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N McKee

Publications and source records attributed to N McKee.

12 recordsLinked to original sources
PubMed2001

Effects of ischemia on sarcoplasmic reticulum Ca(2+) uptake and Ca(2+) release in rat skeletal muscle.

In this study, we investigated the hypothesis that prolonged ischemia would impair both sarcoplasmic reticulum (SR) Ca(2+) uptake and Ca(2+) release in skeletal muscle. To induce total ischemia (I), a tourniquet was placed around the upper hindlimb in 30 female Sprague-Dawley rats [wt = 256 +/- 6.7 (SE) g] and inflated to 350 mmHg for 4 h. The contralateral limb served as control (C). Immediately after the 4 h of ischemia, mixed gastrocnemius and tibialis anterior muscle was sampled from both limbs, and both crude muscle homogenates and SR vesicles were prepared. In another 10 control animals (CC), muscles were sampled and prepared exactly the same way, but immediately after anesthetization. Ca(2+) uptake and Ca(2+) release were measured in vitro with Indo-I on both homogenates and SR vesicles. As hypothesized, submaximal Ca(2+) uptake was lower (P < 0.05) in I compared with CC and C, by 25 and 45% in homogenates and SR vesicles, respectively. Silver nitrate (AgNO(3))-induced Ca(2+) release, which occurred in two phases (phase 1 and phase 2), was also altered in I compared with CC and C, in both muscle homogenates and SR vesicles. With ischemia, phase 1 peak Ca(2+) release was 26% lower (P < 0.05) in SR vesicles only. For phase 2, peak Ca(2+) release was 54 and 24% lower (P < 0.05) in SR vesicles and homogenates, respectively. These results demonstrate that prolonged skeletal muscle ischemia leads to a reduced SR Ca(2+) uptake in both homogenates and SR vesicles. The effects of ischemia on SR Ca(2+) release, however, depend on both the phase examined and the type of tissue preparation.

Adenosine Triphosphate↗
PubMed2001

Effects of 4-h ischemia and 1-h reperfusion on rat muscle sarcoplasmic reticulum function.

To investigate the hypothesis that ischemia and reperfusion would impair sarcoplasmic reticulum (SR) Ca(2+) regulation in skeletal muscle, Sprague-Dawley rats (n = 20) weighing 290 +/- 3.5 g were randomly assigned to either a control control (CC) group, in which only the effects of anesthetization were studied, or to a group in which the muscles in one hindlimb were made ischemic for 4 h and allowed to recover for 1 h (I). The nonischemic, contralateral muscles served as control (C). Measurements of Ca(2+)-ATPase properties in homogenates and SR vesicles, in mixed gastrocnemius and tibialis anterior muscles, indicated no differences between groups on maximal activity, the Hill coefficient, and Ca(50), defined as the Ca(2+) concentration needed to elicit 50% of maximal activity. In homogenates, Ca(2+) uptake was lower (P < 0.05) by 20-25%, measured at 0.5 and 1.0 microM of free Ca(2+) ([Ca(2+)](f)) in C compared with CC. In SR vesicles, Ca(2+) uptake was lower (P < 0.05) by 30-38% in I compared with CC at [Ca(2+)](f) between 0.5 and 1.5 microM. Silver nitrate induced Ca(2+) release, assessed during both the initial, early rapid (phase 1), and slower, prolonged late (phase 2) phases, in homogenates and SR vesicles, indicated a higher (P < 0.05) release only in phase 1 in SR vesicles in I compared with CC. These results indicate that the alterations in SR Ca(2+) regulation, previously observed after prolonged ischemia by our group, are reversed within 1 h of reperfusion. However, the lower Ca(2+) uptake observed in long-term, nonischemic homogenates suggests that altered regulation may occur in the absence of ischemia.

Animals↗
PubMed2001

Ischemia-induced structural change in SR Ca2+-ATPase is associated with reduced enzyme activity in rat muscle.

