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Biomedical subjects

J C Longhurst

Publications and source records attributed to J C Longhurst.

At least 127 records · Page 7Linked to original sources
PubMed1984

Static contraction of hindlimb muscles in cats reflexly relaxes tracheal smooth muscle.

Static contraction of skeletal muscle is associated with increased ventilation. Although chemical stimulation of afferents from skeletal muscle causes relaxation of tracheal smooth muscle, it is not known if skeletal muscle contraction also causes tracheal relaxation. Therefore, in 10 chloralose-anesthetized cats, I examined the hemodynamic and tracheal smooth muscle responses to hindlimb skeletal muscle contraction induced by stimulating the L7 and S1 ventral roots. Isometric tension was measured in the transverse cervical trachea. During contraction average gastrocnemius tension increased from 0.7 +/- 0.1 to 4.9 +/- 0.6 kg, blood pressure and heart rate increased from 100 +/- 8 to 128 +/- 9 mmHg and from 192 +/- 11 to 202 +/- 13 beats/min, respectively, whereas tracheal tension decreased from 19.7 +/- 0.4 to 17.5 +/- 0.7 g (all P less than 0.02). There were significant (P less than 0.01) linear correlations between change in tracheal tension and maximal developed tension (r = -0.65), tension time (r = -0.68), and average developed tension (r = -0.76). Transection of the L7 and S1 dorsal roots in six cats reduced the tracheal relaxation associated with muscle contraction (pre: 19.9 +/- 0.3 to 17.5 +/- 0.3 g vs. post: 20.3 +/- 0.4 to 20.3 +/- 0.6 g) while average developed gastrocnemius muscle tension was not altered (pre: 1.1 +/- 0.1 to 6.4 +/- 1.1 kg vs. post: 1.2 +/- 0.2 to 6.8 +/- 1.2 kg). Thus static contraction of hindlimb muscles in cats reflexly lowers tracheal tension. This response is related to muscle mass and total tension generated by the contracting skeletal muscle.

Animals↗
PubMed1984

Oxygen consumption and hemodynamic responses during graded treadmill exercise in the dog.

A description is given of a technique that provides a relatively simple means by which O2 consumption and hemodynamic variables can be measured in exercising dogs. We used a multistage submaximal treadmill test to study the responses of 10 foxhounds to dynamic exercise. They were also studied during maximal treadmill exercise. O2 consumption increased from 16.3 +/- 1.7 ml O2 X min-1 X kg-1 at rest to 92.9 +/- 9.7 ml O2 X min-1 X kg-1 at a work load of 6.4 km/h, 20% grade and to 111.9 +/- 9.6 ml O2 X min-1 X kg-1 during maximal exercise. Cardiac output (CO) increased from 6.11 +/- 0.45 l/min at rest to 16.91 +/- 1.46 and 17.66 +/- 0.60 l/min at 6.4 km/h, 20% grade and maximal exercise, respectively. Arteriovenous O2 difference increased from 5.8 +/- 0.3 vol% at rest to 12.0 +/- 0.4 and 13.2 +/- 0.7 vol% at 6.4 km/h, 20% grade and maximal exercise, respectively. Heart rate (HR) increased from 116 +/- 7 beats/min at rest to 250 +/- 8 beats/min at 6.4 km/h, 20% grade and to 278 +/- 6 beats/min during maximal exercise. O2 uptake, CO, and arteriovenous O2 difference increased with the onset of exercise, appeared to level at lower work intensities (6.4 km/h, 4 and 8% grade), and increased significantly at each of the higher work intensities (6.4 km/h, 12, 16, and 20% grade). Additionally, we observed linear relationships between O2 consumption and HR (HR = 1.35 X VO2 + 120.5; r = 0.87; P less than 0.001) and between O2 consumption and CO (CO = 5.91 X VO2 + 216.6; r = 0.96; P less than 0.001). Further, the linear relationship between O2 consumption and CO demonstrated in the present study is similar to that observed in humans.

