Improving hand hygiene adherence in an endoscopy unit.

BACKGROUND AND STUDY AIMS: Although hand hygiene is the most important measure in preventing infection transmission in healthcare settings, adherence to recommendations among healthcare workers is low. We implemented and assessed the impact of a World Health Organization-recommended educational intervention to improve hand hygiene adherence at the endoscopy unit of a Brazilian tertiary hospital. PATIENTS AND METHODS: Hand hygiene adherence and techniques used by healthcare workers of the endoscopy unit in the course of their duties were observed unobtrusively by four nurses from the infection control unit. Data were collected at every opportunity for hand hygiene. Evaluations were carried out before and 1 and 10 months after an educational intervention. The intervention consisted of task-orientated training sessions, with live demonstrations of the multitude of opportunities for hand hygiene and the appropriate techniques. In addition to assessing hand hygiene practices, we also evaluated staff knowledge through standardized questionnaires administered before and after the education intervention. Adherence was defined as hand hygiene/disinfection at an opportunity for hand hygiene. RESULTS: Adherence improved from 21.4 % before the intervention to 63.3 % 1 month and 73.5 % 10 months after the educational intervention. Correct answers to the questionnaire were 82.1 % on pre-intervention test and 85.7 % on post-intervention test. CONCLUSION: Hand hygiene rates were low before the education intervention and improved significantly after it. Against expectations, adherence to hand hygiene practices had increased further at 10 months after the intervention, reinforcing the intervention's positive impact.

Effects of standing on the induction of paroxysmal supraventricular tachycardia.

To evaluate the effects of standing on induction of paroxysmal supraventricular tachycardia, electrophysiologic studies were performed in both the supine and standing positions in 22 patients with atrioventricular (AV) reciprocating tachycardia and in 11 with AV node reentrant tachycardia. AV reciprocating tachycardia was induced in 9 of the 22 patients with AV reciprocating tachycardia when they were in the supine position and in 17 when standing. The effective refractory period of the AV node markedly shortened, from 275 +/- 72 to 203 +/- 30 ms (n = 16, p less than 0.005) after standing. The effective refractory period of the accessory pathway shortened slightly, from 293 +/- 75 to 278 +/- 77 ms (n = 8, p less than 0.005), after standing. AV node reentrant tachycardia was induced in 3 of the 11 patients with AV node reentrant tachycardia when they were in the supine position and in 6 when standing. The effective refractory periods of the slow pathway and fast pathway shortened markedly, from 293 +/- 72 to 216 +/- 40 ms (n = 6, p less than 0.025) and from 416 +/- 85 to 277 +/- 50 ms (n = 10, p less than 0.005), respectively, after standing. Plasma norepinephrine levels increased during standing both in patients with AV reciprocating and in those with AV node reentrant tachycardia (n = 11, p less than 0.005, n = 8, p less than 0.005, respectively). In conclusion, standing, which is associated with increased sympathetic tone, changed the electrophysiologic properties of the reentrant circuits, facilitating induction of AV reciprocating tachycardia and AV node reentrant tachycardia.

Prolonged and fractionated right atrial electrograms during sinus rhythm in patients with paroxysmal atrial fibrillation and sick sinus node syndrome.

Intraatrial catheter mapping of the right atrium was performed during sinus rhythm in 92 patients: Group I = 43 control patients without paroxysmal atrial fibrillation or sick sinus node syndrome; Group II = 31 patients with paroxysmal atrial fibrillation but without sick sinus node syndrome; and Group III = 18 patients with both paroxysmal atrial fibrillation and sick sinus node syndrome. Atrial electrograms were recorded at 12 sites in the right atrium. The duration and number of fragmented deflections of the atrial electrograms were quantitatively measured. The mean duration and number of fragmented deflections of the 516 atrial electrograms in Group I were 74 +/- 11 ms and 3.9 +/- 1.3, respectively. The criteria for an abnormal atrial electrogram were defined as a duration of greater than or equal to 100 ms or eight or more fragmented deflections, or both. Abnormal atrial electrograms were observed in 10 patients (23.3%) in Group I, 21 patients (67.7%) in Group II and 15 patients (83.3%) in Group III (Group II versus Group I, p less than 0.001; Group III versus Group I, p less than 0.001). The mean number of abnormal electrograms per patient with an abnormal electrogram was 1.3 +/- 0.7 in Group I, 2.5 +/- 1.9 in Group II and 3.5 +/- 2.5 in Group III (Group I versus Group II, p less than 0.01; Group II versus Group III, p less than 0.05). A prolonged and fractionated atrial electrogram characteristic of paroxysmal atrial fibrillation can be closely related to the vulnerability of the atrial muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of blood pressure changes on development and regression of electrocardiographic left ventricular hypertrophy: a 26 year longitudinal study.

