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Biomedical subjects

F Haddad

Publications and source records attributed to F Haddad.

At least 19 recordsLinked to original sources
PubMed2006

Effect of vital capacity manoeuvres on arterial oxygenation in morbidly obese patients undergoing open bariatric surgery.

BACKGROUND: Arterial oxygenation may be compromised in morbidly obese patients undergoing bariatric surgery. The aim of this study was to evaluate the effect of a vital capacity manoeuvre (VCM), followed by ventilation with positive end-expiratory pressure (PEEP), on arterial oxygenation in morbidly obese patients undergoing open bariatric surgery. METHODS: Fifty-two morbidly obese patients (body mass index >40 kg m-2) undergoing open bariatric surgery were enrolled in this prospective and randomized study. Anaesthesia and surgical techniques were standardized. Patients were ventilated with a tidal volume of 10 mL kg-1 of ideal body weight, a mixture of oxygen and nitrous oxide (FiO2 = 40%) and respiratory rate was adjusted to maintain end-tidal carbon dioxide at a level of 30-35 mmHg. After abdominal opening, patients in Group 1 had a PEEP of 8 cm H2O applied and patients in Group 2 had a VCM followed by PEEP of 8 cm H2O. This manoeuvre was defined as lung inflation by a positive inspiratory pressure of 40 cm H2O maintained for 15 s. PEEP was maintained until extubation in the two groups. Haemodynamics, ventilatory and arterial oxygenation parameters were measured at the following times: T0 = before application of VCM and/or PEEP, T1 = 5 min after VCM and/or PEEP and T2 = before abdominal closure. RESULTS: Patients in the two groups were comparable regarding patient characteristics, surgical, haemodynamic and ventilatory parameters. In Group 1, arterial oxygen partial pressure (PaO2) and arterial haemoglobin oxygen saturation (SaO2) were significantly increased and alveolar-arterial oxygen pressure gradient (A-aDO2) decreased at T2 when compared with T0 and T1. In Group 2, PaO2 and SaO2 were significantly increased and A-aDO2 decreased at T1 and T2 when compared with T0. Arterial oxygenation parameters at T1 and T2 were significantly improved in Group 2 when compared with Group 1. CONCLUSION: The addition of VCM to PEEP improves intraoperative arterial oxygenation in morbidly obese patients undergoing open bariatric surgery.

Adult↗
PubMed2006

Short-term strength training and the expression of myostatin and IGF-I isoforms in rat muscle and tendon: differential effects of specific contraction types.

In skeletal muscle, an increased expression of insulin like growth factor-I isoforms IGF-IEa and mechano-growth factor (MGF) combined with downregulation of myostatin is thought to be essential for training-induced hypertrophy. However, the specific effects of different contraction types on regulation of these factors in muscle are still unclear, and in tendon the functions of myostatin, IGF-IEa, and MGF in relation to training are unknown. Female Sprague-Dawley rats were subjected to 4 days of concentric, eccentric, or isometric training (n = 7-9 per group) of the medial gastrocnemius, by stimulation of the sciatic nerve during general anesthesia. mRNA levels for myostatin, IGF-IEa, and MGF in muscle and Achilles' tendon were measured by real-time RT-PCR. Muscle myostatin mRNA decreased in response to all types of training (2- to 8-fold) (P < 0.05), but the effect of eccentric training was greater than concentric and isometric training (P < 0.05). In tendon, myostatin mRNA was detected, but no changes were seen after exercise. IGF-IEa and MGF increased in muscle (up to 15-fold) and tendon (up to 4-fold) in response to training (P < 0.01). In tendon no difference was seen between training types, but in muscle the effect of eccentric training was greater than concentric training for both IGF-IEa and MGF (P < 0.05), and for IGF-IEa isometric training had greater effect than concentric (P < 0.05). The results indicate a possible role for IGF-IEa and MGF in adaptation of tendon to training, and the combined changes in myostatin and IGF-IEa/MGF expression could explain the important effect of eccentric actions for muscle hypertrophy.

Animals↗
PubMed2006

Similar acute molecular responses to equivalent volumes of isometric, lengthening, or shortening mode resistance exercise.

