarinic receptor subtype-specific antagonists pirenzepine (M1) 2 mg or AFDX-116 (M2) 2 mg. Antinociception was tested using a mechanical stimulus after each injection. Baseline withdrawal threshold did not change postoperatively. Intrathecal neostigmine, but not saline caused antinociception on both of the first two postoperative days. In contrast, intrathecal neostigmine caused no antinociception in another similar study performed at least 5 days after surgery. Pirenzepine, but not AFDX-116, abolished antinociception from neostigmine, suggesting an action on M1 subtype muscarinic receptors. Intrathecal neostigmine is antinociceptive in sheep during the acute postoperative period, and these data suggest that spinal cholinergic tone, and hence intrathecal neostigmine's analgesic effect, may be enhanced during the acute postoperative period.

Analgesia, Epidural↗

PubMed1995

Cardiorespiratory and spinal cord blood flow effects of intrathecal neostigmine methylsulfate, clonidine, and their combination in sheep.

BACKGROUND: Intrathecal neostigmine may produce analgesia by itself and may enhance analgesia from spinal clonidine. Before clinical trials, the spinal cord blood flow effects of these drugs alone and in combination should be examined in animals. METHODS: Conscious, nonpregnant ewes with indwelling vascular and thoracic spinal catheters received intrathecal injection of 0.2 or 2 mg neostigmine, 0.2 mg clonidine, or 2 mg neostigmine plus 0.2 mg clonidine. Mean systemic and pulmonary arterial and central venous pressures, heart rate, and cardiac output were monitored, arterial blood was sampled for blood gas tensions and pH, and spinal cord blood flow was determined by colored microsphere injection before and at 15, 60, and 240 min after spinal study drug injection. RESULTS: Neostigmine alone did not affect cardiorespiratory variables or spinal cord blood flow. Intrathecal clonidine alone decreased systemic arterial and central venous pressures, whereas these effects were not observed with addition of neostigmine. Clonidine or neostigmine alone or the combination of clonidine and neostigmine did not affect spinal cord blood flow. CONCLUSIONS: Intrathecal neostigmine alone or in combination with clonidine does not reduce spinal cord blood flow, an important preclinical toxicity issue. These results provide additional support for initial clinical trials of intrathecal neostigmine for analgesia.

Animals↗

PubMed1995

Computer-controlled epidural infusion to targeted cerebrospinal fluid concentrations in humans. Clonidine.

BACKGROUND: Pharmacokinetically designed infusions have been demonstrated to achieve rapidly and maintain desired concentrations of drug in plasma after intravenous administration. In this study we tested whether a similar approach, targeting concentrations in cerebrospinal fluid (CSF), could be used with epidural administration of the alpha 2-adrenergic analgesic clonidine. METHODS: After institutional review board approval and informed consent had been obtained, seven healthy volunteers received a clonidine infusion through a lower lumbar epidural catheter. Infusion of clonidine (10 micrograms/ml) was controlled by the STANPUMP program for sequential 75-min periods to targeted CSF clonidine concentrations of 25, 50, 75, and 150 ng/ml. Before reprogramming to the next higher targeted concentration, mean arterial blood pressure and heart rate were measured; blood was obtained for clonidine and catecholamine assays; and visual analog score for sedation and pain to immersion of foot and hand in ice water were obtained. CSF was collected during infusion with an indwelling lumbar intrathecal catheter and was analyzed for clonidine, catecholamines, and acetylcholine. RESULTS: CSF clonidine concentrations rapidly increased and were maintained at steady values with the stepped infusion, although observed concentrations were consistently greater than targeted. The relation between CSF clonidine concentration and analgesia in the foot was similar to that previously observed after epidural bolus administration. Clonidine also was associated with concentration-dependent sedation; decreased mean arterial blood pressure, heart rate, and CSF norepinephrine concentration; and increased CSF acetylcholine concentration. CONCLUSIONS: This study suggests that pharmacokinetically designed infusions of drugs in the epidural space in humans can maintain steady concentrations of drug in CSF. In addition to providing a useful tool for investigation of mechanisms of action and drug interactions, this technique may improve analgesia and diminish side effects from epidurally administered analgesics.

Adult↗

PubMed1994

NMDA causes release of nitric oxide from rat spinal cord in vitro.

