Biomedical subjects

R M McAllister

Publications and source records attributed to R M McAllister.

At least 19 recordsLinked to original sources

PubMed2003

Effects of hypothyroidism on the skeletal muscle blood flow response to contractions.

Hypothyroidism is associated with impaired blood flow to skeletal muscle under whole body exercise conditions. It is unclear whether poor cardiac and/or vascular function account for blunted muscle blood flow. Our experiment isolated a small group of hindlimb muscles and simulated exercise via tetanic contractions. We hypothesized that muscle blood flow would be attenuated in hypothyroid rats (HYPO) compared with euthyroid rats (EUT). Rats were made hypothyroid by mixing propylthiouracil in their drinking water (2.35 x 10-3 mol/l). Treatment efficacy was evidenced by lower serum T3 concentrations and resting heart rates in HYPO (both P<0.05). In the experimental preparation, isometric contractions of the lower right hindlimb muscles at a rate of 30 tetani/min were induced via sciatic nerve stimulation. Regional blood flows were determined by the radiolabelled microsphere method at three time points: rest, 2 min of contractions and 10 min of contractions. Muscle blood flow generally increased from rest ( approximately 5-10 ml/min per 100 g) through contractions for both groups. Further, blood flow during contractions did not differ between groups for any muscle (eg. red section of gastrocnemius muscle; EUT, 59.9 +/- 14.1; HYPO, 61.1 +/- 15.0; NS between groups). These findings indicate that hypothyroidism does not significantly impair skeletal muscle blood flow when only a small muscle mass is contracting. Our findings suggest that impaired blood flow under whole body exercise is accounted for by inadequate cardiac function rather than abnormal vascular function.

Animals↗

PubMed2001

Skeletal muscle oxidative capacity and exercise tolerance in rats with heart failure.

PURPOSE: Past research has shown the development of exercise intolerance after myocardial infarction (MI). The purpose of this study was to test the hypothesis that reductions in oxidative enzyme activity, in a variety of skeletal muscles, coincide with the development of exercise intolerance in a rat model of chronic heart failure (CHF) induced by MI. METHODS: The animals were initially divided into two groups: sham-operated controls (Sham) and animals in which a MI was surgically induced. MI rats were then subdivided into two groups according to left ventricular end-diastolic pressure (LVEDP): <20 mm Hg [small MI (SMI)] and > 20 mm Hg [large MI (LMI)]. Exercise tolerance was measured by performing a progressive run to fatigue test (RTF). Citrate synthase (CS), 3-hydroxyacyl CoA dehydrogenase (HADH), and malate dehydrogenase (MDH) activities were measured in six hindlimb muscles. RESULTS: After approximately 6 wk of recovery, LVEDP differed among groups (P < 0.05): Sham (1 +/- 1 mm Hg, N = 7), SMI (7 +/- 2 mm Hg, N = 7), and LMI (30 +/- 2 mm Hg, N = 6). RTF was 20 +/- 1 min for Sham, 25 +/- 3 min for SMI, and 11 +/- 2 min for LMI (P < 0.05 for LMI vs Sham, SMI). Significant reductions in enzyme activity were found for all three enzymes in the red portion of the gastrocnemius muscles of LMI. However, no significant correlation was found between RTF and CS, HADH, or MDH in any muscle of the three groups of animals. DISCUSSION: The results of the present study demonstrate that severe left ventricular dysfunction is associated with reductions in exercise tolerance and modest decreases in oxidative enzyme activities in selected muscles. It does not appear, however, that the development of exercise intolerance in CHF and oxidative enzyme activities are mechanistically related to one another.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2001

Effects of nitric oxide synthase inhibition on vascular conductance during high speed treadmill exercise in rats.