At the Radiation Effects Research Foundation, medical examinations have been conducted biennially since 1958 on a fixed population of approximately 20,000 individuals. Blood pressure measurements and electrocardiographic (ECG) recordings are available for 6,569 individuals who were monitored for at least 11 of the 13 2 year intervals between 1958 and 1984. Data from 601 individuals who had satisfied the Foundation's ECG diagnostic criteria of left ventricular hypertrophy ("Kagan-Yano code") on at least one occasion were reviewed. Both the development and the regression of ECG left ventricular hypertrophy were ascertained in 61 subjects (17 men and 44 women). During the course of development of ECG left ventricular hypertrophy, hypertension (including borderline cases) was noted in 83.3% of the subjects. The most common pattern of ECG left ventricular hypertrophy development was high voltage, followed by ST-T changes. In about half of these cases, the condition of hypertrophy regression was associated with lowering of blood pressure, marked by the disappearance of high voltage ECG readings.

Arrhythmogenic properties of the ventricular myocardium in cardiomyopathic Syrian hamster, BIO 14.6 strain.

STUDY OBJECTIVE: Incidence of spontaneous cardiac arrhythmias and inducibility of ventricular arrhythmias in the cardiomyopathic hamster, BIO 14.6 strain, were examined. DESIGN: A 3 min electrocardiogram (ECG) was recorded weekly to 50 weeks of age. Programmed ventricular stimulation was then performed with single and double ventricular premature stimuli during both sinus rhythm and ventricular pacing, and with brief bursts of ventricular pacing to induce ventricular arrhythmias. EXPERIMENTAL MATERIAL: 19 male cardiomyopathic and 10 age matched normal hamsters from 16 to 50 weeks were used for recording the 3 min ECG; 11 cardiomyopathic and 10 normal hamsters aged 50 to 55 weeks were used for the induction of ventricular arrhythmias. MEASUREMENTS AND MAIN RESULTS: Spontaneous and sporadic ventricular premature contractions were documented in 8.3% of 218 ECGs from the cardiomyopathic hamsters between the ages of 30 and 46 weeks, whereas no ventricular arrhythmia was recorded in normal hamsters throughout the entire follow up period. Non-sustained ventricular tachycardia (NSVT) was induced in 7/11 cardiomyopathic hamsters by single ventricular premature stimulus. Either NSVT or ventricular fibrillation was induced in all cardiomyopathic hamsters with a significantly prolonged intraventricular conduction delay and refractory period. In contrast, neither NSVT nor ventricular fibrillation was induced in normal hamsters. CONCLUSION: This study provides the first evidence of the high arrhythmogenicity of the ventricles in cardiomyopathic hamsters.

Enzyme immunoassay of angiotensin I.

A very sensitive and specific enzyme immunoassay has been developed for angiotensin I. Angiotensin I was coupled to beta-D-galactosidase by a novel cross-linking reagent, N-(meta-maleimidobenzoyloxy)succinimide. No decrease in the enzyme activity was observed during the coupling procedure. In the angiotensin I-beta-D-galactosidase conjugate, 0.39 mol immunoreactive angiotensin I/mol enzyme were present. A competitive assay with the enzyme-labeled angiotensin I was performed. Antibody-bound and free labeled antigen were separated from each other by the second antibody method, and the enzyme activity of the former was estimated. Using this assay, angiotensin I could be detected in the range of 1.2--50 pg. The sensitivity was 4.5-fold higher than that of the usual RIA. This assay distinguished clearly angiotensin I from angiotensin II, angiotensin III, and (Sar1, Ile8)-angiotensin II. The present method was applied to measure PRA in dogs; the results correlated fairly well with those obtained by the RIA (r = 0.94).