Anatomic studies have localized nitric oxide synthase (NOS) activity in the rat spinal cord dorsal horn and intermediolateral cell column. Behavioral and electrophysiologic studies suggest that N-methyl-D-aspartate (NMDA) stimulates nitric oxide synthesis in the dorsal horn. This report describes a novel bioassay to determine directly in vitro whether NMDA causes release of nitric oxide from rat spinal cord. Modified Krebs-Henseleit solution at 26 degrees C was perfused over spinal cord slices from adult male rats, then dropped onto a ring of endothelium-denuded rat aorta. Following preconstriction with phenylephrine, NMDA (10(-10) to 10(-3) M) alone or with other drugs was added to the perfusion solution and vascular tension measured. NMDA-containing solutions applied directly on the preconstricted vessels without exposure to spinal cord tissue had no effect on vessel tone. In contrast, NMDA via the spinal cord perfusion caused concentration-dependent vascular relaxation, which was blocked by MK-801, hemoglobin, methylene blue, and several arginine analogues which inhibit NOS. [14C]citrulline assay suggested NOS in rat spinal cord was non-endothelial in nature. NMDA perfusion of spinal cord slices in vitro causes vascular relaxation in this bioassay due to actions on NMDA receptors and which is consistent with release of nitric oxide. These results support previous anatomical, behavioral, and electrophysiologic studies in rat spinal cord and describe a novel, sensitive, and simple bioassay for nitric oxide release from neural tissue in vitro.

Amino Acid Oxidoreductases↗

PubMed1994

Dosimetry of intravenously administered oxygen-15 labelled water in man: a model based on experimental human data from 21 subjects.

Models based on uniform distribution of tracer in total body water underestimate the absorbed dose from H2(15)O because of the short half-life (2.04 min) of 15O, which leads to non-uniform distribution of absorbed dose and also complicates the direct measurement of organ retention curves. However, organ absorbed doses can be predicted by the present kinetic model based on the convolution technique. The measured time course of arterial H2(15)O concentration following intravenous administration represents the input function to organs. The impulse response of a given organ is its transit time function determined by blood flow and the partition of water between tissue and blood. Values of these two parameters were taken from the literature. Integrals of the arterial input function and organ transit time functions were used to derive integrals of organ retention functions (organ residence times). The latter were used with absorbed dose calculation software (MIRDOSE-2) to obtain estimates for 24 organs. From the mean values of organ absorbed doses, the effective dose equivalent (EDE) and effective dose (ED) were calculated. From measurements on 21 subjects, the average value for both EDE and ED was calculated to be 1.2 microSv.MBq-1 compared with a value of about 0.5 microSv.MBq-1 predicted by uniform water distribution models. Based on the human data, a method of approximating H2(15)O absorbed dose values from body surface area is described.

Adult↗

PubMed1994

Spinal cholinergic alpha-2 adrenergic interactions in analgesia and hemodynamic control: role of muscarinic receptor subtypes and nitric oxide.

Intrathecal injection of neostigmine enhances antinociception from clonidine while it counteracts clonidine-induced hypotension. This study further examined the pharmacology of neostigmine-clonidine interactions in the spinal cord and focused on the roles of muscarinic receptor subtypes and local nitric oxide synthesis. Spinal neostigmine counteracted clonidine-induced decreases in blood pressure and heart rate in conscious sheep and this effect was blocked by spinal injection of the M2 muscarinic antagonist, AFDX-116, but not by the M1 muscarinic antagonist, pirenzepine. Carbamylcholine injected spinally alone increased blood pressure and heart rate and these effects and neostigmine's hemodynamic interaction with clonidine were blocked by spinal injection of the nitric oxide synthase inhibitor, N-methyl-L-arginine. The authors also investigated antinociceptive interactions by using a mechanical pressure stimulus on the forelimb of conscious sheep. Spinal clonidine produced dose-dependent antinociception, which was enhanced by neostigmine and antagonized by N-methyl-L-arginine. NADPH diaphorase staining of sheep spinal cord revealed dense localization to the superficial dorsal horn and the intermediolateral cell column. These results suggest that counteraction of spinal clonidine-induced hypotension by neostigmine is due to stimulation of spinal M2 muscarinic receptors and synthesis of nitric oxide. Nitric oxide synthesis is also necessary for clonidine-induced antinociception in sheep.

