A comparison of ankle foot orthoses with foot abduction orthoses to prevent recurrence following correction of idiopathic clubfoot by the Ponseti method.

The Ponseti method of clubfoot management requires a period of bracing in order to maintain correction. This study compared the effectiveness of ankle foot orthoses and Denis Browne boots and bar in the prevention of recurrence following successful initial management. Between 2001 and 2003, 45 children (69 feet) with idiopathic clubfeet achieved full correction following Ponseti casting with or without a tenotomy, of whom 17 (30 clubfeet) were braced with an ankle foot orthosis while 28 (39 clubfeet) were prescribed with Denis Browne boots and bar. The groups were similar in age, gender, number of casts and tenotomy rates. The mean follow-up was 60 months (50 to 72) in the ankle foot orthosis group and 47 months (36 to 60) in the group with boots and bars. Recurrence requiring additional treatment occurred in 25 of 30 (83%) of the ankle foot orthosis group and 12 of 39 (31%) of the group with boots and bars (p < 0.001). Additional procedures included repeat tenotomy (four in the ankle foot orthosis group and five in the group treated with boot and bars), limited posterior release with or without tendon transfers (seven in the ankle foot orthosis group and two in the group treated with boots and bars), posteromedial releases (nine in the orthosis group) and midfoot osteotomies (five in the orthosis group, p < 0.001). Following initial correction by the Ponseti method, children managed with boots and bars had far fewer recurrences than those managed with ankle foot orthoses. Foot abduction appears to be important to maintain correction of clubfeet treated by the Ponseti method, and this cannot be achieved with an ankle foot orthosis.

Effect of felodipine on myocardial and renal injury induced by aldosterone-high salt hypertension in uninephrectomized rats.

It has been recently shown that calcium channel blockers might have a protective effect on cardiac fibrogenesis induced by aldosterone. The objective of this study was to evaluate the protective effect of felodipine, a dihydropyridine calcium channel blocker, against heart and kidney damage caused by aldosterone-high sodium intake in uninephrectomized rats. Wistar rats were divided into three groups: CNEP (uninephrectomized + 1% NaCl in the drinking water, N = 9); ALDO (same as CNEP group plus continuous infusion of 0.75 microg/h aldosterone, N = 12); ALDOF (same as ALDO group plus 30 mg*kg(-1)*day(-1) felodipine in the drinking water, N = 10). All results were compared with those of age-matched, untreated rats (CTL group, N = 10). After 6 weeks, tail cuff blood pressure was recorded and the rats were killed for histological analysis. Blood pressure (mmHg) was significantly elevated (P < 0.05) in ALDO (180 +/- 20) and ALDOF (168 +/- 13) compared to CTL (123 +/- 12) and CNEP (134 +/- 13). Heart damage (lesion scores - median and interquartile range) was 7.0 (5.5-8.0) in ALDO and was fully prevented in ALDOF (1.5; 1.0-2.0). Also, left ventricular collagen volume fraction (%) in ALDOF (2.9 +/- 0.5) was similar to CTL (2.9 +/- 0.5) and CNEP (3.4 +/- 0.4) and decreased compared to ALDO (5.1 +/- 1.6). Felodipine partially prevented kidney injury since the damage score for ALDOF (2.0; 2.0-3.0) was significantly decreased compared to ALDO (7.5; 4.0-10.5), although higher than CTL (null score). Felodipine has a protective effect on the myocardium and kidney as evidenced by decreased perivascular inflammation, myocardial necrosis and fibrosis.

