Routine choledochotomy with cholecystectomy.
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Cholecystectomy↗
Biomedical subjects
J W Manning
Publications and source records attributed to J W Manning.
Choledocholithiasis, endoscopic sphincterotomy or common bile duct exploration.
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Common Bile Duct↗
Lung mechanics and oxygen consumption during spontaneous ventilation and severe heart failure.
The effects of acute heart failure on lung mechanics and oxygen consumption (VO2) during normocarbic spontaneous ventilation were studied in 21 anesthetized pigs. Heart failure severe enough to double oxygen extraction (O2ex) was induced with intravenous esmolol boluses and infusion. Compared to normal, the inspiratory elastic work of breathing (Wel) increased from 335 +/- 371 (mean +/- SD) to 559 +/- 48 mm Hg.ml (p less than 0.003) during heart failure, lung compliance (CL) fell from 121 +/- 144 to 22 +/- 15 ml/mm Hg (p less than 0.05), and respiratory power climbed from 140 +/- 200 to 245 +/- 214 mm Hg.ml.min-1 (p less than 0.002). These mechanical changes were accompanied by a decrease in both VO2 (221 +/- 61 to 191 +/- 50 mlO2/min, p less than 0.05) and oxygen delivery (DO2) (680 +/- 240 to 260 +/- 90 mlO2/min, p less than 0.004). The VO2/DO2 ratio doubled (p less than 0.0002), confirming increased O2ex. In conclusion, severe acute heart failure decreased CL, and increased Wel and respiratory power significantly. The depressed cardiac output limits both DO2, and to some extent, VO2. However, a greater proportion of the delivered O2 is consumed, supplying indirect evidence which suggests that the respiratory muscles' VO2 increases as a consequence of increased power expenditure.
Acute Disease↗
Role of sympathetic nerve activity in endotoxin induced hypotension in cats.
Within 10 min of intravenous (iv) injection of E. coli endotoxin (1 mg X kg-1) in alpha-chloralose anaesthetised cats, mean blood pressure (MBP) fell significantly to 86% of the pre-endotoxin level. There followed a gradual decline in MBP, so that after 60 min MBP was depressed to 49% of the pre-endotoxin level. Preganglionic splanchnic nerve (PSN) activity decreased significantly before the rapid fall in MBP. There followed a gradual decrease in PSN activity coincident with the significant fall in MBP, so that 60 min after iv injection of E. coli endotoxin PSN activity fell to 40% of the pre-endotoxin level. Heart rate did not differ significantly from the pre-endotoxin level in the control group. However, the hypotension and the reduction of PSN activity following endotoxin were abolished by intracisternal (ic) pretreatment with phentolamine (0.5 mg X kg-1). The heart rate in this group increased significantly, by 15% at 10 min and was maintained until the end of the experiment. These results indicate that in E. coli endotoxin hypotension the blood pressure falls together with the reduction in sympathetic outflow; and suggests that stimulation of central alpha-adrenergic receptors leads to an inhibition of activity in brainstem sympathetic pathways.
Animals↗
Effect of naloxone on baroreflex, sympathetic tone and blood pressure in the cat.
Studies were designed to determine the effect of naloxone on sympathetic nerve activity and blood pressure and, also to investigate the central effect of naloxone in relation to the baroreflex system in alpha-chloralose-anesthetized cats. Following intravenous injection of naloxone (2 mg/kg), preganglionic splanchnic nerve (PSN) activity significantly increased in parallel to the increase in blood pressure. Set gain (mmHg-1) of carotid sinus baroreflex together with the operational range (mmHg) was increased after naloxone. Intraventricular (4th) injection of naloxone (0.2 mg/kg) produced identical responses in blood pressure and PSN activity as well as an altered set gain and range of the baroreflex. Additionally, the pressor response to carotid hypotension and medullary pressor area stimulation were augmented during naloxone activation but not the pressor response to posterior hypothalamus stimulation. The depressor responses to stimulation of both carotid sinus nerve and medullary depressor region were facilitated by naloxone. These data suggest that naloxone has an effect on the central autonomic blood pressure regulatory circuits which participate in the carotid sinus baroreflex system.