The present study was undertaken to test the hypothesis that the contraction mode of action [static-isometric (Iso), shortening-concentric (Con), or lengthening-eccentric (Ecc)] used to stress the muscle provides a differential mechanical stimulus eliciting greater or lesser degrees of anabolic response at the initiation of a resistance training program. We performed an acute resistance training study in which different groups of rodents completed four training sessions in either the Iso, Con, or Ecc mode of contraction under conditions of activation and movement specifically designed to elicit equivalent volumes of force accumulation. The results of this experiment indicate that the three modes of contraction produced nearly identical cell signaling, indicative of an anabolic response involving factors such as increased levels of mRNA for IGF-I, procollagen III alpha1, decreased myostatin mRNA, and increased total RNA concentration. The resulting profiles collectively provide evidence that pure mode of muscle action, in and of itself, does not appear to be a primary variable in determining the efficacy of increased loading paradigms with regard to the initiation of selected muscle anabolic responses.

Animals↗
PubMed2006

A prospective analysis of fenestrated endovascular grafting: intermediate-term outcomes.

PURPOSE: To assess the intermediate-term outcomes following fenestrated grafting for juxtarenal aneurysms. MATERIALS AND METHODS: A prospective trial was conducted on patients with short proximal necks, who were considered to be high-risk for open repair and unacceptable for conventional endovascular repair. Devices were designed from reconstructed CT data. Follow-up studies included CT, duplex ultrasound, and KUB and occurred at hospital discharge, 1, 6, and 12 months and annually thereafter. RESULTS: One hundred and nineteen patients were treated (2001-2005). Mean age and aneurysm size were 75 years and 65 mm, respectively, and 82% were male. A total of 302 visceral vessels were inferior to the fabric seal (a mean of 2.5 vessels per patient), with the most common design incorporating two renal arteries and the SMA (58%). All prostheses were implanted successfully without any acute visceral artery loss. The mean follow-up was 19 months (0-42 months). One patient died within 30 days of device implantation. Kaplan-Meier estimates of survival at 1, 12, 24, and 36 months are 0.99, 0.92, 0.83 and 0.79. There were no ruptures or conversions. Pre-discharge imaging noted 11 type I and type III endoleaks. The 30-day endoleak rate was 10% (all type II). Aneurysm sac size decreased (>5 mm) in 51, 79 and 77% at 6, 12 and 24 months, respectively. One patient had sac enlargement within the first year, associated with a persistent type II endoleak. In-stent stenoses occurred in 12 renal arteries and one SMA. Six renal arteries and the SMA stenosis were treated and two renal stenoses are awaiting treatment. Ten of 231 stented renal arteries occluded (three prior to discharge), one of which was recanalized. One component separation was treated with an extension at 2 years. CONCLUSIONS: The placement of endovascular prostheses with graft material incorporating the visceral arteries is safe and appears to be effective at preventing rupture. Continued follow-up to assess the long-term benefit, aneurysm sac behavior and effect of stenting upon the visceral ostia remains critical.

Aged↗
PubMed2006

Regulation of antisense RNA expression during cardiac MHC gene switching in response to pressure overload.

Hypertension has been shown to cause cardiac hypertrophy and a shift in myosin heavy chain (MHC) gene expression from the faster alpha- to slower beta-MHC isoform. The expression of the beta- and alpha-MHC pre-mRNAs, mRNAs, as well as the newly discovered antisense beta-RNA were analyzed in three regions of the normal control (NC) and 12-day pressure-overloaded (AbCon) hearts: the left ventricle apex, left ventricle base, and the septum. The RNA analyses in the AbCon heart targeted both the 5' and the 3' ends of each RNA molecule. beta-MHC mRNA expression significantly increased relative to control in all three regions, regardless of the target site (5' or 3' end). In contrast, beta-MHC pre-mRNA expression in the AbCon heart depended on the site of the measurement (5' vs. 3' end). For example, whereas the pre-mRNA did not change when targeted at the 3' end (last intron), it increased significantly in the AbCon heart when measurement targeted the 5' end (2nd intron) of the 25-kb molecule. Analyses of the antisense beta-RNA revealed that its expression in the AbCon heart was significantly decreased relative to control regardless of its measurement site. A negative correlation was observed between the beta-mRNA expression and the antisense beta-RNA (P < 0.05), suggesting an inhibitory role of antisense RNA on the sense beta-MHC gene expression. In contrast, a positive correlation was observed between the antisense beta-RNA and the alpha-MHC pre-mRNA (P < 0.05). This latter observation along with the alpha-MHC gene position relative to that of the beta-antisense suggest that the alpha-MHC sense and beta-antisense transcription are coregulated likely via common intergenic regulatory sequences. Our results suggest that the increased beta-MHC expression in the AbCon heart not only is the result of increased beta-MHC transcription but also involves an antisense beta-RNA regulation scheme. Although the exact mechanism concerning antisense regulation is not clear, it could involve modulation of both transcriptional activity of the beta-MHC gene and posttranscriptional processing.