Effect of felodipine on myocardial and renal injury induced by aldosterone-high salt hypertension in uninephrectomized rats

It has been recently shown that calcium channel blockers might have a protective effect on cardiac fibrogenesis induced by aldosterone. The objective of this study was to evaluate the protective effect of felodipine, a dihydropyridine calcium channel blocker, against heart and kidney damage caused by aldosterone-high sodium intake in uninephrectomized rats. Wistar rats were divided into three groups: CNEP (uninephrectomized + 1 percent NaCl in the drinking water, N = 9); ALDO (same as CNEP group plus continuous infusion of 0.75 µg/h aldosterone, N = 12); ALDOF (same as ALDO group plus 30 mg·kg-1·day-1 felodipine in the drinking water, N = 10). All results were compared with those of age-matched, untreated rats (CTL group, N = 10). After 6 weeks, tail cuff blood pressure was recorded and the rats were killed for histological analysis. Blood pressure (mmHg) was significantly elevated (P < 0.05) in ALDO (180 ± 20) and ALDOF (168 ± 13) compared to CTL (123 ± 12) and CNEP (134 ± 13). Heart damage (lesion scores - median and interquartile range) was 7.0 (5.5-8.0) in ALDO and was fully prevented in ALDOF (1.5; 1.0-2.0). Also, left ventricular collagen volume fraction ( percent) in ALDOF (2.9 ± 0.5) was similar to CTL (2.9 ± 0.5) and CNEP (3.4 ± 0.4) and decreased compared to ALDO (5.1 ± 1.6). Felodipine partially prevented kidney injury since the damage score for ALDOF (2.0; 2.0-3.0) was significantly decreased compared to ALDO (7.5; 4.0-10.5), although higher than CTL (null score). Felodipine has a protective effect on the myocardium and kidney as evidenced by decreased perivascular inflammation, myocardial necrosis and fibrosis.

Partial potentials of selected cardiac muscle regions and heart activity model based on single fibres.

We present single fibre heart activity model (SFHAM) based on the current flow through the five bunches of fibres of the cardiac muscle (CM). The five effective fibres are identified and assigned to the appropriate segments of CM. Analytical functions describing ionic flows along the fibres are derived and proposed. The parameters determining the shapes and amplitudes of the functions proposed are obtained on the basis of standard 12-lead ECG measurements after numerical fitting procedures concentrating on the QRS-waves. As a consequence, five independent courses of partial, transient potentials are obtained representing: anterior, inferior, lateral, posterior walls, and interventricular septum activities, respectively. Moreover, to check our theoretical results we compare the potentials calculated with those from physical measurements performed on the patient's body surface. We expect that SFHAM will permit detection of pathological changes in particular fragments of CM.

A novel technique for isolating functional mast cells from the heart.

OBJECTIVE AND DESIGN: The purpose of this study was to determine the feasibility of adapting peritoneal and pleural mast cell isolation techniques to recover cardiac mast cells that retain their functional response to the secretagogue, compound 48/80. METHODS: Using a novel protocol in rats, viable epicardial mast cells were recovered by aspiration of HBSS injected into the pericardial space. Functionality of these cells was determined by ELISA quantification of histamine release in response to compound 48/80, calcium ionophore A23187 and substance P. Mast cell phenotype was determined based on the presence of chymase and tryptase demonstrated by immunofluorescence, alcian blue-safranin staining, and Western blotting. RESULTS: Mast cells isolated in this manner have low basal rates of histamine release and are highly responsive to these secretagogues. These epicardial mast cells were of the connective tissue type, which is consistent with previous reports characterizing cardiac mast cells isolated from the heart by enzymatic dispersion techniques. CONCLUSIONS: This novel pericardial aspiration technique facilitates the straightforward characterization of isolated epicardial mast cell functionality in a controlled in vitro environment, furthering our understanding of their contribution to myocardial disease.

[Obstructive sleep apnea syndrome and upper airway resistance syndrome. Gender-related differences]. / Obstruktives Schlafapnoesyndrom und Upper Airway Resistance Syndrom: Geschlechtsspezifische Unterschiede.

