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T J Ruigrok

Publications and source records attributed to T J Ruigrok.

At least 91 records · Page 5Linked to original sources
PubMed1985

Morphology of primary afferents to the spinal cord of the turtle Pseudemys scripta elegans.

The morphology of primary afferents to the spinal cord of the turtle Pseudemys scripta elegans was studied by means of intra-axonal injections of horseradish peroxidase. A total of 74 collaterals arising from 34 different afferents in 22 animals was investigated. Within this sample, a division into three morphologically distinct collateral types appeared possible. Collaterals of the same parent axon could always be classified to the same type. Type A collateral arborizations could be found within area I-II and III of the spinal grey matter. The number of presynaptic boutons per collateral varied considerably. However, collaterals of the same parent axon usually possessed a similar general appearance. Type B collaterals terminated within area IV and V-VI. The general shape and number of boutons could differ considerably between collaterals of different parent fibers but also between collaterals of the same axon. Type C collaterals formed terminal arborizations in the lateral parts of areas IV, V, VI and VII-VIII and demonstrated a fair constancy in general appearance and number of presynaptic boutons. Type A collaterals are thought to be derived from fibers innervating various cutaneous receptors. Terminal arborizations of type C collaterals are fully overlapping with the dorsal dendritic trees of turtle lumbar motoneurons. It is suggested that type C collaterals form contacts with these motoneurons and arise from muscle spindle innervating afferents. The origin of type B collaterals is less clear, attractive possibilities may be found in joint and/or tendon organs.

Afferent Pathways↗
PubMed1985

Sarcolemmal disruption during the calcium paradox.

Reperfusion of an isolated heart with calcium-containing solution after a short period of calcium-free perfusion may result in irreversible cell damage (calcium paradox). The ultrastructure of the sarcolemma of the rabbit heart during the calcium paradox was studied by using fast freezing devices. This method excluded ultrastructural changes induced by chemical fixation and cryoprotection. In addition, thin-section and conventional freeze-fracture electron microscopy were used. During reperfusion with calcium-containing solution disruption of the sarcolemma was observed, which was attended with formation of unilamellar and multilamellar vesicles and aggregation of intramembrane particles. These ultrastructural changes are explained in terms of calcium- and proton-induced lateral phase separation and fusion processes in the lipid bilayer of the sarcolemma.

Animals↗
PubMed1985

Post-extra systolic potentiation: influence of calcium and verapamil in rat and rabbit hearts.

The interactions of the inotropic effects of verapamil (0.05-2.0 mumol l-1), calcium (0.33-5.2 mmol l-1) and post extra systolic potentiation (PESP) as induced by paired stimulation were studied in isolated rabbit and rat hearts under isovolumic and isotonic conditions. At low doses of verapamil, contractions were depressed, but those elicited by paired stimulation showed less depression than contractions of the same rate during single stimulation and even exceeded the unpotentiated contractions without verapamil. At high doses of verapamil contractility could not be restored by paired stimulation. Although contractions were restored to control level by an increase in extra-cellular calcium they were still abnormal in the sense that PESP could not be elicited. The excitation-contraction (e-c) uncoupling due to low calcium perfusion could be counteracted by paired stimulation but e-c uncoupling due to high dose verapamil could not be reversed by paired stimulation. Our results support the view that PESP does not only depend on augmented slow channel calcium influx but also on an enhanced calcium shift within the sarcoplasmic reticulum. We are doubtful about the idea that PESP can be used clinically to counteract the negative inotropic effect of high doses of verapamil.

Animals↗
PubMed1985

Different effects of thiopental in severe hypoxia, total ischemia, and low-flow ischemia in rat heart muscle.

The effect of thiopental (100 mg X 1(-1] during total ischemia, low-flow ischemia, and severe hypoxia with maintained flow was investigated in the isolated perfused rat heart. During total ischemia the rate of decline of tissue creatine phosphate and adenosine triphosphate was no different in thiopental-treated and untreated hearts. The development of ultrastructural damage during total ischemia, the release of creatine kinase on reperfusion, and the exacerbation of ultrastructural damage after reperfusion were unaffected by thiopental. When thiopental was added to the perfusate during hypoxia and during low-flow ischemia at a normal pH(7.4), creatine kinase release during reoxygenation and during reperfusion was significantly less (P less than 0.005 and P less than 0.05, respectively) than in the untreated groups. After low-flow ischemia at a low pH (6.5), creatine kinase release was no different in thiopental-treated and untreated hearts. Thus, thiopental afforded protection of the myocardium in hypoxia and low-flow ischemia at pH 7.4 but not in total ischemia and low-flow ischemia at pH 6.5. The data are consistent with the hypothesis that during total ischemia and low-flow ischemia at pH 6.5, acidosis favors the entry of thiopental into the cell, causing inhibition of mitochondrial function and reduction of ATP production. During hypoxic perfusion and low-flow ischemia at pH 7.4, when the decrease in pH is less, the cardiodepressant effect of thiopental may offset any deleterious effect of the drug on intracellular organelles such as mitochondria.