Animals↗
PubMed2005

Isometric resistance exercise fails to counteract skeletal muscle atrophy processes during the initial stages of unloading.

This study tested the hypothesis that an isometric resistance training paradigm targeting the medial gastrocnemius of adult rodents is effective in preventing muscle atrophy during the early stages of hindlimb unloading by maintaining normal activation of the insulin receptor substrate-1 (IRS-1)/phosphoinositide-3 kinase (PI3K)/Akt signaling pathway. This pathway has been shown to simultaneously create an anabolic response while inhibiting processes upregulating catabolic processes involving expression of key enzymes in the ubiquitination of proteins for degradation. The findings show that during the 5 days of unloading 1) absolute medial gastrocnemius muscle weight reduction occurred by approximately 20%, but muscle weight corrected to body weight was not different from normal weight-bearing controls (P < 0.05); 2) normalized myofibril fraction concentration and content were decreased; and 3) a robust isometric training program, known to induce a hypertrophy response, failed to maintain the myofibril protein content. This response occurred despite fully blunting the increases in the mRNA for of atrogin-1, MURF-1, and myostatin, e.g., sensitive gene markers of an activated catabolic state. Analyses of the IRS-1/PI3K/Akt markers indicated that abundance of IRS-1 and phosphorylation state of Akt and p70S6 kinase were decreased relative to normal control rats, and the resistance training failed to maintain these signaling markers at normal regulatory level. Our findings suggest that to fully prevent muscle atrophy responses affecting the myofibril system during unloading, the volume of mechanical stress must be augmented sufficiently to maintain optimal activity of the IRS-1/PI3K/Akt pathway to provide an effective anabolic stimulus on the muscle.

Animals↗
PubMed2004

IL-6-induced skeletal muscle atrophy.

Chronic, low-level elevation of circulating interleukin (IL)-6 is observed in disease states as well as in many outwardly healthy elderly individuals. Increased plasma IL-6 is also observed after intense, prolonged exercise. In the context of skeletal muscle, IL-6 has variously been reported to regulate carbohydrate and lipid metabolism, increase satellite cell proliferation, or cause muscle wasting. In the present study, we used a rodent local infusion model to deliver modest levels of IL-6, comparable to that present after exercise or with chronic low-level inflammation in the elderly, directly into a single target muscle in vivo. The aim of this study was to examine the direct effects of IL-6 on skeletal muscle in the absence of systemic changes in this cytokine. Data included cellular and molecular markers of cytokine and growth factor signaling (phosphorylation and mRNA content) as well as measurements to detect muscle atrophy. IL-6 infusion resulted in muscle atrophy characterized by a preferential loss of myofibrillar protein (-17%). IL-6 induced a decrease in the phosphorylation of ribosomal S6 kinase (-60%) and STAT5 (-33%), whereas that of STAT3 was increased approximately twofold. The changes seen in the IL-6-infused muscles suggest alterations in the balance of growth factor-related signaling in favor of a more catabolic profile. This suggests that downregulation of growth factor-mediated intracellular signaling may be a mechanism contributing to the development of muscle atrophy induced by elevated IL-6.

Animals↗
PubMed2004

Pretranslational markers of contractile protein expression in human skeletal muscle: effect of limb unloading plus resistance exercise.

Previously, it has been shown that the human ground-based model consisting of unilateral limb suspension (ULLS) induces atrophy and reduced strength of the affected quadriceps muscle group. Resistance exercise (RE) involving concentric-eccentric actions, in the face of ULLS, is effective in ameliorating these deficits. The goal of the present study was to determine whether alterations in contractile protein gene expression, e.g., myosin heavy chain and actin, as studied at the pretranslational level, provide molecular markers concerning the deficits that occur in muscle mass/volume during ULLS, as well as its maintenance in response to ULLS plus RE. Muscle biopsies were obtained from the vastus lateralis muscle of 31 middle-aged men and women before and after 5 wk of ULLS, ULLS plus RE, or RE only. The RE paradigm consisted of 12 sessions of 4 sets of 7 concentric-eccentric knee extensions. Our findings show that there were net deficits in total RNA, total mRNA, and actin and myosin heavy chain mRNA levels of expression after ULLS (P < 0.05), whereas these alterations were blunted in the two groups receiving RE. Additional observations involving IGF-I and its associated receptor and binding proteins suggest that RE postures the skeletal muscle for signaling processes that favor a greater anabolic state relative to that observed in the ULLS group. Collectively, these findings suggest that molecular markers of contractile protein gene expression serve as useful subcellular indicators for ascertaining the underlying mechanisms regulating alterations in muscle mass in human subjects in response to altered loading states.