Dynamic responses of active and inactive renin in patients with essential and renovascular hypertension.

We studied the dynamic responses of inactive renin and the form of renin released by the kidney in the hypertensive patients. Significant increase of active renin concentration (p less than 0.01) and decrease of the percentage of inactive renin concentration (p less than 0.01) after sodium depletion was observed in 15 essential hypertensive subjects with normal plasma renin activity. In eight of 15 patients, significant increase of inactive renin concentration (p less than 0.01) was observed after sodium depletion. In the remaining seven patients, no significant change of inactive renin concentration was demonstrated. A small increase of active and inactive renin concentration was observed following sodium depletion in six essential hypertensive subjects with low plasma renin activity (PRA). In the unilateral renal hypertension after upright tilting, active renin concentration in the renal vein of the affected kidney was significantly (p less than 0.02) higher than that in the renal vein of the non-affected kidney and the inferior vena cava. Inactive renin concentration in the renal vein of the affected kidney was significantly (p less than 0.02) lower than that in the renal vein of the nonaffected kidney and the inferior vena cava. In four of five cases, the inactive renin concentration in the femoral artery was less than that in the inferior vena cava. Therefore, we might conclude that only active renin was released from the affected kidney, and active renin became inactive by unknown mechanisms; the ischemic kidney might also activate inactive renin.

Prorenin is sorted into the regulated secretory pathway independent of its processing to renin in mouse pituitary AtT-20 cells.

A native human prorenin and a mutant of its processing site (Arg-43 to Gln) were expressed in mouse pituitary AtT-20 cells which process prorenin to renin and have both regulated and constitutive secretory pathways. The native prorenin was processed to renin and secreted in a regulated manner. Although the mutant precursor was not processed, it was also secreted in a regulated manner. These results suggest that prorenin is sorted into the regulated pathway, stored in secretory granules and released by stimulus whether it is processed to renin or not.

Electrophysiologic properties of atrial muscle in paroxysmal atrial fibrillation.

The electrophysiologic properties of atrial muscle were studied by programmed atrial stimulation in 42 patients with paroxysmal atrial fibrillation (PAF) and in 53 control patients without PAF. Single premature atrial stimulation was given at the right atrial appendage following 8 basic stimuli with a basic cycle length of 500 ms. Repetitive atrial firing (RAF) was defined as the occurrence of 2 or more successive premature atrial activations following single premature atrial stimulation. Fragmented atrial activity (FAA) was defined as an increase by more than 75% of the duration of the atrial electrogram in response to a single premature stimulation. Interatrial conduction delay was defined as an increase of the conduction time by more than 50 ms in response to a single premature stimulation. RAF was induced in 26 of 42 patients (61.9%) with PAF and in 14 of 53 control patients (26.4%). FAA and interatrial conduction delay were elicited in 69.0 and 80.9% of patients with PAF and in 34.0 and 56.6% of control patients, respectively. In 16 patients with PAF in whom RAF was not induced, FAA developed in 11 patients (68.8%). In 88.1% of 42 patients with PAF and in 41.5% of 53 controls, RAF or FAA, or both, were elicited by atrial premature stimulation. It is concluded that the incidence of RAF and FAA were significantly higher in patients with PAF than in the control group, and the induction of RAF or FAA, or both, was closely related to the vulnerability of the atrial muscle to atrial fibrillation.

Role of cathepsin B as prorenin processing enzyme in human kidney.