Adenosine Triphosphate↗
PubMed1985

Possible mechanisms involved in the development of the calcium paradox.

Reperfusion of an isolated heart with calcium-containing solution after a short period of calcium-free perfusion may result in excessive influx of calcium into the cells and irreversible cell damage (calcium paradox). This paper describes the possible routes of calcium entry that occurs during the phase of calcium repletion, and the possible mechanisms involved in the development of the calcium paradox damage. The routes of calcium entry include the glycocalyx, the slow channels, the Na+-Ca2+ exchange mechanism, passive diffusion, and abnormal sites of calcium entry. In addition to an increased influx of calcium, a loss in the ability of the sarcolemma to remove calcium from the cells may contribute to the net gain of tissue calcium. The calcium paradox damage itself, which follows the massive influx of calcium into the myocardial cells, may be a result of calcium-triggered energy dependent reactions and a concomitant acidification of the cytoplasm. Mechanical factors may also be involved in the development of the calcium paradox.

Acid-Base Equilibrium↗
PubMed1984

Morphology of lumbar motoneurons innervating hindlimb muscles in the turtle Pseudemys scripta elegans: an intracellular horseradish peroxidase study.

Motoneurons in the turtle lumbar spinal cord, electrophysiologically identified as innervating a muscle belonging to a functional group, were injected with horseradish peroxidase by electrophoresis. A total of 45 motoneurons were reconstructed from transverse sections. Eleven motoneurons were identified as innervating knee extensor muscles, eight as innervating hip retractor and knee flexor muscles, 14 as supplying ankle and/or toe extensors, and 12 as innervating ankle and/or toe flexor muscles. The cell bodies were elongated and spindle-shaped in the transverse plane. The mean equivalent soma diameter was calculated to be 33.4 micrometers. The mean axon conduction velocity was 15.7 m/second. Significant, though rather weak, positive correlations were found between soma diameter, axon diameter, and axon conduction velocity. The axons of the reconstructed motoneurons did not reveal a recurrent axon collateral. However, a few unidentified motoneurons did possess such collaterals. The dendritic trees were restricted to the ipsilateral side of the cord, but reached out in lateral, ventral, and ventromedial directions to the subpial surface. Easily recognizable and characteristic dendrites were found both in the dorsal dendritic tree and in the dorsomedial dendritic tree. Correlations were calculated between the soma diameter and (1) the number of first-order dendrites, (2) the mean diameter of the first-order dendrites, and (3) the combined diameter of the first-order dendrites. In each case no correlations or only weak correlations were found. Fair correlations were observed between the diameter of a first-order dendrite and the number of terminal dendritic branches (r = .61) and the combined dendritic length (r = .78). However, correlations between the combined diameter of all first-order dendrites per neuron and the total number of terminal dendritic branches and the total combined dendritic length of a neuron were extremely weak. The overall appearance of turtle spinal motoneurons is comparable to that observed in other "lower" vertebrates such as frog and lizard. However, similarities are also observed between certain morphometric parameters in turtle and cat lumbar motoneurons.

Animals↗
PubMed1984

The organization of motoneurons in the turtle lumbar spinal cord.

The distribution of motoneurons in the lumbosacral spinal cord of the turtle Pseudemys scripta elegans was studied by using the technique of retrograde transport of horseradish peroxidase. A total of 19 different hindlimb muscles were injected with varying amounts of horseradish peroxidase. The resulting distribution of labeled motoneurons was studied in both longitudinal and transverse sections of spinal cord. Motoneurons innervating a particular hindlimb muscle are clustered in longitudinally arranged motorpools. Motorpools of different muscles can show considerable overlap in both the rostrocaudal and transverse planes. The distribution of the various motorpools demonstrates a somatotopic organization of motoneurons within the lumbar spinal cord. Motoneurons innervating more distally positioned muscles are generally found in the more caudal segments, while motoneurons supplying proximal muscles are distributed throughout almost the whole lumbosacral intumescence. Motoneurons innervating anterodorsally positioned muscles are found in the ventrolateral part of area IX in the ventral horn, while more dorsomedially positioned motoneurons innervate the posteroventral muscles. These features are consistent with observations in other tetrapods, although the somatotopic representation of motoneurons is more evident in higher vertebrates such as chicken and cat. The observed motorpool distribution is discussed in relation to the presumed ontogeny of the spinal cord and hindlimb muscles and also in relation to the functions of the investigated muscles.