Adult↗
PubMed2004

IL-6-174G/C genotype is associated with the bone mineral density response to oestrogen replacement therapy in post-menopausal women.

A reduction in interleukin-6 (IL-6) activity may contribute to the beneficial effects of hormone replacement therapy (HRT) on the menopausal decline in bone mineral density (BMD). We have examined this hypothesis using a genetic strategy. The -174C (rather than G) IL-6 gene variant is associated with lower IL-6 expression. As such, we might anticipate the C allele to be associated with a greater response to HRT. We have tested this hypothesis. Mean three-site [spine (L1-L4), neck of femur, and Ward's triangle] BMD was measured in 65 women in a 1-year randomised controlled trial of HRT with 0.625 mg oestrogen/day and 0.15 mg norgestrel (n=30). Baseline BMD was genotype-independent for both the control and HRT group. In the control group, the percentage change in BMD after 1 year was similar between genotypes (P=0.45). In contrast, in the HRT group, the rise was genotype-dependent. Those homozygous for the G allele showed a 3.62 (2.14)% increase in BMD compared with 10.44 (4.68)% for the C-homozygous group. Heterozygotes had an intermediate BMD increase of 5.6 (2.82)% [ P=0.006 ( P value for interaction between HRT and genotype was 0.04)] Although the study was limited by its small sample size, these are the first data to demonstrate the importance of IL-6 genotype in determining response to oestrogen therapy, rather than its physiological withdrawal.

Bone Density↗
PubMed2004

Clinical and radiographic assessment of the young adult with symptomatic hip dysplasia.

Acetabular dysplasia is a major precursor of osteoarthritis of the hip. It is important to identify patients before the development of osteoarthritis, because these patients may be candidates for joint-preserving surgery, such as pelvic osteotomy. Patients with hip dysplasia, and no osteoarthritis, present with unique findings on history and physical examination. On history, patients should be questioned for symptoms unique to dysplasia, such as locking, snapping, and feelings of instability. Physical examination should look for signs of labral disease, by using the impingement test. Patients suspected of having symptomatic dysplasia should have plain radiographs, including an anteroposterior radiograph of the pelvis taken with the patient standing, a false profile view, and an abduction view of the hip. The anteroposterior radiograph of the pelvis and false profile view will help to quantify the degree of the dysplasia. The abduction view is important in determining the patient's eligibility for joint-preserving hip surgery. Computed tomography scanning and magnetic resonance imaging are reserved for patients who are operative candidates. Computed tomography scanning can aid in the planning of complex pelvic osteotomies. Magnetic resonance imaging especially is useful for delineating labral disease. It is this combination of history, physical examination, and radiographic workup that will allow successful treatment of the dysplastic hip before the development of osteoarthritis.

Bone Diseases, Developmental↗
PubMed2004

Pain in the well-fixed, aseptic titanium hip replacement. The role of corrosion.

We have investigated nine patients with cemented Furlong (JRI, London, UK) titanium hip replacements who presented with early pain despite a well-fixed, aseptic prosthesis. All were followed up clinically and radiologically at regular intervals. Pain was located in the thigh and was worse at night. Radiographs showed cortical hypertrophy of the femur around the tip of the stem. Eight of the nine patients subsequently required single-stage revision using an uncemented prosthesis, which relieved the pain. At revision, the pH of the tip of the stem was found to be highly acidic with macroscopic evidence of corrosion consisting of multiple layers of titanium oxides when studied by X-ray dispersive analysis. Cemented titanium implants have a potential for crevice corrosion leading to cortical hypertrophy and intractable pain.

Aged↗
PubMed2003

Transcriptional regulation of IGF-I expression in skeletal muscle.