Renin is synthesized from an inactive precursor, prorenin, through cleavage at a pair of basic amino acids catalyzed by prorenin processing enzyme (PPE). A lysosomal protease, cathepsin B, has been suggested to be a strong candidate for PPE. However, there still remains a possibility that other protease(s) can also catalyze prorenin processing. We studied the subcellular distribution of PPE in human renal cortex using pure recombinant prorenin as a PPE assay substrate. PPE and renin activities, and cathepsin B activity and protein were colocalized in the lysosomal fraction. The PPE activity was completely inhibited by a cathepsin B specific inhibitor, CA074. Taken together with the immunohistochemical data showing that cathepsin B and PPE are colocalized in dense secretory granules of juxtaglomerular cells of kidney, we conclude that cathepsin B is the authentic PPE in human kidney.

Depressor effect of intraventricular administration of calcium on spontaneously hypertensive rats.

The role of central Ca2+ in the regulation of blood pressure (BP) was investigated in conscious spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY). Ten microliters of a high Ca2+ solution (Ca2+: 32.6 mM) administered intracerebroventricularly (i.c.v.) decreased the mean arterial pressure (MAP) for more than 20 min in SHR (n = 7, P < 0.005), while no change of MAP was observed in the WKY (n = 6). This depressor response to Ca2+ i.c.v. was dose-dependent at Ca2+ concentrations between 16.3 and 65.2 mM. We also investigated the effect of high Ca2+ i.c.v. in SHR after pretreatment with Ca2+ channel blockers, diltiazem (60 micrograms/10 microliters) or nisoldipine (4, 8, 16 and 32 micrograms/10 microliters), administered i.c.v., the autonomic ganglion blocker, hexamethonium (50 mg/kg), administered i.v. and alpha-methyl-p-tyrosine (100 and 400 micrograms/10 microliters) delivered i.c.v. Pretreatment with i.c.v. diltiazem (n = 8) or nisoldipine (n = 5 for 8 micrograms, n = 6 for 4, 16, 32 micrograms) abolished and/or blunted the decrease of MAP due to high Ca2+. Hexamethonium administered i.v. (n = 6) also canceled the depressor action of i.c.v. Ca2+. Pretreatment with 100 micrograms of i.c.v. alpha-methyl-p-tyrosine could not prevent the depressor action of i.c.v. Ca2+; however, 400 micrograms of alpha-methyl-p-tyrosine administered i.c.v. abolished the effect of i.c.v. Ca2+. Furthermore Ca2+ channel blockers administered i.c.v. in themselves increased MAP in SHR (P < 0.05). These results suggest that central Ca2+ is involved in the central regulation of BP in SHR. This effect may be mediated through changes in sympathetic activity.

Contribution of the central interaction between calcium and sodium to hemodynamic regulation in spontaneously hypertensive rats.

The contribution of the central interaction between calcium and sodium to hemodynamic regulation was assessed in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats. The effect of a high calcium solution (Ca2+, 130 mg/dl, 10 microliters) infused into the cerebral ventricle (i.c.v.) on hemodynamic responses induced by a high sodium solution (Na+, 1,000 mEq/1, 10 microliters) i.c.v. and the mechanism by which high Ca2+ affects the hemodynamic responses induced by high Na+ i.c.v. were studied. High Na+ i.c.v. induced a pressor response with tachycardia in the SHRs, but induced a pressor response with reflex bradycardia in the WKYs. Prior treatment with high Ca2+ i.c.v. attenuated the pressor response induced by high Na+ i.c.v. (+55.6 +/- 4.4 to +33.1 +/- 3.2 mmHg, P < 0.01) and restored reflex bradycardia (+86.4 +/- 7.7 to -26.7 +/- 7.6 bpm, P < 0.01) in SHRs. Whereas prior treatment with high Ca2+ i.c.v. attenuated the pressor response (+35.7 +/- 2.0 to +22.2 +/- 4.0 mmHg, P < 0.05), it did not alter the degree of reflex bradycardia (-81.7 +/- 7.1 to -69.2 +/- 120 bpm, n.s.) in WKYs. Ganglionic blockade attenuated the pressor response (+56.9 +/- 3.5 to +42.9 +/- 2.3 mmHg, P < 0.05) and restored reflex bradycardia (+82.1 +/- 10.3 to -65.9 +/- 11.0 bpm, P < 0.01) in SHRs, whereas, inhibition of arginine vasopressin attenuated the pressor response without modification of the tachycardic response.(ABSTRACT TRUNCATED AT 250 WORDS)

Specific 125I-endothelin-1 binding sites in the atrioventricular node of the porcine heart.