To determine the functional role of nitric oxide (NO) in regulating vascular conductance during high intensity dynamic exercise in skeletal muscles composed of all major fibre types, female Wistar rats (277 +/- 4 g; n = 7) were run on a motor-driven treadmill at a speed and gradient (60 m min(-1), 10 % gradient) established to yield maximal oxygen uptake (V(O2,max)). Vascular conductance (ml min(-1) (100 g)(-1) mmHg(-1)), defined as blood flow normalised to mean arterial pressure (MAP), was determined using radiolabelled microspheres during exercise before and after NO synthase (NOS) inhibition with N (G)-nitro-L-arginine methyl ester (L-NAME; 10 mg kg(-1), I.A.). The administration of L-NAME increased MAP from pre-L-NAME baseline values, demonstrating that NOS activity is reduced. The administration of L-NAME also reduced vascular conductance in 20 of the 28 individual hindlimb muscles or muscle parts examined during high speed treadmill exercise. These reductions in vascular conductance correlated linearly with the estimated sum of the percentage of slow twitch oxidative (SO) and fast twitch oxidative glycolytic (FOG) types of fibres in each muscle (Deltaconductance = -0.0082(%SO + %FOG) - 0.0105; r = 0.66; P < 0.001). However, if the reduction in vascular conductance found in the individual hindquarter muscles or muscle parts was expressed as a percentage decrease from the pre-L-NAME value (%Delta = (pre-L-NAME conductance - post-L-NAME conductance)/ pre-L-NAME conductance x 100), then the reduction in vascular conductance was similar in all muscles examined (average %Delta = -23 +/- 2 %). These results suggest that NO contributes substantially to the regulation of vascular conductance within and among muscles of the rat hindquarter during high intensity exercise. When expressed in absolute terms, the results suggest that the contribution of NO to the regulation of vascular conductance during high intensity exercise is greater in muscles that possess a high oxidative capacity. In contrast, if results are expressed in relative terms, then the contribution of NO to the regulation of vascular conductance during high intensity exercise is similar across the different locomotor muscles located in the rat hindlimb and independent of the fibre type composition.

Animals↗

PubMed2001

Thyroid status influences baroreflex function and autonomic contributions to arterial pressure and heart rate.

The effect of thyroid status on arterial baroreflex function and autonomic contributions to resting blood pressure and heart rate (HR) were evaluated in conscious rats. Rats were rendered hyperthyroid (Hyper) or hypothyroid (Hypo) with triiodothyronine and propylthiouracil treatments, respectively. Euthyroid (Eut), Hyper, and Hypo rats were chronically instrumented to measure mean arterial pressure (MAP), HR, and lumbar sympathetic nerve activity (LSNA). Baroreflex function was evaluated with the use of a logistic function that relates LSNA or HR to MAP during infusion of phenylephrine and sodium nitroprusside. Contributions of the autonomic nervous system to resting MAP and HR were assessed by blocking autonomic outflow with trimethaphan. In Hypo rats, the arterial baroreflex curve for both LSNA and HR was shifted downward. Hypo animals exhibited blunted sympathoexcitatory and tachycardic responses to decreases in MAP. Furthermore, the data suggest that in Hypo rats, the sympathetic influence on HR was predominant and the autonomic contribution to resting MAP was greater than in Eut rats. In Hyper rats, arterial baroreflex function generally was similar to that in Eut rats. The autonomic contribution to resting MAP was not different between Hyper and Eut rats, but predominant parasympathetic influence on HR was exhibited in Hyper rats. The results demonstrate baroreflex control of LSNA and HR is attenuated in Hypo but not Hyper rats. Thyroid status alters the balance of sympathetic to parasympathetic tone in the heart, and the Hypo state increases the autonomic contributions to resting blood pressure.

Animals↗

PubMed2001

Interaction of gender and exercise training: vasomotor reactivity of porcine skeletal muscle arteries.