BACKGROUND: The aim of this study was to assess potential gender-related differences in the clinical presentation and polysomnographic parameters of patients with obstructive sleep apnea syndrome (OSAS) and upper airway resistance syndrome (UARS). PATIENTS AND METHODS: The polysomnographic variables and medical histories of 165 women with OSAS and 66 women with UARS from two sleep disorder clinics, presenting consecutively between 2000 and 2006 were retrospectively analyzed. These women were matched with an identical number of men, presenting during the same time frame, by diagnostic category (UARS/OSAS), age, and BMI. RESULTS: The relative percentage of women diagnosed with UARS varied dependent on their menopausal status. Postmenopausal women presented significantly less frequently with UARS than pre- and perimenopausal women. The adjusted odds ratio for a diagnosis of OSAS vs UARS was 5.5 (CI: 2.3;13.2; P=0.001) compared to premenopausal women. UARS women had a 30 min higher subjective sleep need than UARS men (8.2+/-1.1 vs 7.7+/-1.1 h/night; P=0.028). UARS women consumed significantly more prescription drugs than UARS men (P=0.017), and presented with a significantly lower quality of life score than their male counterparts (P=0.021). The quantitative snoring measure during sleep did not indicate significant gender differences between diagnostic categories and gender. CONCLUSIONS: Clinical presentation and polysomnographic parameters in patients with OSAS and UARS show distinct gender-related differences. These differences should be considered when patients present with signs and symptoms of OSAS or UARS.

Rat cardiac mast cell maturation and differentiation following acute ventricular volume overload.

OBJECTIVE: Cardiac mast cell numbers increase significantly within 12 h following the creation of an aortocaval (AV) fistula in rats and play a central role in mediating adverse left ventricular remodeling. We studied whether this increase was related to maturation of resident immature mast cells. METHODS: We measured percentages of immature and mature cardiac mast cells at 1, 2 and 7 days following AV-fistula or sham surgery and in non-surgical control rats using the alcian-blue safranin reaction. RESULTS: Relative to sham-operated and control rats, there was a significant shift from immature to a greater percentage of mature cardiac mast cells at 1 day and 2 days post-fistula that returned to a normal distribution by 7 days. CONCLUSIONS: We conclude that the acute increase in mast cell density following volume overload is due to a paracrine response in the heart that stimulates the maturation and differentiation of resident immature cardiac mast cells.

Spontaneous histamine secretion during isolation of rat cardiac mast cells.

OBJECTIVE: To test the hypothesis that spontaneous release of histamine occurring during an isolation protocol may modify responses of rat cardiac mast cells (connective tissue-type mast cells) to secretagogues. METHODS: We assessed two protocols for enzymatic dispersion utilizing collagenase, hyaluronidase, and deoxyribonuclease; with protease (Protocol 1, n = 8) or without protease (Protocol 2, n = 3). Spontaneous release of histamine was quantified following mechanical and enzymatic dispersion of the whole heart. RESULTS: Total histamine loss (Mean +/- SEM) was 963+/-92 and 833+/-60 ng/g of tissue weight following Protocols 1 and 2. Percentages of histamine release from cell isolates following Protocol 1 were 40+/-5%, 41+/-6%, and 51+/-7% at 0, 30, and 300 microg/mL of compound 48/80. CONCLUSIONS: Enzymatic dispersion of cardiac mast cells affects their response to secretagogues.

Contribution of ventricular remodeling to pathogenesis of heart failure in rats.

We previously reported an approximately 50% incidence of rats with symptoms of congestive heart failure (CHF) at 8 wk postinfrarenal aorto-caval fistula. However, it was not clear whether compensatory ventricular remodeling could continue beyond 8 wk or whether the remaining animals would have developed CHF or died. Therefore, the intent of this study was to complete the characterization of this model of sustained volume overload by determining the morbidity and mortality and the temporal response of left ventricular (LV) remodeling and function beyond 8 wk. The findings demonstrate an upper limit to LV hypertrophy and substantial increases in LV volume and compliance, matrix metalloproteinase activity, and collagen volume fraction associated with the development of CHF. There was an 80% incidence of morbidity and mortality following 21 wk of chronic volume overload. These findings indicate that the development of CHF is triggered by marked ventricular dilatation and increased compliance occurring once the myocardial hypertrophic response is exhausted.

Alterations in myocardial collagen content affect rat papillary muscle function.

