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Biomedical subjects

J H Mitchell

Publications and source records attributed to J H Mitchell.

At least 163 records · Page 9Linked to original sources
PubMed1983

Effect of hemodialysis on left ventricular function. Dissociation of changes in filling volume and in contractile state.

Prior studies of the effect of hemodialysis on left ventricular function have not distinguished between the removal of uremic toxins and the change in cardiac filling volume. To separate these effects, left ventricular function was examined by serial echocardiography in five stable hemodialysis patients before and after three different dialysis procedures: (a) hemodialysis with volume Loss, (b) ultrafiltration (volume loss only), and (c) hemodialysis without volume loss. The patients were similarly studied under control conditions and after increased (5 degrees of head-down tilt for 90 min) and decreased (lower body negative pressure) cardiac filling volume. After hemodialysis with volume loss, end-diastolic volume (EDV) decreased from 167 to 128 ml (P less than 0.001) and end-systolic volume (ESV) decreased from 97 to 51 ml (P less than 0.001) without a change in stroke volume (SV). Ejection fraction increased from 42 to 52% (P less than 0.001) and mean velocity of circumferential fiber shortening (VCF) increased from 0.61 to 1.04 circumferences (circ)/s (P less than 0.001). After ultrafiltration, EDV decreased from 167 ml to 124 ml (P less than 0.001) and SV from 73 ml to 39 ml (P less than 0.001), without significant changes in ESV or VCF. In contrast to the maneuvers in which volume loss occurred, after hemodialysis without volume loss ESV decreased from 95 to 66 ml (P less than 0.001) and SV increased from 74 ml to 97 ml (P less than 0.001) without changes in EDV. EF increased from 44 to 59% (P less than 0.001) and VCF increased from 0.64 to 1.26 circ/s (P less than 0.001). Ventricular function curves plotted from data obtained under conditions of altered cardiac filling volume before and after the three dialysis maneuvers demonstrate that ultrafiltration produced a pure Frank-Starling effect, while hemodialysis with or without volume loss produced a shift in the ventricular function curves, which demonstrated an increase in the contractile state of the left ventricle. The changes in left ventricular function produced by regular hemodialysis are the combined effects of a decrease in EDV and an increase in the contractile state of the left ventricle.

Creatinine↗
PubMed1983

Left ventricular volumes and contractility during hemorrhagic hypotension: dimensional analysis and biplane cinefluorography.

Biplane cinefluorography was used to study left ventricular volume and contractility in hemorrhagic hypotension in nine dogs. A blood loss of 42% of the total blood volume caused end-diastolic volume to fall 20% without any change in end-diastolic pressure. There were decreases in cardiac output (63%), end-systolic volume (23%), stroke volume (63%), ejected fraction (27%); and dP/dt DP 40 (47%) during hemorrhage. Without treatment of shock and dP/dt returned to the prehemorrhage level and the ejected fraction increased despite a decrease in end-diastolic volume, indicating a positive inotropic effect. Peripheral vascular resistance decreased after 2 h of hypotension at the same low cardiac output. These data suggest that in the spleen-intact dogs peripheral circulatory failure and not left ventricular dysfunction causes irreversibility in hemorrhagic hypotension.

Animals↗
PubMed1982

A new model for the assessment of regional ventricular wall motion.

A new model is proposed for the quantitative analysis of segmental left ventricular wall motion from contrast left ventriculograms and scintigraphic cardiac-gated blood-pool images. This model was tested in dogs using implanted lead beads in the myocardium and contrast left ventriculography. Measured values of bead position and displacement were in good agreement with the estimated values determined by the model. Segmental left ventricular wall motion was also measured in 21 patients in whom both cardiac-gated blood-pool scintigrams and contrast left ventriculograms were obtained within minutes of one another. Wall motion values obtained using the end diastolic and end systolic frames of the gated blood-pool studies and the contrast left ventriculograms correlated favorably in the 60 degrees left anterior oblique view.

Animals↗
PubMed1982

Dimensional analysis of right and left ventricles during positive-pressure ventilation in dogs.

Our purpose was to determine the effects of controlled ventilation with positive end-expired pressure (PEEP) on ventricular dimensions and to relate changes in shape to changes in stroke volume and left ventricular volumes. Left and right ventricular dimensions were measured using biplane cinefluorography of dogs with radiopaque markers implanted in their hearts, and left ventricular volumes were derived from left ventricular dimensions by assuming that the left ventricle conformed to the shape of a nonprolate ellipsoid. As PEEP increased from 0 to 5, 10, and 15 cmH2O, stroke volume fell 36%, and all three left ventricular end-diastolic dimensions fell, with apex-base falling 5%, anterior-posterior falling 7%, and septal-lateral falling nearly twice as much, 12%. This resulted in a 11.3 cm3 fall in left ventricular end-diastolic volume. The right ventricular end-diastolic dimensions changed in opposite directions with respect to each other as the level and PEEP was raised to 15 cmH2O; one axis fell 3.2 mm, and the midpoint of the right ventricular free wall moved outward by 1.7 mm. Thus the fall in cardiac output (and stroke volume) during PEEP was associated with a fall in left ventricular end-diastolic volume and a change both left and right ventricular configurations. It is not known whether the left ventricular septal-lateral narrowing is the consequence of lateral wall compression by the lungs or encroachment on the left ventricle by the septum.