The purpose of the present study was to test the hypothesis that gender influences exercise training-induced adaptations of vascular reactivity of porcine arteries that provide blood flow to skeletal muscle and femoral and brachial arteries. Male and female Yucatan miniature swine were exercise trained on a motor-driven treadmill or cage confined for 16-20 wk. Contractile responses of arterial rings were evaluated in vitro by determining concentration-response curves for endothelin-1 (ET-1; 10(-10) to 10(-7) M) and norepinephrine (NE; 10(-10) to 10(-4) M). Relaxation responses of arteries precontracted with 30 microM PGF(2alpha) were examined for endothelium-dependent agents [bradykinin (BK; 10(-11) to 10(-6) M), ACh (10(-10) to 10(-4) M), and a Ca(2+) ionophore, A-23187 (10(-6) M)] and a endothelium-independent agent [sodium nitroprusside (10(-10) to 10(-4) M)]. Arteries from female pigs developed greater contractile force in response to ET-1 than arteries from male pigs, whereas contractile responses to NE and KCl were similar in arteries from both genders. Femoral arteries from females exhibited greater endothelium-mediated vasorelaxation (BK and ACh) than did those from males. In contrast, brachial arteries of males were more responsive to BK and ACh than brachial arteries of females. Exercise training increased ET-1-induced contractions in arteries from males (without endothelium) but not in arteries from females. Training had no effect on endothelium-dependent relaxation in arteries from males but increased relaxation responses in brachial arteries from females. We conclude that both gender and anatomic origin of the artery influence exercise training-induced adaptations of vascular reactivity of porcine skeletal muscle conduit arteries.

Animals↗

PubMed2000

Thyroid status and response to endothelin-1 in rat arterial vessels.

We have previously reported that changes in thyroid status are associated with significant alterations in skeletal muscle blood flow during exercise and that changes in endothelium-dependent vasodilation may contribute to these blood flow abnormalities. The purpose of this study was to test the hypothesis that altered endothelium-dependent vasoconstriction is also associated with changes in thyroid status. To test this hypothesis, rats were rendered hypothyroid with propylthiouracil (Hypo, n = 14) or hyperthyroid with triiodothyronine (Hyper, n = 14) over approximately 3 mo. Treatment efficacy was confirmed by altered (P < 0.05) citrate synthase activity in several hindlimb skeletal muscles from Hypo and Hyper, compared with that in muscles from euthyroid rats (Eut, n = 12). Vascular rings were prepared from abdominal aortae, and responses to several vasoactive agents were determined in vitro. As found previously, maximal acetylcholine-induced vasorelaxation was modulated by thyroid status (Eut, 47 +/- 9; Hypo, 28 +/- 6; Hyper, 68 +/- 5%; P < 0.05). Contractile responses of vascular rings with intact endothelium to the endothelium-derived constrictor endothelin-1 (ET-1), however, were similar among groups across a range of ET-1 concentrations. In addition, maximal responses [Eut, 3.75 +/- 0.47; Hypo, 2.72 +/- 0.25; Hyper, 3.22 +/- 0.42 g; not significant (NS)] and sensitivities (Eut, 8.12 +/- 0.09; Hypo, 8.10 +/- 0.06; Hyper, 8.28 +/- 0.09 -log M; NS) to ET-1 were similar among groups. If these findings from the conduit-type abdominal aorta extend into resistance vasculature, it appears that changes in endothelium-dependent vasoconstriction do not contribute to skeletal muscle blood flow abnormalities associated with thyroid disease states.

Acetylcholine↗

PubMed1998

Evidence for immune system involvement in reflex sympathetic dystrophy.

Skin biopsies from patients with reflex sympathetic dystrophy were immunostained using a variety of antisera. An incidental finding with S100 staining was the presence of numerous Langerhans cells in the epidermis. All patients had significant pain at the time of biopsy, and all had symptoms refractory to treatment. The potential implications of this finding are discussed.

Adult↗

PubMed1998

Acetylcholine is a vasodilator of porcine skeletal muscle arteries.