Analgesia↗

PubMed1993

Neostigmine counteracts spinal clonidine-induced hypotension in sheep.

BACKGROUND: Intraspinal clonidine injection produces analgesia free of respiratory depression, but also decreases blood pressure and causes sedation. Spinal neostigmine injection alone increases blood pressure in animals and enhances clonidine-induced analgesia. METHODS: To test whether neostigmine would alter clonidine-induced hypotension, nine chronically prepared sheep received intrathecal injections of saline or neostigmine (150, 300, 1,000 micrograms) followed in 15 min by 200 micrograms clonidine. RESULTS: Clonidine plus saline decreased mean arterial pressure by 12 +/- 3% associated with small, statistically nonsignificant decreases in heart rate, cardiac output, and systemic vascular resistance. Prior injection of neostigmine diminished hypotension 60 min after clonidine injection in a dose-dependent manner. To further define the time course and pharmacology of this interaction, seven other sheep received intrathecal saline, neostigmine (1,000 micrograms), or neostigmine plus methylatropine (1,000 micrograms) 75 min prior to 200 micrograms clonidine. With this longer interval between injections, neostigmine abolished clonidine-induced hypotension, and this protective effect was inhibited by methylatropine. To test whether rostral spread of neostigmine in cerebrospinal fluid would alter its hemodynamic effects, we injected intrathecal neostigmine into the upper cervical site. Intrathecal neostigmine increased mean arterial pressure and heart rate at this site to a degree similar to that in the thoracic area, with no effect on behavioral or arterial blood gas tensions. CONCLUSIONS: These data are consistent with neostigmine's counteraction of clonidine-induced hypotension by a spinal muscarinic mechanism and support investigation of spinal alpha 2-adrenergic-cholinergic combinations for pain therapy.

Animals↗

PubMed1993

A cholinergic interaction in alpha 2 adrenoceptor-mediated antinociception in sheep.

Intraspinal administration of alpha 2 adrenergic agonists produces analgesia, but clinical application of these agents is limited by dose-dependent sedation and hypotension. Recently, neostigmine has been demonstrated to counteract hypotension in sheep and enhance antinociception to tail flick in rats from spinally administered alpha 2 adrenergic agonists. We investigated this spinal interaction further in chronically prepared, conscious sheep, testing antinociception with a mechanical pressure stimulus on the forelimb. Clonidine produced dose-dependent antinociception which was antagonized by idazoxan and enhanced by neostigmine, although it was unaltered by methylatropine. Clonidine increased acetylcholine in cerebrospinal fluid, an effect potentiated by physostigmine and blocked by idazoxan. The highly lipid-soluble alpha 2 adrenergic agonists dexmedetomidine and clonidine produced antinociception, whereas the poorly lipid-soluble ST-91 (2,[2,6-diethylphenylamino]-2-imidazoline) produced antinociception only at much larger doses and did not affect cerebrospinal fluid levels of acetylcholine. In human volunteers, epidurally administered clonidine increased cerebrospinal fluid acetylcholine levels at the time of peak analgesia. These results support the existence of an interaction between alpha 2 adrenergic and cholinergic mechanisms of analgesia at the spinal level and underscore the importance of lipid solubility in the actions of spinally administered drugs in sheep.

Acetylcholine↗

PubMed1992

The vascular mechanism of ephedrine's beneficial effect on uterine perfusion during pregnancy.

Sensitivity to the vasoconstricting actions of adrenergic agents is altered during pregnancy and is drug-, regional vascular bed-, and endothelium-dependent. To examine whether the uterine perfusion-sparing property of ephedrine is due to local actions, we examined the effects in vitro of ephedrine and the alpha-adrenergic agonist metaraminol (10(-10)-10(-3) M) in uterine and femoral vessels, with and without functional endothelium, from nonpregnant and pregnant ewes. Both agents produced dose-dependent contractions in all vascular rings. In all cases metaraminol was more potent (by analysis of the concentration producing a 50% maximal response [EC50]) and efficacious (by maximal effect). Pregnancy increased constriction from both agents in femoral arterial rings, whereas pregnancy decreased constriction from both agents in uterine arterial rings. However, the ratio of maximal effect at femoral versus uterine rings during pregnancy was greater for ephedrine (5.2 +/- 0.6) than metaraminol (1.9 +/- 0.3). This difference was further accentuated by endothelium removal. Constriction to both agents was abolished by phentolamine (10(-5) M). These data suggest that both ephedrine and metaraminol constrict uterine and systemic vessels by actions on alpha adrenoceptors, and that ephedrine may spare uterine perfusion during pregnancy due to more selective constriction of systemic vessels than that caused by metaraminol.