We investigated the influence of myocardial collagen volume fraction (CVF, %) and hydroxyproline concentration (microg/mg) on rat papillary muscle function. Collagen excess was obtained in 10 rats with unilateral renal ischemia for 5 wk followed by 3-wk treatment with ramipril (20 mg. kg(-1). day(-1)) (RHTR rats; CVF = 3.83 +/- 0. 80, hydroxyproline = 3.79 +/- 0.50). Collagen degradation was induced by double infusion of oxidized glutathione (GSSG rats; CVF = 2.45 +/- 0.52, hydroxyproline = 2.85 +/- 0.18). Nine untreated rats were used as controls (CFV = 3.04 +/- 0.58, hydroxyproline = 3.21 +/- 0.30). Active stiffness (AS; g. cm(-2). %L(max)(-1)) and myocyte cross-sectional area (MA; micrometer(2)) were increased in the GSSG rats compared with controls [AS 5.86 vs. 3.96 (P < 0.05); MA 363 +/- 59 vs. 305 +/- 28 (P < 0.05)]. In GSSG and RHTR groups the passive tension-length curves were shifted downwards, indicating decreased passive stiffness, and upwards, indicating increased passive stiffness, respectively. Decreased collagen content induced by GSSG is related to myocyte hypertrophy, decreased passive stiffness, and increased AS, and increased collagen concentration causes myocardial diastolic dysfunction with no effect on systolic function.

beta-blockade prevents sustained metalloproteinase activation and diastolic stiffening induced by angiotensin II combined with evolving cardiac dysfunction.

Angiotensin II (Ang II)-mediated sympathostimulation may worsen the progression of cardiac failure, although the nature and mechanisms of such interactions are largely unknown. We previously demonstrated that Ang II combined with evolving cardiodepression (48-hour tachycardia pacing, 48hP) induces marked chamber stiffening and increases metalloproteinases (MMPs). Here, we test the hypothesis that both abnormalities stem from sympathostimulatory effects of Ang II. Forty-eight dogs were instrumented to serially assess conscious ventricular mechanics, MMP abundance and activity, and myocardial histopathology. 48hP combined with 5 days of Ang II (15+/-5 ng. kg(-1). min(-1) IV) more than doubled chamber stiffness (end-diastolic pressure >25 mm Hg, P<0.001), whereas stiffness was unchanged by Ang II or 48hP alone. In vitro and in situ zymography revealed increased MMP abundance and activity (principally 92-kDa gelatinase) from Ang II+48hP. Both stiffening and MMP changes were prevented by cotreatment with high-dose atenolol (which nearly fully inhibited isoproterenol-induced inotropy) but not partial beta-blockade. Myocellular damage with fibroblast/neutrophil infiltration from Ang II+48hP was also inhibited by high- but not low-dose atenolol, whereas collagen content was not elevated with either dose. These data support a role of sympathostimulation by Ang II in modulating myocardial MMP abundance and activity and diastolic stiffening in evolving heart failure and suggest a novel mechanism by which beta-blockade may limit chamber remodeling and diastolic dysfunction.

Differential expression of natriuretic peptides and their receptors in volume overload cardiac hypertrophy in the rat.

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) upregulation are genetic markers for the chronic hypertrophic phenotype but also have important acute physiologic effects on salt and water balance and blood pressure control. The presence of a dual NP-system led us to hypothesize a differential expression of ANP and BNP in response to an acute hemodynamic stress of volume overload in the left ventricle (LV) and right ventricle (RV). Accordingly, we examined the temporal relationship between the RV and LV expression of ANP and BNP mRNA and NP receptor mRNA levels on days 1, 2, 3, and 7 after induction of aortocaval fistula in the rat. LV end-diastolic pressure was increased 1.5-fold by day 3 and 2.0-fold by day 7 compared to control (P<0.05). LV weight increased by day 7 compared to control (2.34+/-0.04 vs 3.07+/-0.10 mg/g, P<0.05) while RV weight did not change over the 7 days. There was a 7-fold increase of ANP mRNA in LV at day 1, which was sustained through day 7, while LV BNP mRNA levels did not differ from controls over the 7 days. In contrast, RV mRNA transcript levels for ANP and BNP were increased >2-fold by day 2 and this increase was sustained throughout 7 days. NP clearance receptor was decreased by 75% by day 7 in the LV but did not change in the RV. Thus, LV ANP mRNA levels increased before the onset of LV hypertrophy and RV BNP mRNA levels increased in the absence of RV hypertrophy. The disparate response of BNP and the NP clearance receptor transcript levels in the LV and RV may be related to differences in load and/or differential expression of the NP system in the LV and RV in response to acute haemodynamic stress.