Animals↗
PubMed1983

Stimulation of pancreatic afferents reflexly activates the cardiovascular system in cats.

Chemical stimulation of afferents from the stomach and gallbladder has been shown reflexly to activate the cardiovascular system. It is not known, however, whether stimulating afferents from the pancreas evoke similar reflex activity. Therefore we recorded the cardiovascular responses in cats anesthetized with methoxyflurane, while we applied capsaicin (200 micrograms/ml) and bradykinin (0.001-1,000 micrograms/ml) to the surface of the pancreas. Topically applying these algesic substances evoked cardiovascular responses that included increases in systemic arterial pressure, heart rate, left ventricular dP/dt at 40-mmHg developed pressure and systemic vascular resistance. Bilateral vagotomy at the level of the diaphragm did not diminish the cardiovascular responses evoked by capsaicin or bradykinin. In contrast, removal of the celiac and superior mesenteric ganglia abolished the cardiovascular responses demonstrated previously when capsaicin or bradykinin was applied to the pancreas. We conclude that afferent endings in the pancreas can be stimulated reflexly to increase cardiovascular function in cats. This reflex activation represents a potential mechanism for eliciting the cardiovascular changes observed during acute pancreatitis, particularly the marked vasoconstriction that may lead to renal failure.

Afferent Pathways↗
PubMed1983

Effects of static muscular contraction on impulse activity of groups III and IV afferents in cats.

Static contraction of the hindlimb muscles, induced by electrical stimulation of the ventral roots, reflexly increases arterial blood pressure and heart rate. Although stimulation of groups III and IV muscle afferents is believed to cause these reflex increases, the responses of these afferents to a level of static contraction that increases arterial pressure have not yet been determined. Therefore, in barbiturate-anesthetized cats, afferent impulses arising from endings in the gastrocnemius muscle were recorded from the L7 or S1 dorsal roots, while the cut peripheral end of the L7 ventral root was stimulated. In addition, the effects of capsaicin (100-200 micrograms) and bradykinin (25 micrograms) on the activity of the groups III and IV afferents stimulated by contraction were examined. Contraction of the gastrocnemius muscle to a level equal to or greater than that needed to cause a pressor response stimulated 12 of 19 (63%) group III afferents and 13 of 19 (68%) group IV afferents. However, the discharge patterns of the group III afferents stimulated by contraction were very different from those of the group IV fibers. No relationship was found between those fibers stimulated by contraction and those stimulated by chemicals. Our results suggest that although both groups III and IV muscle afferents contribute to the reflex cardiovascular increases evoked by static exercise, group III fibers were likely to be stimulated by the mechanical effects of muscular contraction, whereas at least some group IV fibers were likely to be stimulated by the metabolic products of muscular contraction.

Afferent Pathways↗
PubMed1983

Stimulation of splanchnic afferents reflexly relaxes tracheal smooth muscle in dogs.

Although chemical stimulation of abdominal visceral afferents has been shown to reflexly increase cardiovascular and ventilatory function, the effect of stimulating these afferents on airway smooth muscle is unknown. Therefore, we recorded transverse smooth muscle tension from an innervated segment of trachea in chloralose-anesthetized dogs while we topically applied capsaicin (200 micrograms/ml) and bradykinin (0.01-10 micrograms/ml) to the serosal surfaces of the stomach, small intestine, and gallbladder. Application of these irritant substances to the stomach and small intestine decreased tracheal tension and increased mean arterial pressure. However, application of capsaicin and bradykinin to the gallbladder had only small effects on both of these variables. Cutting the splanchnic nerves abolished or greatly attenuated the decreases in tension and increases in mean arterial pressure, whereas cutting the vagi had no effect on them. We conclude that stimulation of splanchnic afferent endings in the stomach and small intestine reflexly relaxes tracheal smooth muscle in dogs. This effect may be one component of the constellation of autonomic responses reflexly evoked by abdominal visceral pain and inflammation.