The purpose of this study was to test the hypothesis that porcine skeletal muscle arteries exhibit concentration-dependent vasodilation in response to acetylcholine (ACH) as observed in other mammals. We conducted three experiments. First, vasorelaxation responses to ACH were examined in isolated segments of femoral and brachial arteries, mounted on myographs and studied in vitro. Second, we determined whether resistance arteries from porcine skeletal muscle exhibit vasodilation in response to ACH by isolating second order arterioles (2-A) from the medial (MHT), deep-long (LOH) and lateral (LAT) heads of the triceps brachii muscles of four pigs. The rationale for selection of arterioles from these muscles was that these muscles represent muscles composed primarily of slow-oxidative, fast-oxidative-glycolytic, and fast-glycolytic muscle fiber types, respectively. 2-As were isolated and cannulated with micropipettes and intraluminal pressure set at 60 cm H2O. In both sets of in vitro experiments, we determined responses to an endothelium-independent dilator, sodium nitroprusside (10(-10)-10(-4) M), and to endothelium-dependent agents ACH (10(-10)-10(-4) M), and bradykinin (BK; 10(-11)-10(-6) M). Third, we used transcutaneous ultrasound imaging to measure changes in artery diameters and Doppler-principle measurements of blood flow velocities to estimate changes in total blood flow in the femoral vascular bed. Results reveal that ACH and BK produced similar vasorelaxation responses in femoral and brachial arteries and vasodilation of skeletal muscle 2-As. Also, ACH produced increases in blood flow and decreases in vascular resistance in the femoral vascular bed. These results indicate that the arterial tree of porcine skeletal muscle exhibits ACH-induced, endothelium-dependent vasodilation.

Acetylcholine↗

PubMed1998

Adaptations in control of blood flow with training: splanchnic and renal blood flows.

Acute exercise is associated with large increases in cardiac and active skeletal muscle blood flows and reduced blood flows to inactive muscle, skin, kidneys, and organs served by the splanchnic circulation. Splanchnic and renal blood flows are reduced in proportion to relative exercise intensity. Increased sympathetic nervous system outflow to splanchnic and renal vasculature appears to be the primary mediator of reduced blood flows in these circulations, but the vasoconstrictors angiotensin II and vasopressin also make important contributions. Human and animal studies have shown that splanchnic and renal blood flows are reduced less from resting levels during acute exercise after a period of endurance exercise training. Investigations of mechanisms involved in these adaptations suggest that reductions in sympathetic nervous system outflow, and plasma angiotensin II and vasopressin concentrations, are involved in lesser splanchnic and renal vasoconstriction exhibited by trained individuals. In addition, a reduced response to the sympathetic neurotransmitter norepinephrine in renal vasculature may contribute to greater blood flow to the kidney during acute exercise after training. Greater splanchnic and renal blood flows during acute exercise following training are potentially beneficial in that disturbance from homeostasis would be less in the trained state. Additionally, increased splanchnic blood flow in the trained state may confer benefits for glucose metabolism during prolonged exercise.

Adaptation, Physiological↗

PubMed1998

Effects of hyperthyroidism on vascular contractile and relaxation responses.

Previous research has shown that skeletal muscle blood flow, at rest and during muscular contractions, is elevated in the hyperthyroid state. We hypothesized that reduced vascular contractile and enhanced endothelium-dependent relaxation responses contribute to these observations. To test these hypotheses, male rats were administered triiodothyronine (Hyper, n = 27; 300 micrograms/kg) for 6-12 wk. Compared with euthyroid control rats (Eut, n = 27), Hyper exhibited left ventricular hypertrophy (Eut, 2.01 +/- 0.04 mg/g body wt; Hyper, 2.70 +/- 0.06; P < 0.0005) and greater oxidative enzyme activity in several skeletal muscles (all P < 0.0005). Vascular rings, 2-3 mm in axial length, were prepared from abdominal aortas, and responses to vasoactive agents were determined in vitro. Compared with Eut, vascular rings with intact endothelium from Hyper exhibited reductions in contractile responses to norepinephrine (NE) across a range of NE concentrations (P < 0.05). Maximal tension developed in response to NE was reduced approximately 30% in hyperthyroidism (Eut, 3.8 +/- 0.2 g; Hyper, 2.6 +/- 0.4; P < 0.01). Contractile responses to NE were not different between Eut and Hyper in rings denuded of endothelium. Maximal vasorelaxation responses to acetylcholine (ACh), after precontraction with NE (10(-7) M), were enhanced in the hyperthyroid state (Eut, 65.1 +/- 4.8%; Hyper, 84.0 +/- 7.1; P < 0.05). Enhanced vasorelaxation to ACh was also observed when precontraction was induced by prostaglandin F2 alpha. These findings indicate that vascular contractile and relaxation responses are altered in male hyperthyroid rats.