The effect of non-antihypertensive doses of angiotensin converting enzyme inhibitor on myocardial necrosis and hypertrophy in young rats with renovascular hypertension.

In renovascular hypertensive rats, low doses of angiotensin converting enzyme (ACE) inhibitors have been found to prevent myocardial hypertrophy independent of blood pressure level. This finding would suggest humoral rather than mechanical control of myocyte growth. The aim of this study was to examine the effect of nonantihypertensive doses of ACE inhibitor on myocardial hypertrophy and necrosis in hypertensive rats. Renovascular hypertension (RHT) was induced in four-week-old Wistar rats. Twenty-eight animals were treated for four weeks with three doses of ramipril (0.01, 0.1 or 1. 0 mg/kg/day, which are unable to lower blood pressure. Fourteen animals were not treated (RHT group). A sham operated, age/sex-matched group was used as control (n = 10). Myocardial histology was analysed in 3 microm thick sections of the ventricle stained with either haematoxylin-eosin, reticulin silver stain or Masson's trichrome. There was a significant correlation between systolic blood pressure and left ventricular to body weight ratio in both sets of animals: untreated plus controls and ramipril-treated rats. ACE inhibition prevented myocyte and perivascular necrosis and fibrosis in a dose-dependent manner. We conclude that myocardial hypertrophy in rats with renovascular hypertension is directly related to arterial pressure, and that this relationship is not affected by nonantihypertensive doses of ACE inhibitor. Myocardial necrosis/fibrosis and coronary artery damage induced by angiotensin II are prevented by ACE inhibitor in a dose-dependent manner, despite the presence of arterial hypertension.

Augmentation of spinal arthrodesis with autologous bone marrow in a rabbit posterolateral spine fusion model.

STUDY DESIGN: Posterolateral spinal fusion with autologous bone marrow aspirate in addition to autograft iliac crest bone graft in a rabbit model. OBJECTIVE: To demonstrate that the addition of autologous bone marrow can have positive effects on bone formation and spinal fusion. SUMMARY OF BACKGROUND DATA: Bone marrow has been shown to contain osteoprogenitor cells. A number of studies have demonstrated that bone formation is possible with autologous marrow injection into orthotopic sites such as that performed in femur fracture models. METHODS: A bone paucity model of posterolateral spine fusion was developed. The control animals received 0.8 g of morselized autogenous iliac crest bone graft harvested from a single iliac crest. The graft was mixed with 2 mL of clotted peripheral blood. In the experimental group, 2 mL of bone marrow aspirated from the opposite iliac crest was substituted for the peripheral blood clot. All rabbits were killed at 12 weeks, and the specimens were subjected to evaluation by posteroanterior radiography for the presence of fusion, computed tomography for bone volume, and biomechanical testing for stiffness. RESULTS: Successful fusion was achieved in 61% of the animals in the experimental group versus 25% in the control group (P < 0.05). The fusion mass in the experimental group had a mean volume of 919 +/- 387 mm3 versus 667 +/- 512 mm3 for the control group, as measured from computed tomography images. The results of the biomechanical testing validated the radiographic scoring system. The stiffness in specimens, graded as having a radiographic score of 4, was significantly greater than in specimens with radiographic scores of 1 and 2. CONCLUSION: In cases for which an adequate quantity of autogenous bone graft is not available, addition of bone marrow may facilitate greater bone formation and successful fusion.

[Large intracranial tumors invading skull base]. / Duze guzy wewnatrzczaszkowe przerastajace podstawe czaszki.