Animals↗
PubMed1982

Reflex cardiovascular depression induced by capsaicin injection into canine liver.

Capsaicin was injected into the portal circulation of 29 dogs after a blood delay pathway was constructed between the liver and right heart, through which capsaicin-contaminated blood could be replaced while systemic hemodynamics were maintained constant. Capsaicin (500 micrograms) rapidly decreased left ventricular systolic pressure (-10%), mean arterial pressure (-12%), heart rate (-4%), renal vascular resistance (-7%), maximal rate of left ventricular pressure rise (dP/dtmax) (-12%), and dP/dt at 25 mmHg developed left ventricular pressure (-15%) in animals with paced hearts. Left ventricular end-diastolic pressure did not change. Vagus nerve interruption at the level of the diaphragm did not alter hemodynamic changes occurring during capsaicin injections, but anterior hepatic nerve interruption eliminated the changes, suggesting that the cardiovascular responses were reflex in origin and that the principal afferent pathway traverses the hepatic nerve. This study demonstrates that activation of afferent fiber receptors within the liver tissue can contribute to neural regulation of the cardiovascular system, but the natural stimulus for these receptors is not known.

Animals↗
PubMed1982

Reflex relaxation of tracheal smooth muscle by thin-fiber muscle afferents in dogs.

Although the reflex cardiovascular and ventilatory responses evoked by stimulation of groups III and IV muscle afferents have been extensively investigated, less is known about the effects of stimulation of these afferents on airway caliber. Therefore, in 11 chloralose-anesthetized dogs, we recorded transverse smooth muscle tension from an innervated segment of the trachea, while we stimulated groups III and IV muscle afferents with capsaicin and bradykinin. Injection of both substances into the arterial supply of the skinned hindlimb evoked dose-dependent decreases in tracheal tension, whereas injection into the femoral vein either increased tension or had no effect on it. Injection of capsaicin and bradykinin into the arterial supply of the gracilis muscle also decreased tracheal tension. In addition, cutting the sciatic, gracilis, and femoral nerves abolished the decreases in tracheal tension caused by injection of capsaicin and bradykinin into the arterial supply of the hindlimb. We conclude that chemical stimulation of groups III and IV muscle afferents causes reflux relaxation of tracheal smooth muscle in dogs.

Animals↗
PubMed1982

Distribution of cardiac output during static exercise in the conscious cat.

Blood flows to major organs were measured in conscious cats to study the changes in the distribution of cardiac output during voluntary static (isometric) exercise. Five animals were operantly conditioned to hold a bar against a fixed resistance for 30 s. Organ flows were measured during rest and exercise by injecting 25-micrometer radioactive microspheres into the left atrium or left ventricle. Increases were observed during exercise in heart rate (18%), mean arterial pressure (25%), left ventricular systolic pressure (17%), and rate of left ventricular development (26%). Static exercise produced significant changes in flow (ml . min-1 .g-1) to the kidneys (-1.09 +/- 0.24), spleen (-0.85 +/- 0.21), and exercising muscles (+0.13 +/- 0.08), while flows to liver, heart, brain, and nonexercising muscle were not significantly changed from control levels. Denervation of the left kidney abolished the decrease in flow to that kidney during exercise. Thus, static exercise appears to produce a significant increase in blood flow to exercising muscles and significant reductions in blood flow to spleen and kidneys. The reduction in renal blood flow is mediated by a neural mechanism.

Animals↗
PubMed1982

Effects of capsaicin and bradykinin on afferent fibers with ending in skeletal muscle.

Capsaicin, injected into the arterial supply of the skinned hindlimb of dogs, evokes reflex increases in cardiovascular function. Moreover, the cardiovascular reflexes evoked by capsaicin are very similar to those evoked by static exercise. The afferent fibers initiating these reflex increases have not been identified electrophysiologically, although their endings are believed to be located in skeletal muscle. We have, therefore, attempted to determine which afferent fibers are stimulated by capsaicin. In anesthetized dogs, we recorded impulses from afferent fibers with endings in either the gastrocnemius or gracilis muscles and injected capsaicin (10-30 microgram/kg) into the abdominal aorta. Capsaicin stimulated 24 of 34 group IV (C fiber) endings, but only 5 of 19 group III (A delta fiber) endings. By contrast, bradykinin (0.5-1.5 microgram/kg) stimulated 17 of 33 group IV endings and 9 of 19 group III endings. Impulse activity for the 24 group IV afferents stimulated by capsaicin increased from 0.7 +/- 0.1 to a peak of 9.3 +/- 1.4 imp/sec. Firing started 6 +/- 1 seconds after injection and remained above control levels for 24 +/- 5 seconds. Capsaicin had no significant effect on the firing rate of 30 group I and II muscle afferents. Our results suggest that group IV muscle afferents are primarily responsible for causing the reflex increases in cardiovascular function evoked by injecting capsaicin into the arterial supply of the skinned hindlimb of dogs. Moreover, capsaicin is likely to be a useful pharmacological tool with which to determine the reflex autonomic effects caused by stimulation of group IV muscle afferents.