Afferent Pathways↗
PubMed1983

Cardiovascular reflexes arising from the gallbladder of the cat. Effects of capsaicin, bradykinin, and distension.

We have studied the cardiovascular responses which can be evoked when the gallbladder is stimulated pharmacologically or mechanically. To determine the potential for reflex cardiovascular activation, we applied capsaicin, a selective thin-fiber agonist, to the serosal surface of the gallbladder. This algesic substance evoked cardiovascular responses which included increases in mean arterial pressure (MAP) by 14%, heart rate (HR) by 3%, left ventricular dP/dt at 40 mm Hg developed pressure (dP/dt DP40) by 14%, and systemic vascular resistance (SVR) by 19%. There were no demonstrable effects on the cardiovascular system when this same substance was applied to the surface of the liver. Bilateral vagotomy at the level of the diaphragm did not alter the responses to capsaicin. Right atrial overdrive pacing did not reduce the positive inotropic effect elicited when the gallbladder was stimulated. Removal of the celiac and superior mesenteric ganglia, or selective denervation of the gallbladder, abolished the cardiovascular responses which were evoked previously. beta-Adrenergic blockade, however, abolished only the reflex chronotropic and intropic responses. Thus, the potential for eliciting reflex cardiovascular alterations by stimulating gallbladder afferents with capsaicin was established. In subsequent studies, stimulating the gallbladder with bradykinin, an endogenous polypeptide, evoked a reflex activation of the cardiovascular system similar to that seen with capsaicin (MAP = 14%; HR = 4%; dP/dt DP40 = 18%; SVR = 14%). These reflex responses were dose dependent, were produced by mucosal as well as serosal application of this substance, and were eliminated by bilateral splanchnic nerve action. In contrast to capsaicin and bradykinin, distension of the gallbladder did not cause any cardiovascular alterations. We conclude that stimulation of gallbladder afferents by the algesic substance capsaicin or by bradykinin, an endogenous substance that under certain conditions may be formed in bile, can induce significant reflex activation of the cardiovascular system.

Adrenergic beta-Antagonists↗
PubMed1983

Bradykinin-induced cardiovascular reflexes from the gallbladder in cats.

To determine whether bradykinin, an algesic substance produced in certain inflammatory states, can stimulate gallbladder receptors to cause significant cardiovascular reflexes, we applied this agent to the serosal surface of the gallbladder in cats anesthetized with methoxyflurane. As a control, bradykinin was also applied to the serosal surface of the liver surrounding the gallbladder. Significant cardiovascular reflexes were obtained from the gallbladder in an increasing, dose related fashion over a range of concentrations from 50 pg/ml to 100 micrograms/ml of bradykinin. The cardiovascular responses occurred after a latency of 13 +/- 0.92 seconds (mean +/- SE) and included increases in mean arterial pressure, systemic vascular resistance, heart rate and myocardial contractility (dP/dt at 40 mmHg developed pressure). There was also a small but significant increase in left ventricular end-diastolic pressure, but no change in aortic flow. Application of bradykinin to the liver did not evoke any cardiovascular responses. Bilateral vagus nerve transection just above the diaphragm did not alter the cardiovascular responses to application of bradykinin on the gallbladder. However, the hemodynamic responses were partially diminished by right splanchnic nerve transection and were completely eliminated by bilateral splanchnic nerve transection. We conclude that bradykinin, a substance that is formed within the gastrointestinal tract and possibly in bile, can stimulate gallbladder receptors to induce significant reflex activation of the cardiovascular system.

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

Sympathoadrenal mechanisms in hemodynamic responses to gastric distension in cats.

