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C G Nichols

Publications and source records attributed to C G Nichols.

At least 91 records · Page 5Linked to original sources
PubMed1991

ATP dependence of KATP channel kinetics in isolated membrane patches from rat ventricle.

The dependence of KATP channel activity on [ATP] has been examined in isolated membrane patches from rat ventricular myocytes. The steady-state [ATP] dependence of channel open probability could be described by a sigmoidal relationship with the ki ([ATP] causing half-maximal inhibition of open probability) = 25 microM and Hill coefficient of 2. Description of channel open- and closed-time distributions required at least 2, and 3, time constants, respectively. Long open-channel lifetimes decreased with [ATP]; unconditional mean channel closed-times increased with [ATP]. Step decrease (jump) in bathing [ATP] resulted in a delay (of up to hundreds of milliseconds) followed by a pseudo-exponential rise of current (with a time constant of up to hundreds of milliseconds). The time course of channel current after changes of [ATP] (or the ATP-analogue AMP-PNP) was shown to be predominantly determined by the time course of diffusion into the tip of the electrode and to the membrane. This time course of diffusion of ATP into the pipette tip had to be taken into account when analyzing the current response to [ATP] steps. Several possible kinetic models of the ATP-dependent regulation of channel activity were considered. Adequate explanation of the data required a model with sequential ATP-binding sites. The model can account for the time course of channel opening after steps of [ATP], as well as for the steady-state dependence of P0 on [ATP]. The model predicts [ATP]-dependent closed and open lifetimes as were observed experimentally.

Adenosine Triphosphate↗
PubMed1991

Adenosine triphosphate-sensitive potassium channels in the cardiovascular system.

ATP is normally available in cells at millimolar concentrations and is "buffered" by intracellular pools of other high-energy phosphates, such as creatine phosphate. Thus intracellular [ATP] [( ATP]i) may seem an unlikely candidate for a regulatory signal inside cells. Recent evidence suggests, however, that [ATP]i regulates the behavior of a class of potassium (KATP) channels that are found throughout the cardiovascular system. KATP channels are present in cardiac, skeletal, and vascular smooth muscle. The channels are inhibited by micromolar [ATP]i, and this inhibition is relieved by micromolar [ADP]i. We present evidence in support of the idea that variations of [ATP]i and [ADP]i, even within normal concentration ranges, may influence cellular function in the heart and vascular system via a direct action on the KATP channel. Furthermore, very specific modulators of KATP channel activity are available. We discuss the mechanism of action of these agents and their interaction with endogenous modulators and consider their potential roles in cardiovascular therapy.

Adenosine Triphosphate↗
PubMed1991

ATP-sensitive potassium channel modulation of the guinea pig ventricular action potential and contraction.

The role of ATP-sensitive potassium (KATP) channels in modulating the action potential and contraction of guinea pig ventricular myocytes was investigated. Under voltage clamp, the maximum whole-cell KATP channel conductance was estimated (195 +/- 10 nS, n = 6) by exposing the cells to complete metabolic blockade (2 mM cyanide in the presence of 10 mM 2-deoxy-glucose). In isolated inside-out membrane patches, the ATP dependence of KATP channel activity under relevant conditions was measured (half-maximal inhibition at 114 microM). Under current clamp (with intracellular ATP concentration = 5 mM), the effect of graded KATP channel activation on the action potential and the twitch was estimated by injection of a current (proportional to voltage) that simulated the KATP conductance. As this "conductance" was increased, the action potential was shortened, and contractile amplitude declined, as expected. From the results of these experiments, the quantitative dependence of the action potential duration on intracellular ATP concentration was estimated, without relying on a mathematical model of the cell membrane. The results imply that KATP-dependent action potential shortening is likely to occur if ATP concentration falls below normal levels (approximately 5 mM), as may happen regionally, or globally, during myocardial ischemia.

Action Potentials↗
PubMed1990

Modulation of ATP-sensitive potassium channel activity by flash-photolysis of 'caged-ATP' in rat heart cells.