Animals↗
Time dependence of mechanisms in the renin response to renal nerve stimulation.
The renin release responses to 1 and 5 min of renal nerve stimulation were determined. The left kidneys of alpha-chlorolose-anesthetized cats were pump perfused with blood while stimulating the decentralized renal nerves at different frequencies (0.5 ms, 10 V). With renal blood flow (RBF) held constant, 1 min of renal nerve stimulation increased renin secretion rate (RSR) at 1.0 (128%), 4.0 (168%) and 12.0 (160%) Hz. After 5 min of stimulation the responses were not different. Propranolol pretreatment prevented the increase in RSR at 1.0 Hz, and resulted in decreased RSR at 4.0 and 12.0 Hz. This response pattern occurred after 1 and 5 min of renal nerve stimulation. When renal perfusion pressure (RPP) was held constant, RSR at 1 min into the stimulation period was similar to that found in the constant RBF group. However, after 5 min the 4.0 Hz and 12.0 Hz responses were significantly greater than the 1 min responses (242% and 508%). Propranolol pretreatment resulted in renin responses after 1 min of stimulation which were similar to the beta-blocked constant RBF group. After 5 min of stimulation at 4.0 and 12.0 Hz RSR was greater than control levels. The results illustrate that renal nerve evoked renin release is time-dependent under constant RPP conditions. The data indicate the presence of 3 mechanisms in these responses. A beta-adrenergic receptor operates at all frequencies to increase renin release. When renal vasoconstriction occurs additional mechanisms are involved. One is inhibitory, independent of renal hemodynamic conditions and rapidly activated. The second is excitatory, occurs only under constant RPP conditions, and is activated slowly.
Animals↗
The effects of naloxone on the peripheral sympathetics in cat endotoxin shock.
The effects of naloxone on sympathetic nerve activity during E coli endotoxin hypotension were studied in alpha-chloralose anesthetized cats. Blood pressure and left preganglionic splanchnic nerve (PSN) activity were measured. Naloxone (2 mg/kg) was injected intravenously 30 min after endotoxin. In control group, 30 min after endotoxin, both mean blood pressure (MBP) and PSN activity decreased by 68 +/- 7% and 47 +/- 10%, respectively, and were followed by a gradual decline, so that after 60 min MBP and PSN activity were 54 +/- 8% and 48 +/- 7% of the pre-endotoxin level. The reduced blood pressure recovered to 81 +/- 4% of the pre-endotoxin level 5 min after naloxone. However, the naloxone-induced recovery of blood pressure was transient and there was a decline to the pre-naloxone level within 30 min after the injection. At the end of the experiment (60 min after endotoxin), the level of MBP was significantly higher than in the control group. Similarly, there was a modest recovery in PSN activity (61 +/- 7% of the pre-endotoxin level 5 min after naloxone) that was maintained for 20 min only to decline again. Three of five cats treated with an intermittent bolus injection (2 mg/kg, 30 min and 6 h after endotoxin) of naloxone survived, compared to only one of five nontreated cats. These observations suggest that at least part of the beneficial cardiovascular actions of naloxone in endotoxin shock involves activation of the efferent sympathetic system. To improve longterm survival it may be necessary to continuously administer naloxone.
Animals↗
Pyrimido-pyrimidine derivative, RA642, a central pressor agent in cat endotoxin shock.
The effects of a pyrimido-pyrimidine derivative, RA642, in endotoxin shock were studied. Blood pressure and preganglionic splanchnic nerve (PSN) activity were measured in alpha-chloralosed cats. Within 30 min of intravenous administration of E. coli endotoxin (1 mg/kg), blood pressure and PSN activity were 68 +/- 8% and 47 +/- 10% of control and by 60 min were depressed by 54 +/- 8% and 42 +/- 8%. RA642 (0.25 mg/kg) injected i.v. 30 min after endotoxin, caused blood pressure to recover significantly to 83 +/- 6% of control within 5 min and be maintained at that level. PSN activity was similarly increased to and maintained at 62 +/- 9% of control. The efficacy of RA642 in reversing the lethal consequences of endotoxin shock were dramatic; all treated animals survived whereas the mortality rate of non-treated animals was 83%. This strongly suggests that the central pressor agent, RA642, may have important therapeutic applications in the management of endotoxin shock.