There is presently little information on the efferent mechanisms responsible for the reflex cardiovascular activation during passive gastric distension. Therefore, 40 cats anesthetized with alpha-chloralose were studied with passive gastric balloon distention before and during 1) two repeated gastric distensions, 2) beta-adrenergic blockade with propranolol, 3) alpha-adrenergic blockade with phentolamine, or 4) bilateral adrenalectomy. Before and during each distension mean arterial pressure, heart rate, cardiac output, rate of rise of left ventricular pressure (dP/dt) at 40 mmHg developed pressure and calculated systemic vascular resistance were determined. Repeated gastric distension caused similar hemodynamic responses without tachyphylaxis. beta-Blockade significantly reduced the increase in dP/dt from 893 +/- 362 to 150 +/- 63 mmHg/s. alpha-Blockade significantly altered the changes in mean arterial pressure from 33 +/- 5.0 to -2 +/- 4.7 mmHg and systemic vascular resistance from 0.114 +/- 0.019 to 0.004 +/- 0.031 peripheral resistance units. Bilateral adrenalectomy significantly diminished the contractile response from 525 +/- 107 to 50 +/- 85 mmHg/s but did not significantly alter the pressor and vasoconstrictor responses. We conclude that, during passive gastric distension in cats, the increase in myocardial contractility is mediated by beta-adrenergic-receptor stimulation, whereas the arterial vasoconstrictor and pressor responses are mediated by alpha-adrenergic receptor stimulation. Additionally, during gastric distension a substantial portion of the contractile response is dependent on the integrity of the adrenal glands.

Adrenalectomy↗
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

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

Cardiovascular reflexes elicited by passive gastric distension in anesthetized cats.

Hemodynamic responses to passive gastric distension were examined in alpha-chloralose anesthetized cats. Gastric balloons were distended with 37 degrees C fluid at slow (50 ml/min) and rapid (250 ml/min) infusion rates before and after laparotomy. Passive gastric distension at the slow infusion rate significantly (P less than 0.05) increased mean arterial pressure (MAP) by 28%, dP/dt at 40 mmHg developed pressure by 29%, and systemic vascular resistance (SVR) by 35%. Likewise, the rapid distension rate significantly (P less than 0.05) increased MAP (20%), dP/dt (16%), and SVR (23%). Heart rate, aortic flow, and left ventricular end-diastolic pressure remained unchanged at both distension rates. Cardiovascular responses to passive gastric distension were similar before and after laparotomy. Section of the vagus nerve at the diaphragm did not alter the responses, whereas abdominal splanchnic nerve section significantly (P less than 0.05) reduced the changes in mean arterial pressure and dP/dt. These results indicate that passive gastric distension in the cat elicits cardiovascular reflexes sufficient to increase myocardial oxygen demand. Such a reflex response could potentially contribute to postprandial angina in humans.

Animals↗
PubMed1981

Total plasma creatinine: an accurate measure of total striated muscle mass.

Creatinine is a metabolite unique to striated muscle. Measurement of 24-h urinary creatinine excretion is an established method for estimating striated muscle mass. However, accurate assessment of urinary creatinine excretion is often impractical. We investigated the hypothesis that total plasma creatinine could be used instead of urinary creatinine excretion to estimate body composition. In 24 men, plasma volume and plasma creatinine concentration were measured, and total plasma creatinine was calculated as the product of these two measurements. Other measurements included urinary creatinine excretion, total body water, and anthropometry. Total plasma creatinine correlated strongly with urinary creatinine excretion (r = 0.82) and with weight, total body water, and anthropometrically estimated lean body mass. Muscle mass could be predicted by the equation: 0.88 x total plasma creatinine (mg). To verify this relationship, total plasma creatinine was prospectively measured in four dogs, then their total striated muscle was removed and weighed. Predicted muscle mass was within +/- 3.9% (range = 0.5-10.8%) of observed muscle mass. The ability to estimate muscle mass conveniently and accurately from total plasma creatinine should prove valuable for future studies in physiology and body composition.

Adult↗
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↗
PubMed1981

Chronic training with static and dynamic exercise: cardiovascular adaptation, and response to exercise.