We have used 'caged-ATP' to investigate the kinetic behavior of KATP channels in ventricular cells from rat heart. In whole cells, loaded with 'caged-ATP', an increase of intracellular [ATP] following a UV light flash produced a decrease of KATP channel current that was too slow (tau approximately 300 ms) to be explained by the expected time-course of ATP release (tau approximately 3 ms) and the time-course of channel blockade by ATP (tau approximately 20 ms). In isolated membrane patches, caged-ATP itself caused partial blockade of KATP) channels. Under these conditions, photorelease of ATP caused channel activity to decline further. The results suggest that caged-ATP can bind to the KATP) channel but, on binding, decreases the open probability to a lesser extent than does ATP. Additionally, the observations indicate that for photolytically-generated ATP to bind to the channel, caged-ATP must first unbind (slowly) from the channel. We conclude that 'caged-ATP' is not fully caged with respect to its allosteric action on the KATP channel.

Adenosine Triphosphate↗
PubMed1990

The regulation of ATP-sensitive K+ channel activity in intact and permeabilized rat ventricular myocytes.

1. In isolated rat heart ventricular myocytes exposed to 2 mM-cyanide in the presence of 10 mM-2-deoxyglucose (complete metabolic blockade), there is a time-dependent increase in ATP-sensitive potassium (KATP) channel activity. The increase in KATP channel activity accompanies the decline of twitch amplitude. Channel activation and decline of the twitch amplitude precede the development of a 'rigor' contracture. 2. We measured KATP channel activity in permeabilized cells using the open-cell attached (O-C-A) patch configuration (by establishing a cell-attached patch and then permeabilizing the cell by exposure to saponin). The apparent ATP dependence of KATP channel activity could be described by a sigmoid curve with ki, ATP (ATP concentration required for half-maximum inhibition of channel activity) = 122 microM and H (Hill coefficient) = 1.225. 3. In the O-C-A patch configuration, 10 mM-creatine phosphate (CrP) decreased the apparent ki, ATP from 122 microM to about 10 microM, and the maximal activity (in zero ATP) was decreased to about 30% of the maximal activity in the absence of CrP. 4. In isolated inside-out (I-O) patches, ATP inhibited KATP channel activity at much lower [ATP] than in the O-C-A patch configuration (ki, ATP = 25 microM, H = 2). CrP was without effect on I-O patches. 5. These results are consistent with the hypothesis that the difference in the ATP dependence of KATP channel activity in the O-C-A and I-O patch configurations arises because of ATP consumption in the O-C-A patch configuration. The results suggest that hydrolysis of ATP to ADP by endogenous ATPases leads to the development of gradients of [ATP] and [ADP] between the bath and the 'inside' of the open cell. By re-phosphorylating ADP, CrP is able to dissipate these gradients, revealing the 'true' ATP dependence of channel activity, which is the same as that in the I-O patch configuration. 6. In order to estimate the contribution of KATP channel activity to the rat cardiac action potential at different [ATP] we have made the following measurements. Using electrodes of resistance 2-8 M omega the density of KATP channels was 10.3 +/- 0.1 channels per patch (n = 162).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1990

The role of ATP in energy-deprivation contractures in unloaded rat ventricular myocytes.

Energy-deprivation contractures were investigated in unloaded rat ventricular myocytes. Application of 2 mM cyanide in the presence of 10 mM 2-deoxyglucose (metabolic blockade) led to a rapid shortening "contracture" (maximum speed 1.5 +/- 0.2% control cell length/s). Cells shortened to a constant length of 69 +/- 1.6% of the control length. Removal of cyanide caused cells to shorten further ("recontracture"), before relaxing towards the control length. Cells shortened to 57 +/- 2.0% during the recontracture. Similar behaviour was observed in zero extracellular [Ca2+]. Cells permeabilized with saponin (0.1% w/v) responded to the removal of ATP from the bathing solution, and to readdition of ATP, as intact cells did to complete metabolic blockade and its removal. In these permeabilized cells, the extent and speed of contracture shortening were similar at pCa = 7 and pCa greater than 9. When the bath concentration of ATP ([ ATP]b) was lowered to zero, shortening stopped at about 70% of the control length. However, when [ATP]b was lowered to an intermediate level (4-20 microM), cells contracted to lengths as short as 30% of the control length. Similarly, when [ATP]b was restored from zero to an intermediate concentration (4-20 microM), recontracture shortening continued without relaxation. The peak speed of this Ca2(+)-independent shortening showed a sigmoidal dependence on pMgATP (pMgATP0.5 = 4.0). Phosphocreatine (10 mM) shifted the ATP dependence of Ca2(+)-independent shortening to lower [ATP]b (pMgATP0.5 = 5.0), suggesting that gradients of [ATP] could exist between the bath and the myofilaments. Ca2(+)-independent shortening was inhibited by the chemical phosphatase 2,3-butanedione monoxime (BDM), although BDM did not relax cells from the shortened state during energy deprivation. Using a simple model, we show that the results can be explained by cross-bridge cycling occurring independently of Ca2+ over a "window" range of [MgATP] (0.1-100 microM). Therefore, when [MgATP] falls, cross-bridge cycling occurs and the cell shortens. As [MgATP] falls to very low levels ([ MgATP] less than 1 microM), shortening ceases as the rate of cross-bridge cycling declines. Recontracture occurs on restoring ATP production, because stiffness falls and Ca2(+)-independent cross-bridge cycling initially increases. As [MgATP] rises above 100 microM, Ca2(+)-independent cross-bridge cycling ceases and the cell relaxes towards the control length. We conclude that energy-deprivation contractures, and recontractures, can result from changes in [MgATP] and do not necessarily require changes in [Ca2+]i.