Animals↗

PubMed1992

Intrathecal clonidine and the response to hemorrhage.

Intraspinally administered alpha 2-adrenergic agonists are being examined for postoperative analgesia, yet their effects on the hemodynamic response to acute hemorrhage have not been examined. In this study chronically prepared conscious sheep received thoracic intrathecal saline or clonidine 300 micrograms followed in 15 min by rapid removal of 1,000 ml blood. In saline-treated ewes blood pressure was maintained and heart rate steadily increased during hemorrhage of up to 700 ml blood, with further blood removal resulting in rapid decreases in both variables. In contrast, heart rate never increased and blood pressure was maintained only up to 400 ml blood loss in animals receiving intrathecal clonidine. Compared to saline controls, clonidine did not alter blood pressure or heart rate at the end of hemorrhage or during blood pressure restitution during the next hour. Clonidine inhibited the increase in plasma epinephrine at the end of hemorrhage without altering plasma norepinephrine, vasopressin, renin, or atrial natriuretic factor. Intrathecal idazoxan, a specific alpha 2-adrenergic antagonist, reversed clonidine's effect on blood pressure during hemorrhage. Intravenous DG-5128, a poorly lipid-soluble alpha 2-adrenergic antagonist, also reversed clonidine's effect and additionally completely blocked any reduction in blood pressure and heart rate during hemorrhage. These data suggest that intrathecal clonidine interferes with maintenance of blood pressure during hemorrhage, likely because of a spinal sympatholytic effect, but does not affect the ultimate decrease in blood pressure after rapid removal of 1,000 ml blood. This difference in effect during the two phases of hemorrhage can be explained by the relative importance of the sympathetic nervous system in each.

Adrenergic alpha-Antagonists↗

PubMed1992

Vasopressin and fetal cerebrovascular regulation.

Vasopressin (AVP) may increase cerebral blood flow (CBF) during hypoxemia by selective dilatation of cerebral vessels via endothelium-derived relaxing factor (EDRF) release. To test whether this action is relevant in the fetus, we produced isocapnic hypoxemia in halothane-anesthetized pregnant ewes. Fetal infusion of a V1 AVP antagonist reduced by 55% the increase in CBF during fetal hypoxemia. To test the role of this response during development, we examined the response to AVP in intact and endothelium-denuded femoral and basilar arterial rings in vitro from fetal, newborn, and adult sheep. AVP constricted femoral rings in an endothelium-independent manner, with increased potency in newborn and fetal compared with adult rings. AVP relaxed basilar rings in an endothelium-dependent manner, which was unaffected by indomethacin treatment, with increased potency in newborn and adult compared with fetal rings. We conclude that fetal cerebral vascular endothelium is functional and responsive to AVP and that circulating AVP during fetal hypoxemia contributes to increased CBF via this effect.

Animals↗

PubMed1990

Toxicity studies of butylated hydroxyanisole and butylated hydroxytoluene. I. Genetic and cellular effects.

The cellular effects of the antioxidants butylated hydroxyanisole and butylated hydroxytoluene were studied in a battery of in vitro tests. No evidence of genotoxicity was obtained for either compound in the hepatocyte primary culture/DNA repair test, the Salmonella/microsome mutagenesis test, the adult rat liver epithelial cell/hypoxanthine guanine phosphoribosyl transferase test, or for butylated hydroxyanisole in the Chinese hamster ovary cell/sister chromatid exchange test. Both compounds inhibited intercellular molecular exchange between cultured liver cells, an effect that has been observed for many agents with neoplasm-promoting activity.

Animals↗

PubMed1989

Hyperglycaemia after burn injury.