The quantitative receptor autoradiographic method we used revealed that specific 125I-endothelin-1 binding sites are highly concentrated in the atrioventricular node of the porcine heart. 125I-Endothelin-1 binding to the atrioventricular node, interatrial and interventricular septa was displaced by unlabeled endothelin-1 with Kd values of 53 pM, 2.03 nM and 3.48 nM, respectively. Knowledge of the existence of specific 125I-endothelin-1 binding sites in the porcine heart helps with understanding the physiology of endothelin, a possible endogenous Ca2+ channel agonist.

Electrophysiological abnormalities of the atrial muscle in patients with sinus node dysfunction without tachyarrhythmias.

The duration and the number of fragmented deflections of the right atrial electrograms were assessed and quantitatively measured in 74 patients who underwent endocardial catheter mapping during sinus rhythm. The bipolar electrograms were recorded at 12 sites in the right atrium. An abnormal atrial electrogram was defined as a duration of 100 ms or longer, and/or 8 or more fragmented deflections, according to our previous criteria. The patients were divided into two groups. The control group consisted of 41 age-matched patients with normal sinus node function and without paroxysmal atrial fibrillation. The study group comprised 33 patients with sinus node dysfunction but without tachyarrhythmias. Abnormal atrial electrograms were observed in 8 (19.5%) control patients, and in 16 (48.5%) sinus node dysfunction patients; p < 0.02. The total number of abnormal electrograms was 14 (2.89%) of 483 atrial electrograms in controls, and 36 (9.38%) of 384 in the study group; p < 0.0002. The mean duration (75.6 +/- 17) and the mean number of fragmented deflections (4.1 +/- 2) of the total atrial electrograms in the sinus node dysfunction group was significantly greater than that in controls (70.9 +/- 11 and 3.6 +/- 1, respectively); p < 0.01. The mean number of abnormal electrograms per patient in the study group (1.06 +/- 1.8) was significantly higher than that in the control group (0.3 +/- 0.8); p < 0.05. These data suggest that: (1) there is a significantly greater electrophysiological abnormality of the atrial muscle in patients with sinus node dysfunction but without paroxysmal atrial fibrillation than in age-matched controls, and (2) not only the sinus node but also the atrial muscle is electrophysiologically altered in patients with sinus node dysfunction but without tachyarrhythmias.

Mechanism of the suppression of repetitive atrial firing by isoproterenol--comparison with disopyramide.

To investigate whether isoproterenol (Iso) could suppress the initiation of repetitive atrial firing (RAF), we investigated its effect on RAF in comparison with that of disopyramide (Diso). Extrastimuli at a basic cycle length of 500 ms were delivered from the high right atrium in 49 patients who received an intravenous infusion of Iso (0.01 microgram/kg per min) and in 39 patients given intravenous Diso (2 mg/kg per 10 min). Induction of RAF, the atrial effective refractory period (A-ERP), and the maximum conduction delay (MCD) were measured. Iso abolished the induction of RAF in 13/19 (68%) patients, while Diso did so in 13/22 (59%) patients. Thirty-four of the 41 patients with RAF in the baseline study had an A-ERP < 250 ms and an MCD > 40 ms. Iso significantly decreased the A-ERP from 205 +/- 26 to 194 +/- 23 ms (P < 0.01) and significantly decreased the MCD from 67 +/- 24 to 39 +/- 16 ms (P < 0.0001) in 19 patients with RAF. On the other hand, Diso significantly increased the A-ERP from 203 +/- 31 to 235 +/- 36 ms (P < 0.0001), and significantly diminished the MCD from 68 +/- 31 to 55 +/- 30 ms (P < 0.01) in 22 patients with RAF. In patients with new RAF (n = 7) or re-induced RAF (n = 14) during Iso or after Diso, the MCD was more than 40 ms. Our results suggest that there are two different modes of RAF suppression, i.e. shortening or lengthening of the A-ERP.(ABSTRACT TRUNCATED AT 250 WORDS)

Augmented central pressor action of magnesium in SHR.