Acetylcholine↗

PubMed1997

A review of effects of hypothyroidism on vascular transport in skeletal muscle during exercise.

Hypothyroidism is a common thyroid disease characterized by exercise intolerance. Both exercise capacity and endurance are compromised in the hypothyroid state. Studies involving rats performing treadmill running have shown that blood flows during exercise to high oxidative, extensor-type muscles are lower in hypothyroid rats compared with those in euthyroid rats. Abnormal cardiac and vascular function appear to contribute to this hypoperfusion. Experiments involving isolated arterial vessel segments have demonstrated that potential for constriction is normal in vessels from hypothyroid animals; however, reduced vasodilator potential is associated with hypothyroidism. Dysfunction of both endothelium and vascular smooth muscle appear to contribute to blunted potential for vasodilation. Altered ability to generate vasodilatory substances and/or changes in responses to these vasodilators may account for vascular dysfunction. It appears that impaired vascular function interacts with other factors such as poor myocardial function and changes in energy metabolism to compromise exercise tolerance.

Animals↗

PubMed1997

Short-term exercise training alters responses of porcine femoral and brachial arteries.

The primary purpose of this study was to test the hypothesis that short-term exercise training enhances endothelium-dependent relaxation of porcine femoral and brachial arteries. Miniature swine ran on a treadmill for 1 h at 3.5 miles/h, twice daily, for 7 consecutive days (Trn; n = 8). Compared with sedentary controls (Sed; n = 7), Trn swine exhibited increased skeletal muscle citrate synthase activity (P < 0.05). Vascular rings approximately 3 mm in axial length were prepared from segments of femoral and brachial arteries, and responses to vasoactive agents were determined in vitro. Sensitivity to bradykinin (BK) was enhanced in brachial vascular rings from Trn swine compared with those from Sed swine, as indicated by lower concentration of vasorelaxing agent eliciting 50% of maximal response values [Sed, 8.63 +/- 0.09 (-log M); Trn, 9.07 +/- 0.13; P < 0.05]. This difference between groups was preserved in brachial rings in which formation of nitric oxide and vasodilator prostaglandins were inhibited [Sed, 8.57 +/- 0.17 (-log M); Trn, 8.97 +/- 0.13; P < 0.05]. Sensitivity to BK was not different between Sed and Trn in femoral arterial rings. Relaxation responses to the calcium ionophore A-23187 and sodium nitroprusside were not altered with training. Femoral and brachial arterial rings from Trn swine, compared with those from Sed swine, exhibited augmented vasocontraction across a range of concentrations and increased sensitivity to norepinephrine (all P < 0.05). These findings indicate that responses of porcine femoral and brachial arteries change in response to short-term training. Together with findings from previous studies involving longer term training, our data suggest that vascular adaptations may differ at different time points during long-term endurance exercise training.

Animals↗

PubMed1997

Skeletal muscle biochemical adaptations to exercise training in miniature swine.