In this study, we employed an in vivo model of prolonged ischemia in rat skeletal muscle to investigate the hypothesis that structural modifications to the sarcoplasmic reticulum (SR) Ca2+-ATPase can explain the alterations in Ca2+-ATPase activity that occur with ischemia. To induce total ischemia, a tourniquet was placed around the upper hindlimb in 27 female Sprague-Dawley rats weighing 256 +/- 6.7 g (mean +/- SE) and was inflated to 350 mmHg for 4 h. The contralateral limb served as control (C) to the ischemic limb (I), and the limbs of animals killed immediately after anesthetization served as a double control (CC). Mixed gastrocnemius and tibialis anterior muscles were sampled and used for SR vesicle preparation. Maximal Ca2+-ATPase activity (micromol x g protein(-1) x min(-1)) of C (15,802 +/- 1,246) and I (11,609 +/- 1,029) was 90 and 73% (P < 0.05) of CC (17,562 +/- 1,682), respectively. No differences were found between groups in either the Hill coefficient or the free Ca2+ at half-maximal activity. The fluorescent probes, FITC and N-cyclohexyl-N'-(dimethylamino-alpha-naphthyl) carbodiimide, used to assess structural alterations in the regions of the ATP binding site and the Ca2+ binding sites of the Ca2+-ATPase, respectively, indicated a 26% reduction (P < 0.05) in FITC binding capacity (absolute units) in I (0.22 +/- 0.01) compared with CC (0.29 +/- 0.02) and C (0.29 +/- 0.03). Our results suggest that the reduction in maximal SR Ca2+-ATPase activity in SR vesicles with ischemia is related to structural modification in the region of the nucleotide binding domain by mechanisms that are as yet unclear.

Animals↗
PubMed2000

Compartment syndrome following intravenous regional anesthesia.

PURPOSE: To present two cases of upper extremity compartment syndrome following intravenous regional anesthesia. CLINICAL FEATURES: Case 1: A 57-yr-old man presented for surgical release of a left-hand Dupuytren's contracture. The procedure was performed under iv regional anesthesia with 360 mg lidocaine and sedation with 150 microg fentanyl and 1.5 mg midazolam. Tourniquet time was 107 min at a pressure of 260 mmHg using three different tourniquet sites. Within minutes of tourniquet release, increased forearm muscle tension, hand anesthesia, pallor, and limited motor function developed. Serum CK and myoglobin levels rose. Myoglobinuria was present. Several fasciotomies and aggressive fluid therapy were performed. Patient made almost full recovery. Case 2: A 73-yr-old woman with controlled hypertension had Dupuytren fasciotomy of her right hand under iv regional anesthesia with 200 mg lidocaine and sedation using 75 microg fentanyl and 1.5 mg midazolam. Tourniquet time was 64 min at a pressure of 250 mmHg using three different tourniquet sites. The patient complained of pain at the iv site during injection of local anesthetic, third tourniquet inflation and after deflation of tourniquet. Thirty minutes after arrival in PACU, her fingers were bluish. She complained of pain and swelling of the forearm. Under general anesthesia, fasciectomy was performed. Myoglobin and CPK levels rose. CPK MB was high but troponin was negative. Three days later she developed pulmonary embolism. She was heparinized and subsequently discharged home. She recovered completely. CONCLUSION: Compartment syndrome may have a rapid and severe onset. Etiology of our cases is still not established. We postulate that increased tissue pressure may be the cause. The anesthesiologists must be aware of compartment syndrome during regional anesthesia.

Aged↗
PubMed1999

Methods for creating and animating a computer model depicting the structure and function of the sarcoplasmic reticulum calcium ATPase enzyme.

This paper describes the developmental process used to visualize the calcium ATPase enzyme of the sarcoplasmic reticulum. The steps involved were evaluating scientific information, consulting with scientists, model making, storyboarding, and creating and editing in a computer medium. The product was a computer-generated animation depicting the relationship between the structure and function of the sarcoplasmic reticulum calcium ATPase enzyme.

Calcium-Transporting ATPases↗
PubMed1994

Soft-tissue expansion before total knee arthroplasty in arthrodesed joints. A report of two cases.

We report two cases in which arthrodesed knees were revised to total arthroplasties after the use of soft-tissue expanders. Case 1 had had multiple operations on her knee and had been arthrodesed for septic arthritis two years earlier. Case 2 had had knee arthrodesis for severe osteoarthritis 18 years before revision. In both patients, tissue expanders were used to increase the soft tissues available for cover and to help to mobilise the extensor mechanism. The operations were made much easier, and in both patients a range of motion from 0 degrees to 90 degrees was achieved at operation.

Adult↗
PubMed1992

The peripheral nerve allograft in the primate immunosuppressed with Cyclosporin A: II. Functional evaluation of reinnervated muscle.