Animals↗
PubMed1984

Biochemical properties of membranes isolated from calcium-depleted rabbit hearts.

The purpose of this study was to define the biochemical properties of sarcolemma from the calcium-depleted rabbit heart. Calcium repletion after calcium-free perfusion results in irreversible damage to the heart (calcium paradox). No difference was found in specific activity of the Na+ -Ca++ antiporter in a crude preparation of sarcolemmal vesicles that was isolated from calcium-depleted hearts, compared with control perfused hearts. Likewise, the passive calcium efflux from sarcolemmal vesicles, preloaded with calcium via the Na+ -Ca++ antiporter, showed rates that were identical with control values. This indicates that the sarcolemma calcium permeability is not affected by calcium-free perfusion of the heart. Na+,K+ -ATPase activity in sarcolemma isolated from calcium-depleted hearts was reduced by 75% (P less than 0.005) compared with the control activity. Sarcolemmal phosphoproteins, whether produced by endogenous cyclic AMP- or calcium-calmodulin-dependent protein kinase, were not altered by calcium-free perfusion of the heart. The content of an important calcium-binding site in the myocardial cell, the sialic acid residues, was also estimated. Only a long period (60 minutes) of calcium-free perfusion resulted in a significant decrease (by 68%, P less than 0.025) of sialic acid content in the homogenate but not in the sarcolemma preparation. In hearts that were reperfused for 15 minutes with a normal calcium concentration (1.3 mM), sarcolemmal Na+,K+ -ATPase remained depressed and calcium permeability was still unchanged. It is possible that the sarcolemma isolation method selected a distinct part of the sarcolemma from the calcium-depleted and repleted heart that had no modified glycocalyx and permeability barriers to calcium ions, and that another part of the sarcolemma with altered properties was lost during the isolation procedure. Another possibility is that reconstitution processes during isolation affected membrane permeability properties. The results of the Na+,K+ -ATPase measurements provide evidence that the net calcium gain of the cells after calcium repletion may be associated, in part, with a loss in ability of the sarcolemma to remove calcium from the cytosol.

Animals↗
PubMed1984

Enzyme histochemical changes in retinal ganglion cells and the optic nerve after goldfish optic nerve lesion. A regenerative and hypertrophic phenomena study.

After sectioning of the goldfish optic nerve a number of enzyme histochemical changes are observed in the hypertrophied retinal ganglion cells and in the optic nerve. Between one and eighteen days postoperatively an increase in the amount of acid phosphatase reaction product is noted. The enhanced activity decreased to normal first in the optic nerve, followed by the optic tract and tectum. Four days postoperatively higher levels of activity were noted in the hypertrophic retinal ganglion cells for the enzymes NADH tetrazolium reductase, cytochrome oxidase, glutamate dehydrogenase and lactate dehydrogenase. The same enzymes also showed an activity increase in the lesioned optic nerve after four to ten days postoperatively, beginning at the cut and gradually spreading towards the optic tectum. Between fifteen and eighteen days the activity dropped to normal in the hypertrophic retinal ganglion cells, while in the lesioned nerve raised levels of reaction products could be seen till days thirty-five and/or forty-five. It was concluded that the degeneration of the optic pathway is marked by the increase of acid phosphatase activity, whereas the process of regeneration is characterized by an increase of NADH tetrazolium reductase, cytochrome oxidase, glutamate dehydrogenase and lactate dehydrogenase activities. The possible functional implications of these enzymes in the regenerative phenomena are discussed.

Animals↗
PubMed1983

Protective effect of nifedipine in myocardial ischemia assessed by phosphorus-31 nuclear magnetic resonance.