Animals↗
Neural and vascular interaction in renin response to graded renal nerve stimulation.
The effect of a 1-min period of renal nerve stimulation was studied in alpha-chloralose-anesthetized cats, whose left kidneys were pump perfused. Renal hemodynamics and filtration parameters were unaltered at stimulation frequencies of 2.0 Hz or less; however, renin secretion rates (RSR) increased with frequency reaching 3 times the control level. At higher frequencies renal vasoconstriction occurred and glomerular filtration rate (GFR) fell. RSR was increased but little more than at 2.0 Hz. The RSR response plots were similar to constant-flow and constant-pressure perfused preparations. beta-Adrenergic blockade with propranolol abolished low-frequency responses and resulted in progressive decreases in RSR at higher frequencies. alpha-Adrenergic blockade with phentolamine prevented renal vascular and GFR changes, whereas RSR continually increased up to 12.0 Hz (13.5 times control). Papaverine treatment, to prevent vascular-GFR changes without blocking alpha-receptors, resulted in similar renin responses. The results indicate that the beta-adrenergic receptor mediates increases in RSR in proportion to frequency when vascular-GFR factors are constant. When renal vasoconstriction occurs at high frequencies the beta-receptor mechanism interacts with an inhibiting mechanism indirectly mediated by alpha-adrenergic receptors.
Animals↗
Centrally mediated hypotensive effect of E coli endotoxin in the anesthetized cat.
E coli endotoxin, 1 mg/kg, injected intravenously in cats anesthetized with alpha chloralose caused an initial transient rise followed by a prolonged decrease in systemic blood pressure. The renal blood flow decreased gradually while the nictitating membrane contracted. Calculated renal vascular resistance significantly decreased 10 min after intravenous injection of the endotoxin. E coli endotoxin injected into the cisterna magna (50 micrograms/kg), and the nucleus tractus solitarius (2.5 micrograms/kg) produced an abrupt and persistent fall in the systemic blood pressure, the heart rate, the renal blood flow, and the calculated values for the renal vascular resistance. The pressor response to carotid sinus hypotension (carotid occlusion) was reduced after intracisternal and intravenous injection of E coli endotoxin. The prolonged hypotensive effects caused by the intravenous and intracisternal administration of E coli endotoxin and the reduction of the pressor response to carotid occlusion were abolished by pretreatment with phentolamine (500 micrograms/kg) intracisternally, whereas the initial increase of the blood pressure and transient contraction of the nictitating membrane remained. In conclusion, the hypotensive effect of E coli endotoxin may be mediated by a central autonomic blood pressure regulatory circuit. The endotoxin activates central alpha-adrenergic receptors that are components of a brain stem inhibitory pathway which participate in the baroreflex pressor response. This central mechanism together with the peripheral actions of endotoxin would yield the complex pathophysiological responses seen in endotoxin shock.
Anesthetics↗
Visceral afferents and the fastigial nucleus in vascular and plasma renin adjustments to head-up tilting.