To determine the acute and chronic effects of static and dynamic exercise upon the cardiovascular system, two groups of athletes were studied and compared to untrained control individuals. Thus, 12 long distance runners (LDR) and 17 competitive weight lifters (CWL) were compared to 10 light controls (LC) and 14 heavy controls (HC). The echocardiographically measured left ventricular mass (LVM) was shown to be increased in both groups of athletes. When this mass was related to lean body mass, the LDR demonstrated a significantly increased LVM, whereas the CWL had a LVM similar to that of the HC. During static handgrip exercise, the LDR maintained a relative bradycardia and, consequently, a lower calculated double product when compared to the LC, whereas the CWL reacted similarly to the HC. Further, the LDR demonstrated higher end-diastolic and higher end-systolic volume indices than the LC during static exercise. The exercising stroke volume index and the cardiac index were, however, not significantly different in the LDR compared to the LC. In contrast to the LDR, the cardiovascular dynamics of the CWL changed in a manner very similar to that of the HC during static exercise. This information suggests, therefore, that endurance training alters both the absolute and relative left ventricular mass and the response of the cardiovascular system to static exercise. On the other hand, static exercise training increases the absolute but not the relative left ventricular mass. Also, the immediate hemodynamic response to static exercise is similar in athletes who train with this form of exercise compared to untrained control subjects.

Adult↗
PubMed1980

The spinal cord ventral root: an afferent pathway of the hind-limb pressor reflex in cats.

1. In anaesthetized cats the sciatic nerve was cut and the central end was stimulated at a high frequency and voltage. This caused an increase in arterial blood pressure and a rise in heart rate. The pressure response was diminished by dorsal root section but not completely eliminated until ventral root section (L4-S3). The tachycardia response was abolished by dorsal root section alone. 2. In other cats capsaicin was injected intra-arterially into the hind limb, causing elevations in both blood pressure and heart rate. Similar to the sciatic nerve stimulation experiments, the pressor response was principally reduced by dorsal root section but was further significantly decreased by ventral root section (L1-S3). The rise in heart rate was prevented by dorsal root section alone. 3. It is concluded that, in cats, the afferent pathway of the pressor response to sciatic nerve stimulation and to hind-limb capsaicin injection are conducted principally in the dorsal roots but also to a small extent in the ventral roots of the spinal cord. Although the tachycardia response appears to be conducted only through the dorsal roots, it is possible that at lower resting heart rates and by stimulation of a large population of the unmyelinated skeletal muscle afferents, the ventral root is a functional pathway.

Afferent Pathways↗
PubMed1980

Echocardiographic left ventricular masses in distance runners and weight lifters.

Sixty individuals including 17 competitive weight lifters (CWL), 12 competitive long-distance runners (LDR), 7 amateus (noncompetitive) weight lifters (AWL), 14 heavy controls (HC), and 10 light controls (LC) were studied at supine rest with echocardiographic determination of the left venticular mass (LVM) by the Penn convention. Lean body mass (LBM) was estimated by the Wilmore-Behnke method. The absolute LVM (mean +/- SE) was increased in the two competitive athlete groups compared to controls (LDR: 195 +/- 12; CWL: 190 +/- 10 vs. LC: 122 +/- 10; HC: 151 +/- 9 g). The AWL had a mass (174 +/- 20 g) intermediate between the LDR-CWL and the HC-LC groups. A significant (P = 0.033) correlation of LVM was found with LBM although the correlation coefficient was low (r = 0.276). Normalizing LVM by LBM revealed a significantly higher mass for LDR compared to all other groups but equalized CWL and HC (LDR: 3.2 +/- 0.2; CWL: 2.5 +/- 0.1; AWL: 2.5 +/- 0.2; HC: 2.3 +/- 0.2; LC: 2.0 +/- 0.2 g). These data suggest that training for competitive long-distance running (dynamic training) elevates LVM compared to nonathletic controls and CWL. On the other hand, training for weight lifting (static training) increases absolute LVM but only to the extent that LBM is increased.

Adult↗