Calcium antagonists may protect the myocardium against the consequences of ischemia. Phosphorus-31 nuclear magnetic resonance (31P NMR) was used to study the effect of nifedipine on intracellular acidosis and high energy phosphate depletion during global ischemia. Isolated rat hearts were paced (300 beats/min), perfused with a modified Tyrode solution for 30 min, made totally ischemic for 30 min (37 degrees C) and then reperfused for 30 min. When required, nifedipine (1 mg/l) was added to the perfusion fluid 10 min before ischemia. During ischemia intracellular pH fell from 7.11 +/- 0.03 (mean +/- S.E.M.) to 5.88 +/- 0.04 in the untreated hearts (n = 6), and from 7.11 +/- 0.03 to 5.95 +/- 0.02 in the treated hearts (n = 6). During the first 20 min of ischemia, intracellular pH was significantly higher in the treated than in the untreated hearts (P less than 0.001). Myocardial creatine phosphate (CP) content was depleted after 15 min of ischemia in the untreated hearts, and after 20 min of ischemia in the hearts treated with nifedipine. Myocardial adenosine triphosphate (ATP) content was depleted after 20 min of ischemia in the untreated hearts; ATP content in hearts that received nifedipine amounted to 23.5 +/- 6.2% of control after 30 min of ischemia. In contrast with the untreated hearts, the nifedipine-treated hearts showed a rapid recovery of CP content during reperfusion. The results indicate that nifedipine protects the myocardium against the metabolic consequences of ischemia and reperfusion.

Adenosine Triphosphate↗
PubMed1983

The calcium paradox: an electrophysiological study in the isolated rabbit heart.

In Langendorff perfused rabbit heart (37 degrees C) transmembrane potentials were recorded from the left ventricle with 'floating' microelectrodes. During calcium-free perfusion, action potential duration lengthened by 55.4 +/- 34.9% (n = 8). AV conduction time increased, until Wenckebach and 2 : 1 AV block occurred. Heart rate initially decreased, and later increased although control values were not reached. Upon reperfusion with normal calcium-containing fluid, a few vigorous contractions occurred, which dislodged the intracellular microelectrode. As far as could be established, cells depolarized within 6-60s to values less than -50 mV, and no action potentials could be recorded. During low-calcium (50 mumol l-1) perfusion (n = 5), action potential duration initially increased, but later decreased. When perfusion with normal calcium-containing fluid was resumed when action potentials were still longer than normal, the action potentials shortened initially but returned later to control values. In these hearts, contractions reappeared. However, when perfusion with normal calcium-containing fluid was resumed when action potential duration was shorter than normal, no contractions reappeared, and action potentials remained short during the entire reperfusion period. In six experiments, creatine kinase release was determined during both low-calcium and calcium-free perfusion, and during subsequent periods with normal calcium-containing fluid. During 10 min of low-calcium perfusion, 107 +/- 31 IU g-1 dry weight appeared in the perfusate, and in the subsequent normal calcium perfusion period of 15 min, 438 +/- 88 IU were released. During the 10 min calcium-free period, 141 +/- 40 IU were released, and during 15 min of reperfusion, 2773 +/- 258 IU appeared.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1983

Diminished Na+/K+ and Ca2+ pump activities in the Ca2+ depleted heart: possible role in the development of Ca2+ overload during the Ca2+ paradox.

Experiments were carried out to test the hypothesis that membrane injury associated with Ca2+ depletion of the heart is involved in the development of Ca2+ overload during the Ca2+ paradox phenomenon. Biochemical properties of sarcolemma (SL) and sarcoplasmic reticulum (SR) isolated from the rabbit heart after 10 min of Ca2+-free perfusion were examined. This treatment predisposes hearts to the Ca2+ paradox as assessed by perfusate creatine kinase (CK) activity and heart contractility during reperfusion with Ca2+. Homogenates prepared from Ca2+ depleted heart were examined for their capacity to accumulate Ca2+ in the presence of ATP, which is mainly a property of the SR Ca2+ pump. The initial rate of Ca2+ pumping was 55% less in the Ca2+ depleted heart. The activities of 5'-nucleotidase, Na+/K+-ATPase and Na+/Ca2+ antiporter, and the Ca2+ permeability were studied in isolated SL vesicles. Na+/K+-ATPase activity was 75% less in SL isolated from Ca2+ depleted hearts, no significant changes were observed with the other parameters studied. Calmodulin (CaM) content in SL, assayed by radioimmunoassay, was unchanged. However, a 98% increase was observed in homogenates prepared from Ca2+ depleted hearts. The possible involvement of CaM in the Ca2+ paradox phenomenon is discussed. The data provide evidence that the net Ca2+ gain of myocardial cells in Ca2+ repletion may in part be associated with a loss of the ability of the SL and SR to remove Ca2+ from the cytosol.

Animals↗
PubMed1983

The calcium paradox in isolated frog heart: Ringer revisited.