The present study investigated the role of transcription in the regulation of insulin-like growth factor (IGF)-I expression in skeletal muscle. RT-PCR was used to determine endogenous expression of IGF-I pre-mRNA and mRNA in control (Con) and functionally overloaded (FO) rat plantaris. The transcriptional activities of five different-length IGF-I promoter fragments controlling transcription of a firefly luciferase (FLuc) reporter gene were tested in vitro by transfection of myoblasts or in vivo during FO by direct gene transfer into the plantaris. Increased endogenous IGF-I gene transcription during 7 days of plantaris FO was evidenced by an approximately 140-160% increase (P < 0.0001) in IGF-I pre-mRNA (a transcriptional marker). IGF-I mRNA expression also increased by approximately 90% (P < 0.0001), and it was correlated (R = 0.93; P < 0.0001) with the pre-mRNA increases. The three longest IGF-I exon 1 promoters induced reporter gene expression in proliferating C2C12 and L6E9 myoblasts. In differentiated L6E9 myotubes, promoter activity increased approximately two- to threefold over myoblasts. Overexpression of calcineurin and MyoD increased the activity of the -852/+192 promoter in C2C12 myotubes by approximately 5- and approximately 18-fold, respectively. However, FO did not induce these exogenous promoter fragments. Nevertheless, the present findings are consistent with the hypothesis that the IGF-I gene is transcriptionally regulated during muscle hypertrophy in vivo as evidenced by the induction of the endogenous IGF-I pre-mRNA during plantaris FO. The exon 1 promoter region of the IGF-I gene is sufficient to direct inducible expression in vitro; however, an in vivo response to FO may require elements outside the -852/+346 region of the exon 1 IGF-I promoter or features inherent to the endogenous IGF-I gene.

Animals↗
PubMed2003

Atrophy responses to muscle inactivity. I. Cellular markers of protein deficits.

The goal of this study was to use the model of spinal cord isolation (SI), which blocks nearly all neuromuscular activity while leaving the motoneuron muscle-fiber connections intact, to characterize the cellular processes linked to marked muscle atrophy. Rats randomly assigned to normal control and SI groups were studied at 0, 2, 4, 8, and 15 days after SI surgery. The slow soleus muscle atrophied by approximately 50%, with the greatest degree of loss occurring during the first 8 days. Throughout the SI duration, muscle protein concentration was maintained at the control level, whereas myofibrillar protein concentration steadily decreased between 4 and 15 days of SI, and this was associated with a 50% decrease in myosin heavy chain (MHC) normalized to total protein. Actin relative to the total protein was maintained at the control level. Marked reductions occurred in total RNA and DNA content and in total MHC and actin mRNA expressed relative to 18S ribosomal RNA. These findings suggest that two key factors contributing to the muscle atrophy in the SI model are 1). a reduction in ribosomal RNA that is consistent with a reduction in protein translational capacity, and 2). insufficient mRNA substrate for translating key sarcomeric proteins comprising the myofibril fraction, such as MHC and actin. In addition, the marked selective depletion of MHC protein in the muscles of SI rats suggests that this protein is more vulnerable to inactivity than actin protein. This selective MHC loss could be a major contributor for the previously reported loss in the functional integrity of SI muscles. Collectively, these data are consistent with the involvement of pretranslational and translational processes in muscle atrophy due to SI.

Actins↗
PubMed2003

Atrophy responses to muscle inactivity. II. Molecular markers of protein deficits.

We examined the expression of several molecular markers of protein balance in response to skeletal muscle atrophy induced by spinal cord isolation (SI; i.e., a complete transection of the spinal cord at both a midthoracic and a high sacral level plus complete deafferentation between the two transection sites). This treatment nearly eliminates neuromuscular activity (activation and loading) of the hindlimb muscles while maintaining neuromuscular connectivity. SI was associated with a reduced transcriptional activity (via pre-mRNA analyses) of myosin heavy chain (MHC) and actin. In addition, there was an increased gene expression of enzyme systems impacting protein degradation (calpain-1; plus enzymes associated with polyubquitination processes) that could further contribute to the protein deficits in the SI muscles via degradative pathways. IGF-I receptor and binding protein-5 mRNA expression was induced throughout the 15-day period of SI, whereas IGF-I mRNA was induced at 8 and 15 days. These responses occurred in the absence of an upregulation of translational regulatory proteins (p70 S6 kinase; eukaryotic 4E binding protein 1) to compensate for the decreased protein translational capacity. These data collectively demonstrate that 1). the molecular changes accompanying SI-induced muscle atrophy are not necessarily the reverse of those occurring during muscle hypertrophy, and 2). the rapid and marked atrophy that defines this model of muscle inactivity is likely the result of multifactorial processes affecting transcription, translation, and protein degradation.