A two min orthostatic stress of 30 degrees head-up tilting in alpha-chloralose anesthetized and paralyzed cats results in compensatory changes in cardiovascular parameters (systemic blood pressure, renal perfusion pressure) and renin release. The dynamics of the response leads to shifts in systemic arterial pressure characterized by 3 phases. The initial phase, a fall in systemic pressure, is followed by a rapid compensatory phase with a period that does not exceed 50 s. The near steady-state adjustment in blood pressure and renal vascular resistance represents the third phase, has a longer time constant and is adequately accounted for by both arterial and cardiopulmonary baroreflex mechanisms. Indeed, fixing carotid sinus pressure in the vagotomized cat at high or low levels alters only the magnitude of the steady-state pressure obtained with tilt and not the early rapid compensation of the second phase. By contrast, bilateral lesions of the fastigial nucleus of the cerebellum abates the rapid phase of systemic compensation to tilting. Renin secretion significantly increased (greater than 2 1/2) with tilt and this increase was abolished by vagotomy. By fixing carotid sinus pressure at high or low levels in the vagotomized cat, tilt resulted in only a modest rise in renin secretion. Following fastigial lesions such as upwards trend was abated. Three neural components (cerebellar fastigial pressor, arterial baroreflex and cardiopulmonary baroreflex) appear necessary for the integrated response in cardiovascular adjustment to head-up tilt. The adjustments to orthostatic stress comprise both rapid neural as well as long-term humoral responses.
Afferent Pathways↗
Altered renal vascular tone and plasma renin activity due to fastigial and baroreceptor activation.
The effects of stimulating the cerebellar fastigial nucleus in altering renal vascular resistance were assessed at three levels of carotid sinus pressure (CSP). In alpha-chloralose-anesthetized, vagotomized, and salt-depleted cats, renal vascular resistance changes were established by perfusing the isolated carotid sinus at high (197 +/- 17 mmHg), medium (117 +/- 8 mmHg), and low (60 +/- 7 mmHg) pressure. The hemodynamic state of the perfused kidney was determined from flow-pressure curves. In relative units, the flow resistance in the renal bed was for low CSP, 2.60 PRU100, for medium CSP, 2.25 PRU100, and for high CSP, 1.22 PRU100. The fastigial pressor response was imposed at each flow-presure determination with or without superior cerebellar peduncle lesions. An increase in the resistance with the fastigial stimulation was noted at each of the three hemodynamic states; 14% at low, 26% at medium, and 22% at high CSP. With increased renal vascular resistance evoked through the baroreflex, there was an increase in plasma renin activity. The rise in plasma renin activity could be attributed in large part to an increase in sympathetic renal nerve activity wherein the fastigial pressor response shared a synergistic action at medium and high carotid sinus pressure. The effect of the fastigial stimulation on renal vascular resistance and renin secretion was abolished by transections of the superior cerebellar peduncles.
Animals↗
Carotid baroreflex regulation of plasma renin levels.
The influence of carotid sinus pressure (CSP) on plasma renin activity (PRA) was studied in vagotomized, alpha-chloralose-anesthetized salt-deprived (<1 meq Na+/day) or salt-loaded (100-125 meq Na+day) cats. Changes in renal vascular resistance were produced by varying the pressure in the isolated perfused carotid sinus while maintaining renal blood flow constant in one kidney. Renal flow-pressure determinations were made at high, medium, and low CSP. Venous blood samples were withdrawn for PRA determination by radioimmunoassay after 10 min at each CSP. Low CSP resulted in an increased renal resistance and a dramatic elevation of the PRA in both groups. High CSP also resulted in an increase in PRA (due to contralateral variable-flow kidney) accompanied by a decrease in renal vascular resistance. No difference was found between PRA during medium CSP ad initial control PRA. Propranolol blocked the increase in PRA during low CSP but had no effect on the elevated PRA during high CSP. It is concluded that low CSP produced an increase in PRA that was associated with a reflex activation of renal sympathetic nerves.
Animals↗
Vascular resistance of intestine, muscle and skin during blood pressure oscillation.