Restoration of a normal calcium concentration in the perfusate of isolated hearts after a short period of calcium-free perfusion may result in irreversible cell damage (calcium paradox). We have compared the calcium paradox in rat and frog hearts. Perfusion with zero calcium for 8 min at 37 degrees C predisposed the rat heart to the paradox. After the reintroduction of calcium to the perfusate resting tension rose, developed tension did not recover, ultrastructural changes occurred and enzyme loss was substantial. In the frog heart a calcium paradox did not occur after 8 min of calcium-free perfusion at 23 degrees C. Removal of both potassium and calcium caused a rise in resting tension on reintroduction of control solution, but the rise was only transient and absent if potassium was present during the perfusion with zero calcium. At 37 degrees C no complete calcium paradox occurred after 8 min calcium-free perfusion. Only a small rise in resting tension was apparent, and developed tension partially recovered. A calcium paradox could only be induced in the frog heart after calcium-free perfusion at 37 degrees C for 30 min. Ultrastructural changes were apparent and resting tension rose but even under these conditions the recovery of developed tension was not abolished. Release of creatine kinase was 161 +/- 55 IU/g dry tissue during the 15 min after reintroduction of calcium (n = 5). Calcium-free perfusion for 8 min resulted in a smaller release of creatine kinase over 15 min (39 +/- 11 IU/g dry tissue. n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Bretschneider's histidine-buffered cardioplegic solution and the calcium paradox.

Reperfusion of an isolated heart with calcium-containing solution after a short period of calcium-free perfusion may result in irreversible cell damage (calcium paradox). Experiments were undertaken to determine whether rat hearts could be predisposed to the calcium paradox by perfusion with Bretschneider's calcium-free histidine-buffered cardioplegic solution. Creatine kinase (CK) release during the reperfusion phase was used to quantitate cell damage. Perfusion with cardioplegic solution was performed at 37 degrees and 20 degrees C. Reperfusion after 10 minutes of perfusion with this solution at 37 degrees C resulted in a full calcium paradox. After 120 minutes of perfusion with cardioplegic solution at 20 degrees C, CK release during reperfusion amounted to 30% of the release during a full calcium paradox. This CK release could be further reduced by lowering the coronary flow rate or by adding 50 mumol X L-1 CaCl2 to the cardioplegic solution. It is concluded that a combination of hypothermia, a low coronary flow rate, and a limited duration of exposure to Bretschneider's histidine-buffered cardioplegic solution will minimize the risk of evoking the calcium paradox.

Animals↗
PubMed1982

The distribution of motoneurons innervating hindlimb muscles in the terrapin Pseudemys scripta elegans.

The distribution of motoneurons innervating a number of hindlimb muscles in the spinal cord of the terrapin Pseudemys scripta elegans was studied by means of intramuscularly injected horseradish peroxidase (HRP). It appeared that motoneurons innervating knee extensors were localized more rostrally in the spinal cord than those innervating knee flexors and hip retractors. Muscles on the dorsal side of the limb were positioned more ventrally in the ventral horn compared to motoneurons innervating ventral muscles. Thus, an evident somatotropic organization of motoneurons was demonstrated in the chelonian spinal cord.

Animals↗
PubMed1982

Cardioplegia in the presence or absence of calcium.

The effect of the Bretschneider procedure of myocardial protection on the recovery of dog hearts in the postischemic phase after 90 min of aortic occlusion was studied. In one series of experiments, Bretschneider's calcium-free cardioplegic solution HTP was used; in a second series, 5 X 10(-5) M CaCl2 was added to this solution. The coronary system was perfused with cardioplegic solution (6 degrees C) for 6 min at the onset and for 1 min after 30 and 60 min of ischemic arrest. Functional recovery of the heart and plasma creatine kinase activity during the postischemic phase were not significantly different in the two groups of dogs. It is concluded that low temperature, mode of administration, and composition of Bretschneider's cardioplegic solution HTP protect the heart against the potential danger of exposure to a calcium-free solution.

Animals↗
PubMed1981

Enzyme histochemical changes in some optic projection areas of the goldfish after optic nerve lesions.

Enzyme histological changes have been studied in several optic projection areas after right optic nerve lesion in goldfish. An increase in acid phosphatase activity was found in the optic tectum, nucleus rotundus, nucleus geniculatus lateralis and area pretectalis between 2 and 15 days postoperatively. The enzymes glutamate dehydrogenase, lactate dehydrogenase, NADH tetrazolium reductase, cytochrome oxidase, succinate dehydrogenase and beta-hydroxybutyrate dehydrogenase showed a decrease in activity in all or some of these projection areas. No changes were found in acetylcholinesterase activity after optic nerve lesions. Three weeks postoperatively, all enzyme activities returned to the same level as on the normal side. The results are discussed in relation to possible neurotransmitters in goldfish optic terminals.

Acid Phosphatase↗