Adenosine Triphosphate↗
PubMed1990

Modulation of ATP-sensitive K+ channel activity and contractile behavior in mammalian ventricle by the potassium channel openers cromakalim and RP49356.

We have investigated the effects of potassium channel opening drugs on the ATP-dependence of ATP-sensitive K+ channel activity and on contractile activity in rat and guinea pig ventricular myocytes. The results show that cromakalim (BRL34915), and RP49356, agents reported to open ATP-sensitive K+ channels, do so by shifting the intracellular [ATP] required to cause half-maximal inhibition of channel activity (ki) to higher [ATP]. In guinea pig ventricular myocytes at 37 degrees C, the ki was shifted from 79 to 152 microM by 40 microM cromakalim and, in rat myocytes at room temperature, the ki was also shifted to higher [ATP] by 50 microM RP49356. The effect of externally applied RP49356 on the contractile activity of intact rat ventricular myocytes was investigated. At 100 microM the drug was without effect in the presence of normal bathing solution containing 10 mM glucose. When glucose in the bathing medium had been replaced by 2-deoxyglucose for 84 +/- 2 min, 100 microM RP49356 decreased the twitch amplitude to 23 +/- 4% of control. The negative inotropic effect of 100 microM RP49356 increased with time after perfusion with 2-deoxyglucose, and the negative inotropic effect diminished on reperfusing with glucose; 83 +/- 3 min after reperfusing with glucose, twitch amplitude was decreased by only 52 +/- 6% on exposure to 100 microM RP49356. These results suggest that the effect of the potassium channel opening drugs on contractility and electrical behavior will depend critically on the intracellular [ATP]. The results provide an explanation of how potassium channel openers may become clinically useful as cardioprotective agents without interfering with normal function.

Adenosine Triphosphate↗
PubMed1990

Toxic shock syndrome associated with use of latex nasal packing.

We treated a previously healthy young man who developed toxic shock syndrome 2 days after elective septoplasty with nonabsorbent latex packing. This case emphasizes that non-menstrual wound-associated toxic shock syndrome can occur after surgery that does not involve absorbent splinting or packing and should be considered in patients who present within a few days after surgery with fever, sunburnlike rash, hypotension, and multisystem complaints and laboratory abnormalities.

Adult↗
PubMed1989

The effects of metabolic inhibition on intracellular calcium and pH in isolated rat ventricular cells.

1. Intracellular calcium concentration [( Ca2+]i) and pH (pHi) were measured in single, isolated rat ventricular myocytes using, respectively, the fluorescent indicators Fura-2 and BCECF (2',7'-bis(carboxyethyl-5(6)-carboxyfluorescein). Contraction was measured simultaneously. The intracellular calibration of BCECF is demonstrated. In a HEPES-buffered bathing solution of pH 7.4, pHi had a mean value of 7.16 +/- 0.05 (mean +/- S.E.M.). 2. Addition of NH4Cl (5-20 mM) produced an intracellular alkalosis that was associated with an increase of contraction amplitude. Removal of NH4Cl produced an acidosis and decrease of contraction. 3. The addition of 2 mM-cyanide (CN-) to inhibit oxidative phosphorylation had variable effects on contraction amplitude. Changes of contraction amplitude could largely be accounted for by changes in the systolic Ca2+ transient. 4. CN- addition increased lactic acid production. However, in the majority of experiments, this was not accompanied by an intracellular acidosis. 5. Anaerobic glycolysis was inhibited by either removal of glucose, addition of deoxyglucose, or addition of iodoacetate. Under these conditions the application of CN- decreased systolic [Ca2+]i and contraction amplitude. This was sometimes preceded by a transient increase of systolic [Ca2+]i and contraction amplitude. 6. When glycolysis was inhibited, the subsequent addition of CN- always increased diastolic [Ca2+]i and produced a contracture. The increase of [Ca2+]i occurred before the contracture. However, once the contracture had developed, decreasing [Ca2+]i (by removal of external Ca2+) did not cause relaxation. 7. With glycolysis inhibited, addition of CN- resulted in a large (0.51 +/- 0.05 pH unit) acidosis that was sometimes preceded by an alkalosis. This acidosis was unaffected by removal of external Ca2+ or external alkalinization. Calculations show that some of this acidosis may result from protons released by ATP hydrolysis. 8. If the acidosis produced by metabolic blockade was partly reversed by adding NH4Cl then a contracture immediately developed. This suggests that the acidosis delays the onset of the contracture. 9. We conclude that metabolic inhibition increases diastolic [Ca2+]i. The accompanying acidosis prevents contraction. Once the contracture has developed it is maintained by factors other than increased [Ca2+]i, possibly by a fall of [ATP].