Large intracranial tumours (diameter > 4.5 cm) invading skull base are not frequent. In Department of Neurosurgery in Poznan 22 patients were operated on between 1977-1966. There were 15 males and 7 females. Mean age was 34.78 +/- 15.31 years. The authors analyse the time between the onset of illness and diagnosis, symptoms and neurological condition. Tumour localization was verified by X-rays, computed tomography, cerebral angiography and in some cases magnetic resonance. There were 11 tumours in both fossae--anterior and middle, in 7 tumour site was limited to anterior and in 4--to middle fossa. Extracranial tumour penetration was observed as follows: in 10 cases into paranasal sinuses, 10--orbit, 8--nasopharyngeal cavity and in 4 cases into subtemporal fossa. The authors discuss surgical methods, histological appearances and postoperative complications. Mortality rate was 9% (2 patients died).

Left ventricular adaptation to chronic pressure overload induced by inhibition of nitric oxide synthase in rats.

Recent studies have indicated that chronic inhibition of nitric oxide synthase induces arterial hypertension without myocardial hypertrophy. We investigated the mechanisms of left ventricular (LV) adaptation to this condition. Also, we analyzed the effect of the angiotensin-converting enzyme inhibitor (ACEI), lisinopril, in this experimental model of ventricular pressure overload. Fifty-eight Wistar rats received eight weeks of treatment with either NW-nitro-L-arginine-methyl ester (L-NAME group, n = 19), lisinopril (LISINOPRIL group, n = 19) or the combination of both drugs (LNAMELIS group, n = 20). All results were compared to age and sex matched untreated rats (CONTROL group, n = 18). Tail-cuff blood pressure rose significantly in L-NAME treated rats (195 +/- 29 mm Hg) compared to the CONTROL (141 +/- 12 mm Hg), LISINOPRIL (97 +/- 13 mm Hg), and LNAMELIS (113 +/- 16 mm Hg) groups. There was no myocardial hypertrophy in the chronically hypertensive rats. The ventricular unstressed volume was significantly reduced in the L-NAME group (0.119 +/- 0.027 mL) compared to the CONTROL (0.158 +/- 0.026 mL) indicating a disproportional reduction in ventricular volume related to the myocardial mass. The chamber size modification resulted in a systolic stress which was comparable to the CONTROL even though the isovolumetric systolic pressure was higher. The systolic functional data indicated preserved myocardial contractility in L-NAME. LV compliance was increased in the LISINOPRIL group and myocardial passive stiffness was lower in all treated rats compared to CONTROL. We conclude that LV. adaptation to chronic pressure overload without hypertrophy involves changes in chamber geometry and myocardial diastolic mechanical properties. Also, ACEI fully prevents L-NAME induced hypertension, reduces myocyte cross-sectional area, and myocardial passive stiffness. The combination of L-NAME plus lisinopril decreases the load independent index of myocardial contractility.

ANG II-related myocardial damage: role of cardiac sympathetic catecholamines and beta-receptor regulation.

The objectives of this study were 1) to determine whether ANG II-induced myocardial damage (ANG Dam) is mediated via the beta1-adrenergic receptor, 2) to elucidate whether adrenal medulla or cardiac sympathetic neuron catecholamines are responsible for ANG Dam, and 3) to determine whether the lack of damage after 3 days of elevated ANG II levels is due to beta1-receptor downregulation. To this end, ANG II was administered to rats 1) that were treated with a beta-receptor blocker, 2) after adrenal medullectomy and/or cardiac sympathectomy, and 3) for 3 or 8 days. ANG II caused both myocyte necrosis and coronary vascular damage after adrenal medullectomy but not after cardiac sympathectomy. There was a 38 and 55% decrease in beta-receptor density after 3 and 8 days, respectively, of ANG II infusion, and an upregulation to control levels 5 days after a 3-day ANG II infusion was stopped. We conclude that cardiac sympathetic neuron catecholamines are responsible for ANG Dam and that the acute nature of this damage is associated with a downregulation of beta1-adrenergic receptors.

[Cardiac arrhythmias in sleep apnea. Increased cardiovascular risk caused by nocturnal arrhythmia?]. / Herzrhythmusstörungen bei Schlafapnoe. Erhöhtes kardiovaskuläres Risiko durch nächtliche Arrhythmien?