This study attempted to determine whether central magnesium (Mg) influences the regulation of blood pressure (BP). An intracerebroventricular (icv) injection of a high Mg2+ solution (190.0 mEq/L, 10 microL), made by adding MgC12 to artificial cerebrospinal fluid, increased the mean BP in both conscious spontaneously hypertensive rats (SHR; n = 17, p < 0.001) and Wistar Kyoto rats (WKY; n = 8, p < 0.005). Spontaneously hypertensive rats showed a greater pressor response than WKY (+11.7 +/- 0.9 mm Hg versus +3.5 +/- 1.1 mm Hg, p < 0.001). This pressor response to Mg2+ given icv was dose-dependent in the range of Mg2+ concentration between 47.5 and 190.0 mEq/L in SHR. A high Mg2+ solution (190.0 mEq/L), made by adding MgSO4 given icv, also increased the mean BP in SHR (n = 7, p < 0.001) and WKY (n = 6, p < 0.01), whereas the high osmolarity solution (340 mOsm/kg H2O) given icv did not change the mean BP in either SHR or WKY. Also administered was a high Mg2+ solution icv after either hexamethonium bromide (Hx; 50 mg/kg intravenously) or arginine vasopressin antagonist (aAVP, (CH2)5Tyr(Me)AVP, 30 micrograms/kg i.v.). The pressor response to the high Mg2+ solution was abolished by arginine vasopressin antagonist both in SHR and WKY, although it was not canceled by Hx. A high Mg2+ solution administered icv caused a 3.5-fold increase in plasma arginine vasopressin concentration in SHR (n = 5, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Reliability of QT intervals as indicators of clinical hypercalcemia.

Reliability of corrected QT intervals (QoTc, QaTc, and QeTc) as indicators of clinical hypercalcemia was assessed in 14 hypercalcemic patients. Hypercalcemia was severe to extreme (serum calcium 14.9 to 22.8 mg/dl) in 11, moderate (13.4 mg/dl) in 1, and mild (12.2 and 11.8 mg/dl) in 2 patients. QT intervals during hypercalcemia were compared with those during normocalcemia either before or after development of hypercalcemia. QeTc interval showed neither significant correlation with serum calcium nor any consistent pattern of change with development of hypercalcemia or normalization of serum calcium. In contrast, QoTc and QaTc intervals shortened with development of hypercalcemia and returned toward normal with normalization of serum calcium in all the patients, and showed significant correlation with serum calcium (QoTc: r = -0.77, p less than 0.001, n = 35; QaTc: r = 0.82, p less than 0.001, n = 35). QaTc was short (less than 0.30 s) in all the ECGs in severe and moderate hypercalcemia and in 2 of the 5 ECGs in mild hypercalcemia. Combination of short QoTc (less than 0.18 s) and short QaTc was found to be highly specific for, and was present in 65% of ECGs, in moderate and severe hypercalcemia. Combination of normal QoTc (greater than 0.18 s) and normal QaTc (greater than 0.30 s) was not observed in moderate or severe hypercalcemia. We conclude that QoTc and QaTc intervals are reliable indicators of clinical hypercalcemia.

Inactivation of Saccharomyces cerevisiae by ultrasonic irradiation.