Action Potentials↗
PubMed1989

The mechanism of early contractile failure of isolated rat ventricular myocytes subjected to complete metabolic inhibition.

1. Twitch shortening of isolated rat ventricular myocytes was measured on exposure to complete metabolic blockade (2 mM-cyanide in the presence of 10 mM-2-deoxyglucose). Under these conditions twitch shortening declines to undetectable levels over 1-15 min. This 'early' contractile failure is followed by the development of a maintained contracture. 2. Contractures induced by caffeine (20 mM) were similar in amplitude before and after 'early' contractile failure. This result suggests that 'early' contractile failure is not due to depletion of Ca2+ from the sarcoplasmic reticulum. 3. The action potential shortened as the twitch magnitude declined during 'early' contractile failure, raising the possibility of a causal link. Voltage-clamp experiments show that an enormous increase in K+ conductance (greater than 20-fold) occurs during the period of 'early' contractile failure, and presumably underlies the action potential shortening. 4. If the K+ conductance changes are inhibited by replacement of intracellular K+ with N-methyl glucosamine and inclusion of 2 mM-tolbutamide in intra- and extracellular solutions, good voltage control can be achieved. Under these conditions, 'early' contractile failure did not occur on exposure to complete metabolic blockade and neither Ca2+ current nor the twitch were completely abolished until a maintained contracture had begun to occur. 5. Injection of ATP following 'early' contractile failure could partially restore the twitch and prolong the foreshortened action potential. 6. These results are consistent with the hypothesis that 'early' contractile failure occurring under non-voltage-clamped conditions is due principally to failure of activation of the Ca2+ current because of the shortening of the action potential. Although a decline in the availability of Ca2+ current also occurs, action potential shortening results mainly from increased conductance through ATP-sensitive K+ channels which are activated by a fall of intracellular [ATP]. Contractile failure arises not because of a primary alteration, or defect, in the coupling of excitation to contraction, but because the cell membrane is effectively clamped at a potential close to the K+ equilibrium potential.

Action Potentials↗
PubMed1989

Nucleotide modulation of the activity of rat heart ATP-sensitive K+ channels in isolated membrane patches.

1. We have measured the ATP dependence of KATP channel activity, and the effect of various metabolites on this relationship, in inside-out membrane patches isolated from rat ventricular myocytes. 2. The inhibition of KATP channel activity by ATP could be described as a sigmoid function of [ATP] with a Hill coefficient (HATP) of 2 and a half-maximal inhibition at an ATP concentration (Ki, ATP) of 25 microM, in the presence of 0 mM, or 0.5 mM, total [Mg2+]. The non-hydrolysable ATP analogue, AMP-PNP, also inhibited the channel with Ki, AMP-PNP = 60 microM and HAMP-PNP = 2. 3. Acidosis caused a small, but significant, increase in Ki, ATP from 25 microM at pH 7.25 to 50 microM at pH 6.25, but phosphate and lactate were without effect (at 20 mM) on channel activity. 4. In the absence of ATP or Mg2+, ADP3- inhibited channel activity with Ki, ADP = 275 microM, and HADP = 1.2. Other purine and pyrimidine triphosphates, diphosphates and monophosphates also inhibited the channel with apparent order of inhibitory effectiveness ATP greater than AMP-PNP greater than ADP greater than CTP greater than GDP = AMP = ITP. 5. In the absence of Mg2+, but in the presence of 40 microM-ATP, channel inhibition by GTP, ITP, CTP, GDP, ADP or AMP was additive with inhibition by ATP. 6. In the presence of 0.5 mM-Mg2+ and 40 microM-ATP, inhibition by GTP, GMP and AMP was still additive with inhibition by ATP. The diphosphates ADP and GDP, however, paradoxically increased channel activity in the presence of ATP. This increase in channel activity appeared to result from a competitive increase in Ki, ATP, MgADP did not appear to cause any inhibition of channel activity. 7. We conclude that, in cardiac tissue, KATP channels are regulated by [ATP], and that this regulation is sensitive to other intracellular nucleotides, Mg2+, and pH, but not to phosphate or lactate. A simple, interactive two binding-site model is consistent with the nucleotide-dependent regulation that we observe.