The effect of burn injury on blood sugar levels, serum insulin levels and glucose tolerance was studied in male rats. In the burned group (following 50 per cent surface burn injury), the blood sugar level was significantly increased after burn injury in comparison with control uninjured rats. Hyperglycaemia was blocked by injection of phentolamine (10 mg/kg) for 24 h or propranolol (50 micrograms/kg) 30 min before burn or if the animals were adrenalectomized 4 days before injury. Serum insulin levels were significantly decreased in the scalded rats and their glucose tolerance was impaired. Early hyperglycaemia probably arises as a result of adrenal medullary hyperactivity. The initial rise in blood glucose probably arises from glycogen breakdown, followed later by increased hepatic production of glucose. The 50 per cent body surface scald injury is followed, acutely, by a period of glucose intolerance. In part, this intolerance may be due to decreased serum levels of insulin. The inadequate response of insulin secretion in response to glucose loading may be due to inhibition of insulin secretion by pancreatic beta cells caused by elevated catecholamine levels, possibly in combination with the action of antagonists such as glucagon, which may be secreted in excess as a result of stimulation by catecholamines.

Adrenalectomy↗

PubMed1988

Rat liver foci and in vitro assays to detect initiating and promoting effects of chlorinated ethanes and ethylenes.

Nine chlorinated aliphatics (CAs) were examined in a rat liver foci assay for tumor initiating and promoting activities. In this model, young adult male Osborne Mendel rats were first subjected to a partial hepatectomy, the test chemical was then administered at the maximum tolerated dose in the initiation or promotion phase in conjunction with diethylnitrosamine (DEN; 30 mg/kg b.w.) or phenobarbital (PB; 0.05 percent, w/w, in the diet), and gamma glutamyltranspeptidase (GGT) was used as a putative preneoplastic indicator. When administered in the promotion protocol after initiation with DEN, 1,1-dichloroethane, 1,1,2-trichloroethane (1,1,2-TCE), 1,1,2,2-tetrachloroethane (1,1,2,2-TTCE), tetrachloroethylene (TTCY), and hexachloroethane induced significant increases in GGT+-foci above control levels. 1,1,2,2-TTCE, TTCY, and 1,1,2-TCE also induced significant increases in GGT+-foci when administered in the promotion protocol without DEN initiation. Two variants of GGT+-foci were observed: the classical type associated with PB promotion, and the other, which was more diffuse, less intensely stained, resembling foci undergoing redifferentiation and associated with CAs. A number of CAs were also genotoxic in short-term in vitro tests. Taken together, the studies suggest that CAs may be complete carcinogens in vivo with weak initiating activity and stronger promoting activity.

Animals↗

PubMed1988

Five-year follow-up of Hancock pericardial valves: management of premature failure.

The durability and function of bovine pericardial valves are dependent upon design, preservation, patient factors (age, sex), and site of valve implantation. In 1983, a shelf recall of all Hancock bovine pericardial valves (HPV) was instituted by the manufacturer. This report represents the results of an organized 5-year follow-up in a hospital Prosthetic Valve Registry of 129 HPV implanted in 122 patients (79 males, 43 females) between May 1982 and April 1985 using echo Doppler and careful clinical evaluation. Mean age was 56 +/- 15 years. There were 81 AVR, 33 MVR, 7 DVR, and 1 TVR. Concomitant coronary bypass was performed in 38 patients (31%). Surgery was on a redo basis in 25 patients (20%), urgent in 14 (11%), and for SBE in 8 patients (7%). There were seven hospital deaths (5.7%). Mean follow-up was 44 months (maximum 66 months) for 114 patients (99% complete), representing 417 patient years. There have been 20 late deaths (18%), of which 7 were directly valve related. Linearized frequency of major events (per pt-yr) was: thromboembolism, 1.6%; anticoagulant related hemorrhage, 0.8% (1 late death); prosthetic valve endocarditis 1.3%; primary tissue failure, 5.8%. Patient symptomatology was a more accurate predictor of bioprosthetic failure requiring reoperation than echo Doppler studies, which were completed in 74 of 97 patients examined during scheduled follow-up visits. Twenty-four of the 96 patients (25%) have required re-replacement at a mean interval of 44 months (27-59 months) from initial implantation. This was due to vertical shear starting at the top of the strut anchoring commissural attachments in every case.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Clinical results of pericardial xenograft valves: the Ionescu-Shiley and Hancock valves.