Isometric contractile function was evaluated in primates receiving peripheral nerve allografts and autografts. Twelve adult male cynomolgus monkeys received both sural nerve allografts and autografts to the ulnar nerve in opposite forearms. Half the animals received Cyclosporin A (CsA) immunosuppression (25 mg/kg per day); the remaining animals received placebo. One year following nerve engraftment, isometric contractile muscle function was evaluated in reinnervated abductor digiti quinti and intact abductor pollicis brevis muscles. Maximal twitch tension (Pt), tetanic tension (P(o)), time to peak tension (tpt), rate of rise of twitch tension (DP/dt), and muscle fatigue were evaluated at optimal muscle length (L(o)). All reinnervated muscles distal to nerve autografts and allografts in both Cyclosporin A-immunosuppressed and placebo-treated animals generated equivalent maximal twitch tension, tetanic tension, and time to peak tension, with no significant difference between groups (p > 0.05 by ANOVA). There was a tendency toward increased muscle fatiguability in Cyclosporin A-treated animals (p > 0.05). However, the rate of rise of twitch tension was significantly faster in the reinnervated and intact muscles of Cyclosporin A-treated primates (p < 0.05). Evidence of excellent functional reinnervation across nerve allografts and autografts similar to that seen in histologic and electrophysiologic studies was noted. Cyclosporin A immunosuppression did not significantly enhance recovery of muscle function distal to nerve allografts in this model.

Animals↗
PubMed1987

Repair of anorectal incontinence in an adolescent boy with neonatal anal atresia.

Fecal continence, the ability to retain intestinal contents until evacuation is desired, requires the complex interaction of several factors. They include: the motor action of the sphincters, sensibility of skin and sphincters and function of the rectum and central nervous pathways. Appropriate and effective management is available to treat many disorders of continence. However, the success of these treatments depends on careful delineation of the various contributing factors. The authors present the case of an 18-year-old boy with disabling fecal incontinence, secondary to neonatal anal atresia and its primary management, in order to illustrate the importance of careful assessment of each of the contributing factors. His staged surgical treatment has been successful in returning him to a more normal state.

Adolescent↗
PubMed1986

Metabolic response of skeletal muscle to ischemia.

To evaluate the temporal relationship and potential correlation between intramuscular phosphagen levels, lipid oxidation, and extent of muscle injury, a canine gracilis muscle model was used to study the consequences of a global ischemic episode for up to 7 h duration with reperfusion for 4 h. In this model the contralateral gracilis muscle was prepared identically to the test side but was not subjected to ischemia and thus served as a control. Blood flow, oxygen consumption, and lactate and glycerol release were measured before and after 2- and 7-h ischemic stress periods. The intramuscular metabolites, glycogen, lactate, phosphocreatine, and ATP, as well as free fatty acid conjugated dienes, were measured before, during, and after the ischemic insult. A 2-h ischemic insult resulted in minimal ultrastructural damage and complete regeneration of intramuscular phosphagens and glycogen on reperfusion with complete normalization of lipid oxidation products. In contrast, a 7-h ischemic insult resulted in profound injury at the ultrastructural level with an inability to restore intramuscular phosphagens and glycogen on reperfusion. This severe muscle injury correlated with a 2.5-fold increase in lipid oxidation products (free fatty acid conjugated dienes) and a decline in ATP levels below 5 mumol/g dry wt on reperfusion. Our results emphasize the prolonged glycolytic activity of skeletal muscle during global ischemia and document the increased production of oxygen free radical-mediated lipid oxidation products in irreversibly injured muscle.

Adenosine Triphosphate↗
PubMed1986

Bone and cartilage allotransplantation. A review of 14 years of research and clinical studies.

The authors review their experience of over 14 years in the field of osteochondral allotransplantation. Experimental studies demonstrated the immunogenicity of bone and cartilage, immunosuppression in skeletal transplantation models, and a subset of myeloid cells within bone marrow with strong immunogenic properties. Clinical results of knee joint resurfacing with fresh small-fragment osteochondral allografts have been best in posttraumatic joints. Experience with allograft reconstructions of skeletal defects after tumor surgery has been gratifying as a limb salvage procedure. Microvascular fibular autografts have been an important adjunct in massive reconstructive osteochondral transplantation.

Animals↗