After the blood supply to the head was surgically limited to one common carotid artery in rabbits, the artery was compressed by exertion of stepwise elevated side pressure on a segment of the artery. Systemic arterial pressure rose and began to oscillate when the side pressure was increased to 50 to 60 mmHg. The oscillations were regular and occurred at a rate of 3 to 4 per minute with a wave height of 15 to 45 mmHg. Concomitant with systemic pressure oscillations, and in near synchrony were undulations in the perfusion pressures recorded during constant flow from the vascularly isolated abdominal skin, skeletal muscle and small intestine. With the graded elevation of side pressure on the common carotid artery, mean systemic pressure and perfusion pressure showed a nearly exponential relation. The ratio between the two variables was slightly less than one below the systemic pressure of 120 mmHg and rapidly increased above this level. At ratios greater than one, the peripheral resistance undulations in the isolated areas gave a larger minimum and maximum, a sharper contour and, particularly in the skin, a phase lag in the period of the wave form when compared to the systemic pressure oscillations. These observations highlight the differences in response characteristics of peripheral resistance vessels and those of cardiac output and different consecutive parts of the systemic arteries during periods of intense sympathetic activation.
Animals↗
Responses of the uterine circulation to sympathetic nerve stimulation.
Pregnant and non-pregnant sheep uteri were perfused in situ with arterial blood at a constant flow rate. Unilateral stimulation (1-2 ma, u ms pulse) of the distal end of the severed sympathetic chain (L3-L4) at frequencies between 5 and 25 Hz produced a graded increase in uterine artery pressure in both horns. At 25 Hz, pressure in the horn ipsilateral to the stimulated sympathetic chain increased by 28 +/ 2% in four pregnant animals and 32 +/ 5% in six non-pregnant ewes. The response of the contralateral horn was significantly smaller than that of the ipsilateral horn (P less than or equal to 0.05). The response was alpha-mediated since it was abolished by local injection of dibenzyline into the middle uterine artery. The responses of the pregnant and non-pregnant animals were similar, indicating that pregnancy did not alter the alpha-adrenergic responses of the uterine vasculature.
Animals↗
Repetitively firing medullary neurons responsive to carotid sinus nerve stimulation and norepinephrine infusion.
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Animals↗
Central nervous system control of cardiac rhythm.
Stimulation of sites in the midbrain reticular formation and in the posterior hypothalamus of the cat resulted in a large to modest rise of arterial pressure and the induction of cardiac dysrhythmias. Most frequently, these arrhythmias developed upon cessation of brain stem stimulation but also occurred during the stimulus period in 5 of 23 cats studied. The arrhythmias disappeared upon cooling and reappeared upon rewarming the vagus nerves. The ventricular dysrhythmias also were abolished by methylscopolamine, by bilateral vagatomy, or by extirpation of the stellate ganglia. Simultaneous stimulation of both distal end of the cut right vagus nerve and the decentralized right stellate ganglion caused arrhythmias similar to those observed after diencephalic stimulation. These data are interpreted to indicate that the cardiac arrhythmias evoked by brain stem stimulation result from the interplay of both sympathetic and parasympathetic influences on the heart. The response patterns of a population of medullary neurons activated by carotid sinus nerve stimulation were modified by condition stimuli to posterior hypothalamic sites. From studies on unit activity of brain stem areas known to participate in cardiovascular adjustment, a schema is proposed of hypothalamic-medulla interaction as a central mechanism that may account for the development of ventricular arrhythmias.
Animals↗
Hypothalamic modulation of baroreceptor afferent unit activity.
Unit responses to sinus nerve stimulation were recorded in the medulla. A conditioning stimulus to the posterior hypothalamus produced inhibition of 65% of unit responses to sinus nerve stimulation as early as 7 ms and extending as long as 790 ms after conditioning; 50% recovered after 300 ms. Unit responses to hypothalamic stimulation alone were also recorded in the medulla, some in the same loci as other unit responses to sinus nerve stimulation. They could be activated by contralateral as well as ipsilateral hypothalmic stimulation and showed recurrent bursts of firing over a 1,000-ms poststimulus interval. Evoked potentials and unit responses were recorded in the posterior hypothalamus, some occurring within 10--20 ms poststimulation of the sinus nerve, indicating that baroreceptor information is ascending in a time sufficiently short to involve the hypothalamus in reflex regulation of blood pressure as well as more generalized homeostatic responses which include the cardiovascular system.
Animals↗