Afferent Pathways↗
PubMed1981

Blood pressure and heart rate response to static exercise in relation to electromyographic activity and force development.

5 healthy men performed static knee extension (90 degree knee angle) with one leg for 5 min. In one series of experiments the force was held constant at 20% of the isometric maximal voluntary contraction. In the other the initial force development was also 20%, but the smoothed, rectified electromyographic activity, (SREMG) recorded after 5 s of contraction was kept constant. Heart rate (HR), arterial mean blood pressure (MBP) (measured 20 cm proximally to the elbow in a. brachialis), EMG (surface electrodes) from the lateral portion of m. quadriceps femoris, and force were continuously recorded. HR and MBP increased approximately 40% in the force-constant experiments and approximately 20% in the SREMG-constant experiments. The greatest increase occurred during the first two minutes of contraction. In the force-constant experiments SREMG doubled, with the most marked increases occurring during the very early and late parts of the contraction. SREMG correlated with both HR (r = 0.85) and MBP (r = 0.98). In the SREMG-constant experiments force declined quickly during the first minute and remained at about 12% MVC thereafter. The observed cardiovascular responses to static contraction can best be explained as the result of the combined action of central and peripheral drives, the central drive being related to the central activity for the recruitment of motor units, and the peripheral drive being mediated through chemoreceptors in the exercising muscles.

Adult↗
PubMed1981

Reflex cardiovascular response during injection of capsaicin into skeletal muscle.

In an anesthetized dog, injections of capsaicin, a potent stimulator of small myelinated and unmyelinated fibers that originate as free nerve endings, into a neurally intact donor-perfused hindlimb produced a significant (P less than 0.05) increase in mean aortic pressure (20%), heart rate (12%), cardiac output (28%), and respiratory minute volume (97%). Organ blood flows were measured with 25-micrometers radioactive microspheres. During the injection of capsaicin, there was a decrease in renal blood flow (-25%), but liver, spleen, brain, heart, and skeletal muscle flows remained near control values. After section of the afferent neural connection from the donor perfused hindlimb, the responses to the injection of capsaicin were abolished. These reflex cardiovascular and respiratory responses and changes in organ flow caused by stimulation of capsaicin-sensitive receptors in skeletal muscle are similar to those that occur during induced isometric exercise in the hindlimb.

Animals↗
PubMed1981

Reflex alpha-adrenergic coronary vasoconstriction during hindlimb static exercise in dogs.

We studied 18 alpha-chloralose-anesthetized dogs to determine if alpha-adrenergic coronary vasoconstriction occurs with hindlimb static exercise. Exercise was elicited by spinal cord ventral nerve root stimulation. Regional coronary blood flow was determined by the radioactive microsphere method. Animals were studied under four experimental conditions: control rest and static exercise, rest and static exercise after beta-adrenergic blockade with propranolol (2 mg/kg), rest and exercise after alpha-adrenergic blockade with phentolamine (.35 mg/kg), and rest and exercise after combined alpha- and beta-adrenergic blockade. Myocardial oxygen consumption during exercise was determined during control and during alpha-adrenergic blockade conditions. Control hindlimb static exercise resulted in significant increases in systolic (10.6%) and diastolic (12.5%) arterial pressures, heart rate (12.2%), and double product (24.6%). Associated with the increased demand for oxygen, myocardial oxygen consumption increased (33.6%) as did left ventricular myocardial flow (29.6%). However, left ventricular coronary vascular resistance was unchanged during static exercise. After beta-adrenergic blockade, systolic (12.2%) and diastolic (11.6%) arterial pressures and double product (10.7%) still increased significantly, but heart rate did not change with static exercise. In contrast, alpha-adrenergic vasoconstriction was unmasked as left (LV) and right (RV) ventricular myocardial blood flow decreased (LV: -30.0%, RV: -25.0%) and coronary vascular resistance increased (LV: 52.5%, RV: 45.3%) with static exercise. Combined alpha- and beta-adrenergic blockade abolished the reduction in myocardial blood flow and the increase in coronary vascular resistance which occurred with static exercise after beta-adrenergic blockade. These data suggest that, during static exercise, reflexes from skeletal muscles can cause alpha-adrenergic coronary artery vasoconstriction.

Adrenergic alpha-Antagonists↗