Actins↗
PubMed2003

A chapter in emergency: a surgical trainee's experience.

OBJECTIVES: To assess (1) the exposure a senior house officer (SHO) gains while training in accident and emergency (A&E) and (2) how much this experience benefits a surgical trainee. METHODS: An SHO trained in A&E for a period of six months as part of his surgical rotation. Besides regular daily duties, he prospectively collected details of patients in a logbook. For each patient records of name, age, sex, address, presenting symptoms, specialty, and treatment outcome were noted. Also recorded were courses attended, certificates achieved, and audits performed during this period. RESULTS: A total of 1249 patients were seen during this period. This included 423 (33%) medical, 374 (30%) orthopaedic/trauma, and 268 (21%) paediatric cases. Some 153 (12%) were surgical, 55 urology, 41 patients presented with "pain" symptoms in different body regions (excluding abdominal pains), and 120 patients included all other specialties (psychiatry, ENT, ophthalmology, dental, gynaecology). Twenty (1.6%) practical procedures were performed. The SHO attended two courses (ATLS, ALS), achieved two certificates, and was involved in two audits. CONCLUSIONS: Wide exposure in all specialties and branches of medicine including internal medicine, orthopaedics and trauma, paediatrics, and surgery was gained. As a surgical trainee, training in A&E did not provide hands on practical experience, but was useful in contributing towards general clinical skills.

Adolescent↗
PubMed2002

Transcriptional regulation of the type I myosin heavy chain gene in denervated rat soleus.

Denervation (DEN) of rat soleus is associated with a decreased expression of slow type I myosin heavy chain (MHC) and an increased expression of the faster MHC isoforms. The molecular mechanisms behind these shifts remain unclear. We first investigated endogenous transcriptional activity of the type I MHC gene in normal and denervated soleus muscles via pre-mRNA analysis. Our results suggest that the type I MHC gene is regulated via transcriptional processes in the denervated soleus. Deletion and mutational analysis of the rat type I MHC promoter was then used to identify cis elements or regions of the promoter involved in this response. DEN significantly decreased in vivo activity of the -3,500, -2,500, -914, -408, -299, and -215 bp type I MHC promoters, relative to the alpha-skeletal actin promoter. In contrast, normalized -171 promoter activity was unchanged. Mutation of the betae3 element (-214/-190) in the -215 promoter and deletion of this element (-171 promoter) blunted type I downregulation with DEN. In contrast, betae3 mutation in the -408 promoters was not effective in attenuating the DEN response, suggesting the existence of additional DEN-responsive sites between -408 and -215. Western blotting and gel mobility supershift assays demonstrated decreased expression and DNA binding of transcription enhancer factor 1 (TEF-1) with DEN, suggesting that this decrease may contribute to type I MHC downregulation in denervated muscle.

Animals↗
PubMed2002

[Comparison of nicardipine and isradipine in hypertension following coronary artery bypass graft].

OBJECTIVE: Compare the efficacy of isradipine to that of nicardipine for the control of arterial hypertension following coronary artery bypass graft (CABG). STUDY DESIGN: Clinical prospective, randomised study. MATERIAL AND METHODS: 40 patients ASA II or III, mean age 66 +/- 8 years, scheduled for elective CABG were included. If the mean arterial pressure (MAP) was > or = 100 mmHg within the first six post operative hours, the patients were included and randomly attributed to either one of the 2 groups: Gr I (n = 20) received nicardipine, Gr II (n = 20) received isradipine in bolus then in continuous perfusion. HR, MAP, MPAP, CVP, PCWP, CI, SVRI, PVRI and SVI were recorded at: T0 before administration of drugs, T1 = 2 min after the first bolus. T2 when MAP reached 85 +/- 5 mmHg. T3, T4, T5, T6, T7 and T8 at 5, 10, 30, 60, 90 and 120 min after the continuous perfusion. T9 before stopping the perfusion. RESULTS: No significant changes in HR, CVP, PCWP, MPAP or PVRI at any time in both groups. Significant increase in CI at T2 in both groups. Reduction of MAP at T2 was more important (-27%) in Gr I compared to that in Gr II (-22%). This was mainly due to a significant decrease in SVRI. CONCLUSION: Isradipine is effective in the treatment of arterial hypertension following CABG. However there is not any significant beneficial effect of isradipine over nicardipine.

Aged↗