The primary purpose of this study was to test the hypothesis that endurance exercise training induces increased oxidative capacity in porcine skeletal muscle. To test this hypothesis, female miniature swine were either trained by treadmill running 5 days/wk over 16-20 wk (Trn; n = 35) or pen confined (Sed; n = 33). Myocardial hypertrophy, lower heart rates during submaximal stages of a maximal treadmill running test, and increased running time to exhaustion during that test were indicative of training efficacy. A variety of skeletal muscles were sampled and subsequently assayed for the enzymes citrate synthase (CS), 3-hydroxyacyl-CoA dehydrogenase, and lactate dehydrogenase and for antioxidant enzymes. Fiber type composition of a representative muscle was also determined histochemically. The largest increase in CS activity (62%) was found in the gluteus maximus muscle (Sed, 14.7 +/- 1.1 mumol.min-1.g-1; Trn, 23.9 +/- 1.0; P < 0.0005). Muscles exhibiting increased CS activity, however, were located primarily in the forelimb; ankle and knee extensor and respiratory muscles were unchanged with training. Only two muscles exhibited higher 3-hydroxyacyl-CoA dehydrogenase activity in Trn compared with Sed. Lactate dehydrogenase activity was unchanged with training, as were activities of antioxidant enzymes. Histochemical analysis of the triceps brachii muscle (long head) revealed lower type IIB fiber numbers in Trn (Sed, 42 +/- 6%; Trn, 10 +/- 4; P < 0.01) and greater type IID/X fiber numbers (Sed, 11 +/- 2; Trn, 22 +/- 3; P < 0.025). These findings indicate that porcine skeletal muscle adapts to endurance exercise training in a manner similar to muscle of humans and other animal models, with increased oxidative capacity. Specific muscles exhibiting these adaptations, however, differ between the miniature swine and other species.

Adaptation, Physiological↗

PubMed1996

The epidemiology and management of upper limb peripheral nerve injuries in modern practice.

This paper reports an epidemiological and clinical study of 813 patients with 1,111 peripheral nerve injuries who were treated for upper limb trauma, which included nerve injury, at two plastic surgery units in south-east England, predominantly between the years 1982 and 1991. The frequency distributions of the levels of nerve injury, and the causes of nerve injury in the sample, are presented, together with the surgical management and timing of nerve repair in these patients. 1,018 clinically suspected nerve injuries in 730 patients (91.6% of nerves, 89.8% of patients) were treated by primary nerve repair, elective delayed nerve repair or primary surgical exploration alone. Divisions of 93 nerves in 83 patients (8.3% of nerves, 10.2% of patients) were treated other than by primary repair or elective delayed repair, due to delayed referral from accident and emergency departments, resulting from missed or uncertain diagnosis at presentation or otherwise unaccounted delay in the initial referral.

Adolescent↗

PubMed1996

Effects of exercise training on responses of peripheral and visceral arteries in swine.

Blood flow to skeletal muscle during exercise is greater in the trained state. We hypothesized that intrinsic vasomotor reactivity of arteries to active muscle during training bouts would be altered to favor a relative vasodilation after training. To test this hypothesis, miniature swine were pen confined (Sed; n = 30) or treadmill trained for 5 days/wk over 16-20 wk (Trn; n = 32). Efficacy of training was indicated by myocardial hypertrophy (4.84 +/- 0.11 and 5.81 +/- 0.12 g/kg body wt for Sed and Trn, respectively, P < 0.0005), training bradycardia at several submaximal running speeds of a maximal exercise test, increased running time to exhaustion (26 +/- 1 and 35 +/- 1 min for Sed and Trn, respectively, P < 0.0005), and increased oxidative capacities of several locomotory skeletal muscles. Segments of femoral, brachial, mesenteric, renal, and hepatic arteries were isolated from Sed and Trn swine. Isometric contractile and relaxation properties of vascular rings cut from these segments were determined in vitro. Contractile responses to KCl and norepinephrine (NE) were determined, as were relaxation responses to sodium nitroprusside and adenosine, agents acting directly on vascular smooth muscle, and the endothelium-dependent agents bradykinin and the calcium ionophore A-23187. Responses to vasocontractile and vasorelaxation agents were not different between Sed and Trn swine for vessels serving active muscles (i.e., femoral, brachial). On the other hand, renal arterial rings from Trn swine exhibited lesser contractile responses than those from Sed swine across a range of NE concentrations (P < 0.05) and approximately 25% less maximal contractile response to NE (32.7 +/- 2.6 and 24.2 +/- 2.1 g for Sed and Trn, respectively, P < 0.01). Responses of other vessels serving viscera (i.e., mesenteric, hepatic) were unchanged with training. These data indicate that vasomotor reactivity of porcine conduit-type arteries generally does not change with exercise training. An exception is the lesser contractile response to NE in renal artery, which could permit better preservation of renal blood flow during acute exercise in trained animals.