Between 1979 and 1985, 552 Ionescu-Shiley valves were implanted in 511 patients. The Hancock valve was implanted in 122 patients (129 valves) between 1982 and 1983. Sixty percent of procedures were isolated aortic valve replacements. In the Ionescu series, 59% of these were 19 or 21 mm valves while only 15% of the Hancock valves were of this size. For isolated mitral valve replacement, 76% of Ionescu-Shiley valves were 25 to 27 mm, compared to 36% of the Hancock valves. Patient age, sex, prior operations, concomitant surgery (usually coronary bypass), operative mortality and late deaths were similar for both valves. A mean follow-up of 38 months was obtained for each valve population (99% complete) representing a cumulative 1497 patient-years for the Ionescu-Shiley valve and 375.4 patient-years for the Hancock valve. Actuarial survival for the former was 73 +/- 4% at 72 months, and 65 +/- 14% for Hancock valves at 60 months. The frequency of major events during follow-up (thromboembolism, anticoagulant related hemorrhage, bland perivalvular leak and prosthetic valve endocarditis) were similar, but the frequency of primary tissue valve failure was markedly different for the two valves (1.1% per patient-year for Ionescu-Shiley valves and 5.9% for the Hancock valve). The mean interval to replacement of an Ionescu mitral prosthesis was significantly shorter (23.4 months) than for replacement of an aortic prosthesis (42 months) while the mean interval to replacement of an Ionescu aortic and/or a Hancock aortic or mitral were all similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗

PubMed1988

Clinical performance of Bjork-Shiley mechanical heart valves: a perspective on outlet strut fractures in the 60 degrees and 70 degrees convexo-concave disc models.

The convexo-concave disc model of Bjork-Shiley mechanical heart valve is a significant improvement over the spherical disc model and compares favourably to other valves, including bioprostheses, with respect to hemodynamics, thromboembolism, anticoagulant related hemorrhage and prosthetic endocarditis. A small number of the 60 degrees and 70 degrees welded outlet strut Bjork-Shiley convexo-concave valves are at risk of sudden structural failure. The risk is constant or decreasing with time. Elective explanation is not recommended. The integral outlet monostrut 70 degrees Bjork-Shiley convexo-concave valve demonstrates further improvements in design and durability, and is recommended for use in patients who are appropriate candidates for mechanical cardiac prostheses.

Aortic Valve↗

PubMed1986

Randomised controlled trial of computer assisted management of hypertension in primary care.

The hypothesis that general practitioners would obtain better outcomes for patients with hypertension using a computer than doctors not using a computer was tested. Sixty family physicians were randomised to two treatment strategies. "Test" physicians completed a data collection form after each visit from a patient with hypertension and mailed the forms to the test centre for processing. Computer feedback on management was mailed to the doctors. This encouraged doctors to apply the "stepped care" protocol, supplied charts of diastolic blood pressure v time, and ranked patients' diastolic blood pressures by percentile. Letters were mailed to patients to remind them of appointments. "Control" doctors filled out the same data collection forms as test physicians, but neither doctors nor patients received computer feedback. Physicians who used the computer saw more patients per practice than control doctors (test 50 patients, control 40). For all patients the length of follow up was significantly longer in test practices (test 199 days, control 167), and a smaller percentage dropped out of active treatment in test practices (test 37.5%, control 42.1%). For patients with "moderate" hypertension of a baseline diastolic pressure of greater than 104 mm Hg the mean score of the last recorded pressure was below the goal of 90 mm Hg in test practices (88.5 mm Hg), but it failed to reach this goal in control practices (93.3 mm Hg). A greater average reduction of diastolic pressure was achieved in test practices (test 21.7 mm Hg, control 16.7 mm Hg). Though patients with "moderate" hypertension were better controlled in test practices than in control practices, the patients in test practices visited their doctors less often (test 13.3 visits per patient-year, control 17.4 visits). Among patients with newly detected hypertension test practices achieved a greater reduction in diastolic pressure than control practices (test 15.1 mm Hg v control 11.3 mm Hg) and more sustained control of hypertension (test 323 days per patient-year with a diastolic pressure of 90 mm Hg or less v control 259 days).

Blood Pressure↗