In sleep-disordered breathing (SDB), the greatest clinical relevance attaches to obstructive sleep apnea on account of its high prevalence and its concomitance with diseases of the cardiovascular system. The high mortality rate of untreated patients is believed to be due to the consequences of these latter diseases. Thus, for example, in addition to systemic arterial hypertension, elevated rates of such disorders as pulmonary hypertension, right heart insufficiency, coronary heart disease, myocardial infarction and stroke are also found. Up until quite recently bradycardic and tachycardic arrhythmias occurring during sleep have been held responsible of the increased mortality rate of these patients. Till the mid-eighties the prevalence of bradycardic arrhythmias was reported to be more than 30%. However, the importance of cardiac arrhythmias has been overestimated, as is supported in particular by current studies on large non-selected samples showing a much lower prevalence of apnea-related arrhythmias. In the differential diagnosis, however, consideration must be given to SDB in patients with nocturnal arrhythmias and heart rate variations.

Synergistic exacerbation of diastolic stiffness from short-term tachycardia-induced cardiodepression and angiotensin II.

Synergistic interaction between angiotensin II (Ang II) and evolving cardiodepression may play an important role in worsening chamber function, particularly in diastole. To test this hypothesis, Ang II was infused at 10 or 17 ng.kg(-1).min(-1) in 18 conscious dogs 4 days before and during induction of subacute cardiodepression by 48-hour tachypacing. The lower dose yielded negligible systemic pressure changes. Twelve additional animals served as paced-only controls. Pressure-dimension relations were recorded, and serial endocardial biopsies were obtained to assess histological and metalloproteinase (MMP) changes. Forty-eight-hour pacing alone depressed systolic function but had little effect on diastolic stiffness. Ang II alone only modestly raised diastolic stiffness at both doses and enhanced contractility at the higher dose. These changes recovered toward baseline after a 7-day infusion. However, Ang II (at either dose) combined with 48-hour pacing markedly increased ventricular stiffness (110+/-26% over baseline) and end-diastolic pressure (22+/-1.7 mm Hg). In contrast, pacing-induced inotropic and relaxation abnormalities were not exacerbated by Ang II. Zymography revealed MMP activation (72- and 92-kD gelatinases and 52-kDa caseinase) after a 4-day Ang II infusion (at both doses), which persisted during pacing. Tachypacing initiated 24 hours after cessation of a 7-day Ang II infusion also resulted in diastolic stiffening and corresponded with MMP reactivation. Ang II also induced myocyte necrosis, inflammation, and subsequent interstitial fibrosis, but these changes correlated less with chamber mechanics. Thus, Ang II amplifies and accelerates diastolic dysfunction when combined with evolving cardiodepression. This phenomenon may also underlie Ang II influences in late-stage cardiomyopathy, when chamber distensibility declines.

[Cardiorespiratory polygraphy in differential diagnosis of respiratory insufficiency in patients after coronary artery bypass operation]. / Die kardiorespiratorische Polygraphie zur Differentialdiagnostik der respiratorischen Insuffizienz bei Patienten nach koronarer Bypass-Operation.

BACKGROUND: In intensive care medicine it is well established how to diagnose respiratory insufficiency caused by cardiopulmonary diseases. However, there is no consensus how to diagnose respiratory insufficiency which may be caused by extrapulmonary disturbances of the respiratory apparatus. PATIENTS AND METHODS: In 5 patients we performed postoperatively a cardio-respiratory polygraphy for 12 to 13 hours using Polymesam. This unit allows to record airflow, respiratory movements of the chest and abdomen, arterial oxygen saturation, heart rate, body position and EKG. RESULTS: The present case-series-study demonstrates that patients after arterio-coronary bypass surgery may present respiratory insufficiency caused by extrapulmonary disturbances of the respiratory apparatus (central and obstructive apnea and hyoponea). The respiratory insufficiency occurs during nighttime even when supplemental oxygen (2 to 3 1/min) is delivered. CONCLUSION: We conclude that the cardiopulmonary polygraphy for assessing respiratory insufficiency in patients after coronary bypass surgery is important, in order to avoid severe arterial hypoxemia which may produce cardiovascular instability in these patients.