Adenosine Triphosphate↗
PubMed1988

Anoxic contractile failure in rat heart myocytes is caused by failure of intracellular calcium release due to alteration of the action potential.

Anoxia of the heart causes failure of contraction before any irreversible injury occurs; the mechanism by which anoxia blocks cardiac excitation-contraction coupling is unknown. Studies in whole muscle are confounded by heterogeneity; however, achieving the low oxygen tensions required to study anoxia in a single myocyte during electrophysiological recording has been a barrier in experimental design. Guided by calculations of oxygen transport, we developed a system to insulate myocytes in an open dish from oxygen by a laminar counterflowing argon column, permitting free access to the cell by microelectrodes while maintaining a PO2 less than 0.02 torr (1 torr = 133 Pa). In the absence of glucose, the amplitude of stimulated contraction of anoxic ventricular myocytes fell to zero over 2 min after a lag period attributable to the consumption of endogenous glycogen. The cytosolic calcium concentration transient, measured by indo-1 fluorescence, fell to zero simultaneously with contraction. After the twitch had failed, microinjection of caffeine around the cell still caused a large calcium release and contraction, indicating that sarcoplasmic reticular calcium stores were not depleted. Twitch failure was accompanied by shortening and then failure of the action potential; under voltage clamp, large outward currents, reversing at the resting potential, developed during contractile failure. After failure of action potential-mediated contraction, voltage-clamp depolarization, with a large command voltage to compensate for the series-resistance error due to outward currents, restored normal twitch contraction. We conclude that anoxic contractile failure in the rat myocyte is due to alteration of the action potential and the distal pathways of excitation-contraction coupling remain essentially intact.

Action Potentials↗
PubMed1988

The effects of changes in muscle length during diastole on the calcium transient in ferret ventricular muscle.

1. Ferret papillary muscles were isolated and injected with aequorin to measure intracellular Ca2+ concentration [( Ca2+]i). Developed tension and [Ca2+]i were measured in response to length changes. 2. A maintained reduction in muscle length produced an immediate decrease in developed tension followed by slow decline over 10-20 min. This slow decline in tension was accompanied by a slow decline in the amplitude of the systolic [Ca2+]i rise (the Ca2+ transient). The immediate decrease in tension was accompanied by a prolongation of the Ca2+ transient and an abbreviation of the twitch. 3. Repeated reductions in muscle length timed to occur only during the period of contraction (systolic shortening) produced an immediate decrease of developed tension but the subsequent slow decline was substantially smaller. The slow decline in the amplitude of the Ca2+ transients was also smaller. The prolongation of the Ca2+ transient and abbreviation of the twitch were similar to those observed with a maintained reduction of length. 4. Repeated reductions in muscle length during the period between contractions (diastolic shortening) did not produce the immediate decrease of tension but the slow decline of tension was present. The slow decline in the amplitude of the Ca2+ transients was also present. However no change in the duration of the Ca2+ transient or the twitch was present under these conditions. 5. These results suggest that diastolic muscle length can influence the amplitude of the Ca2+ transients achieved during systole. This conclusion was confirmed by experiments in which the recovery of tension and Ca2+ transients was observed after periods of rest. Both developed tension and Ca2+ transients on recovery from a rest were reduced when the rest occurred at a short length in comparison with a long length. 6. We suggest that muscle length influences resting [Ca2+]i and this in turn affects the Ca2+ transients and developed tension.

Action Potentials↗
PubMed1988

The Anrep effect: an intrinsic myocardial mechanism.