We have investigated the inactivation of Saccharomyces cerevisiae (yeast cells) by ultrasonic irradiation. The amplitude on the vibration face contacting the sample solution was used as an indication of the ultrasonic power intensity. The effects of the amplitude on the vibration face and the initial cell numbers on the sonolytic inactivation of yeast cells have been investigated using a horn-type sonicator (27.5 kHz). The inactivation of the yeast cells by ultrasonic irradiation shows pseudo first-order behavior. The inactivation rate constant varied from 0.0007 to 0.145 s(-1) when the amplitude on the vibration face was in the range of 1-7 microm(p-p). The change in the inactivation rate constant as a function of the amplitude on the vibration face was similar to that of the OH radical formation rate under the same conditions. The threshold of this sonicator was 3 microm(p-p) with the amplitude on the vibration face. The initial cell numbers (from 10(2) to 10(5) mL(-1)) had an influence on the inactivation of the yeast cells by ultrasonic irradiation. The inactivation rate constants varied from 0.023 to 6.4 x 10(-3) s(-1), and the inactivation by ultrasonic irradiation was fastest at the lowest initial cell numbers. In a squeeze-film-type sonicator (26.6 kHz), 90% inactivation of the yeast cells was achieved by ultrasonic irradiation for 60 min.

Central effect of aprotinin, a serine protease inhibitor, on blood pressure in spontaneously hypertensive and Wistar-Kyoto rats.

We examined the effect of centrally administered aprotinin, a serine protease inhibitor, on blood pressure (BP) in conscious spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Twenty-two gauge needles and polyethylene catheters were implanted into lateral cerebroventricle and femoral artery, respectively, at 48 hours before the experiments. In Group 1 (8 SHR, 6 WKY), rats received a bolus intracerebroventricular injection (i.c.v.) of aprotinin (1,000 KIU/kg/10 microliters). A prompt increase of BP was observed in SHR after aprotinin and this elevation of BP was persisted for over 30 minutes (mean BP: 158.8 +/- 2.9 mmHg at control to 168.7 +/- 3.2 at 15 min., p less than 0.01; to 168.3 +/- 3.4 at 30 min., p less than 0.01). On the other hand, BP of WKY decreased gradually after aprotinin (mean BP: 143.0 +/- 3.3 at control to 136.8 +/- 2.7 at 15 min., n.s.; to 134.2 +/- 5.1 at 30 min., p less than 0.05). The intravenous injection (i.v.) of aprotinin (Group 2: 7 SHR, 5 WKY) and the i.c.v. of artificial cerebrospinal fluid (CSF) (Group 3: 5 SHR, 6 WKY) did not affect BP in both SHR and WKY except for the minor transient increase of BP in WKY immediately after artificial CSF i.c.v.. We performed additional experiments to study the contributions of sympathetic nervous system and vasopressin to these changes in BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Histologic analysis of the tibial bone tunnel after anterior cruciate ligament reconstruction using solvent-dried and gamma-irradiated fascia lata allograft.

Anterior cruciate ligament (ACL) reconstruction using free tendon graft requires biologic fixation in the bone tunnel. This report describes the intratunnel histology retrieved from a 47-year-old woman who underwent high tibial osteotomy 17 months after ACL reconstruction using a hybrid graft (a solvent-dried and gamma-irradiated fascia lata allograft as a core wrapped with iliotibial autograft). The patient underwent revision because of pain resulting from osteoarthrotic change, and the graft appeared to be taut and healthy on second-look arthroscopy. The sample was taken from the site of the metaphyseal osteotomy site. Histologic examination of the samples was performed with a light microscope (H&E and Masson trichrome stain). Biologic fixation of the graft to the bone was evident from observation of collagen fiber continuities, resembling Sharpey fibers. Integration of the autograft and allograft seemed to have occurred; the junction between the allograft and the autograft could not be determined. However, there was a difference in ligamentization depending on location. In the peripheral region of the graft (the autograft region), the collagen fibers showed a distinct crimped pattern; the fibroblasts were arranged regularly along the major axis of the collagen fiber bundle. In the central part of the graft (the allograft region), remodeling seemed to be delayed. There were acellular, bubbly or myxoid degeneration areas in which the fiber bundles were less oriented and there was increased vascularity.