Animals↗

PubMed1996

Endothelium-medicated control of the coronary circulation. Exercise training-induced vascular adaptations.

This review discusses the role of the endothelium in the regulation of coronary vascular function. The role of endothelium-mediated mechanisms at rest, during exercise, in exercise training-induced adaptations of coronary function and in the presence of coronary heart disease (CHD) are examined. Mechanisms of control of coronary blood flow are briefly discussed with emphasis on endothelium-mediated control of vascular resistance. The concept that the relative importance of vascular control mechanisms differs as a function of position along the coronary arterial tree is developed and discussed. Metabolic, myogenic and endothelium-mediated control systems contribute in parallel to regulating coronary blood flow. The relative importance of these mechanisms varies throughout the coronary arterial tree. Endothelium-dependent vasodilation contributes to maintenance of resting coronary blood flow but the endothelium's role in dilation of small resistance arteries, thereby increasing coronary blood flow during exercise, remains in question. In contrast, the endothelium plays an essential role in dilation of the conduit coronary arteries during exercise. Atherosclerosis and CHD convert this exercise-induced dilation to a vasoconstriction, apparently due to endothelium dysfunction. Long term increases in physical activity and exercise training alter the control of coronary blood flow. Adaptations in endothelium-mediated control play a role in these changes. However, the effects of the mode, frequency, and intensity of exercise training bouts and duration of training on adaptive changes in endothelial function have not been established. The role of the endothelium in control of the permeability characteristics of the exchange vessels in the coronary circulation is discussed. Current evidence indicates that vascular permeability is a dynamic characteristic of the vessel wall that is controlled, at least in part, by endothelium-dependent phenomena. Also, preliminary results indicate that exercise training alters microvessel permeability and the control of permeability in the coronary circulation. Further research is needed to provide clarification of the effects of exercise training on coronary endothelial control of vascular resistance and vascular permeability in atherosclerosis and CHD.

Adaptation, Physiological↗

PubMed1995

Paradoxical clinical consequences of peripheral nerve injury: conduction of nerve impulses does not occur across the site of injury immediately following nerve division and repair.

The occasional apparent clinical phenomenon of the immediate although transient return of peripheral nerve function after nerve division and primary repair has been previously reported. Electrophysiological findings from the sciatic nerve of the rabbit have been previously presented in support of the concept of the transmission of nerve impulses across a freshly divided and repaired peripheral nerve for a short period until the onset of Wallerian degeneration. This paper presents experimental evidence to show that these findings were misinterpreted and that a compound action potential cannot be transmitted across a surgically repaired division in a peripheral nerve. Observations from previous experimental research in neurophysiology are discussed which confirm these conclusions. The claim that failure to diagnose a peripheral nerve injury at presentation can be explained in some circumstances by "jump transmission" is not based on sound evidence and the concept of "jump transmission" cannot be accepted as a defence for clinicians who fail to diagnose a peripheral nerve injury.

Action Potentials↗

PubMed1995

Paradoxical clinical consequences of peripheral nerve injury: a review of anatomical, neurophysiological and psychological mechanisms.

This paper reviews some of the possible explanations and mechanisms that may be responsible for variation from expected clinical findings soon after nerve injury in certain patients, and for subjective sensations and objective sensibility which can appear to arise from within the autonomous zone of the cutaneous distribution of a divided nerve. A number of features of peripheral innervation, central nervous system physiology and sensory psychology are discussed. These include: (1) the normal extent of overlap- or cross-innervation between the territories of adjacent peripheral nerves; (2) anomalous innervation due to normal anatomical variation; (3) ectopic impulse generation and cross-excitation between neurons in the peripheral nervous system after nerve injury; (4) neurophysiological responses and mechanisms of re-innervation other than axon regeneration across the site of nerve repair; (5) cortical somatotopic reorganisation in response to nerve injury; and (6) phantom sensory phenomena including the psychology of sensory perception.

Animals↗