In cat papillary muscles contracting physiologically, increasing the afterload caused a biphasic change in contractility. In response to an increase in afterload, contractility (as measured by peak shortening, peak developed force, or peak dF/dt) initially decreased (antihomeometric autoregulation) over the first few beats and then increased slowly with t 1/2 of about 3 min at 30 degrees C and about 1 min at 37 degrees C (homeometric autoregulation). The antihomeometric autoregulation is due to decreased active shortening when the afterload is increased, since it also occurs in response to increased afterload in isotonic contractions. The secondary slow increase in contractility is primarily due to the increase in mean diastolic length that occurs as a result of increased afterload. The time course and the magnitude of the biphasic change in contractility are very similar to those observed in response to afterload increase in intact hearts; we suggest that the secondary slow increase in contractility that we observed is a contributory mechanism to homeometric autoregulation (or the Anrep effect), as it is observed in the whole heart.

Animals↗
PubMed1987

Evaluation of cervicothoracic junction injury.

Cervical spine injury is a significant cause of morbidity and mortality in the traumatized patient. Little of the trauma literature addresses injury to the cervicothoracic junction (C7-T1); we were able to find only two studies that evaluated the incidence of injury in this area. The spinal injury registry of St Joseph's Hospital and Medical Center and Barrow's Neurological Institute in Phoenix, Arizona, was reviewed for cervical spine-injured patients. Of the 397 patients with cervical spine injury admitted between January 1980 and June 1985, 37 (9%) had cervicothoracic junction injury. Documentation of signs and symptoms of neck injury was recorded for each patient. All available lateral cervical spine radiographs were evaluated for indirect evidence of injury through the level of C7 as currently recommended in the trauma literature. Films were reviewed after being masked at the middle of the body of C7 thereby visualizing the C6-C7 junction. The incidence of C7-T1 injury in our cervical spine-injured population was 9%. Nine of the patients (24%) had a depressed level of consciousness and had neurologic examination that was not diagnostic of spinal injury. All of the cervical injuries in these patients were diagnosed by radiographic evaluation alone. We recommend that adequate visualization of the cervical spine through the cervicothoracic junction must be the standard for trauma care.

Arizona↗
PubMed1985

The influence of 'diastolic' length on the contractility of isolated cat papillary muscle.

Isometrically contracting cat papillary muscles were studied. Muscle length was changed during diastole and returned to control just before the next contraction such that developed force was always measured at the same length. When the diastolic length was increased from a control length, systolic force at the control length increased slowly over several minutes. When the muscle was then held at the increased length, there was an immediate increase in systolic force followed by a small secondary slow increase. Conversely, a decrease in diastolic length from a control length resulted in a slow decrease in systolic force at the control length. When the muscle was then held at the decreased length there was an immediate decrease in systolic force followed by a small secondary decrease. No change in the time course of contraction accompanied the slow force changes after a maintained change of length or a change of diastolic length alone. The magnitude of the slow change of force was proportional to the duration of time in each diastole for which the length was altered and independent of the onset time of a given duration of diastolic length change. The contractility changes were not linearly related to the amplitude of the diastolic length changes. The potentiating effect of a given stretch was greater than the depotentiating effect of a similar release. The development of inotropic changes as a result of diastolic length changes occurred whether or not the muscle was stimulated during the period of the length changes.

Animals↗
PubMed1985

Selection for increased weaning or yearling weight in Hereford cattle. I. Measurement of selection applied.

Selection was applied from 1964 to 1978 for increased weaning weight (WWL) or yearling weight (YWL) in two Hereford lines with an Angus line maintained as an unselected control line (CL). Each line was maintained with 50 cows and four sires (two sires selected each year and each used for 2 yr). Traits analyzed were birth weight (BW), preweaning daily gain (WDG), weaning weight (WW), weaning conformation grade (WG), weaning condition score (WC), weaning to yearling daily gain (YDG), yearling weight (YW), yearling conformation grade (YG) and yearling condition score (YC). After 15 yr of selection, a total of 3.22 generations of selection had occurred in both WWL and YWL. Average selection differentials in standard measure per generation for WWL, YWL and CL, respectively, were: BW, .44, .51, .0; WDG, .95, .81, .09; WW, .97, .85, .09; WG, .66, .57, .09; WC, .60, .38, -.02; YDG, .30, .79, .38; YW, .80, 1.05, .25; YG, .63, .62, .34 and YC, .45, .64, .24. The proportionate contribution of sire selection (delta S) to the average midparent selection differential per generation (delta M) was 70% in WWL and 76% in YWL. Selection indexes in retrospect were also calculated.

Animals↗