Uphill versus downhill high-intensity training effectiveness in preserving vascular function and exercise performance in runners who reduce their regular endurance training.

Purpose: The COVID-19 restrictions have limited outdoor physical activities. High-intensity training (HIT) may be a valid indoor alternative. We tested whether an indoor HIT is effective in maintaining vascular function and exercise performance in runners who reduce their usual endurance training, and whether a downhill HIT is as effective as an uphill one for such purposes. Methods: Sixteen runners performed the same 6-week HIT either uphill (UP, eight runners) or downhill (DOWN, eight runners). Eight runners continuing their usual endurance training acted as a control group (CON). The following data were collected before vs after our HIT: vascular conductance during rapid leg vasodilation to assess vasodilation capacity; V̇O2max through running incremental test to exhaustion; 2000 m running time; neuromuscular indexes related to lower-limb muscle strength. Results: Both uphill and downhill HIT failed in maintaining the pre-HIT leg vasodilation capacity compared to CON, which was, however, blunted more after uphill than downhill HIT. V̇O2max and 2000 m time were similar after downhill HIT compared to CON, and augmented after uphill HIT compared to CON and DOWN. Indexes of lower-limb muscle strength were similar before vs after HIT and among groups. Conclusion: Our HIT was ineffective in maintaining the pre-HIT leg vasodilation capacity compared to runners continuing their usual low-intensity endurance training, but did not lead to reductions in V̇O2max, 2000 m time performance, and indexes related to lower-limb muscle strength. Our data show an appealing potential for preserving exercise performance with low cardiorespiratory effort via downhill running.

Energy cost and efficiency of Venetian rowing on a traditional, flat hull boat (Bissa).

The total net metabolic power output (E, kW) required to scull a traditional, flat hull boat--the "Bissa", 9.02 m long and weighting about 500 kg including the crew-was assessed at different constant speeds (nu) ranging from 2.44 to 3.75 m s(-1). E increased with the speed: E = 0.417 x e (0.664v ); r (2) = 0.931. The amount of metabolic energy spent per unit distance (C, J m(-1)) to move the "Bissa", calculated by dividing E by the corresponding nu, was a linear function of nu: C = 0.369 nu -0.063; r (2) = 0.821. The hydrodynamic resistance met by the boat in the water--drag (D, N)--was estimated by analysing the decay of the reciprocal of nu as a function of time measured during several spontaneous deceleration tests carried out in still water and by knowing the total mass of the watercraft plus crew. D increased as a square function of speed: D = 12.76 v (2). This allowed us to calculate the drag efficiency (g(d)), as the ratio of D to C: g(d) increased from 8.9 to 13.7% in the range of the speeds tested. The "Bissa" turned out to be as economical as other flat hull, traditional watercrafts, such as the bigger Venetian gondola, and her g(d) was similar to that of other modern and traditional watercrafts.

Adaptations to endurance training in the healthy elderly: arm cranking versus leg cycling.

The effect in healthy elderly subjects of cycle ergometer or arm ergometer training on peak oxygen consumption (VO(2peak)) and ventilatory threshold (VT) was studied. The aim was to determine the benefit of each training modality on specific and cross exercise capacity. The cross-effect was also evaluated as an index of the central nature of the adaptive response to training. Twelve non-smoking healthy males (age: 67 +/- 5 year; body mass: 75 +/- 9 kg) were randomly divided in two age-matched groups of six, performing an arm cranking (ARM) or a cycloergometer (CYC) training (12-week, 30 min, 3 times/week), while a third group of 6 subjects (age: 73 +/- 4 year; body mass: 80 +/- 8 kg) performed no training (control, C). At baseline and following the intervention, subjects carried out an incremental test to exhaustion both on the ergometer on which they trained (specific test) and on the other ergometer (cross test). Respiratory variables were measured breath by breath and heart rate (HR) was recorded. Peak oxygen consumption (VO(2peak)), ventilation (VE(peak)), oxygen pulse (O2P(peak)) and heart rate (HR(peak)) were averaged over the last 10 s of exercise. Following training, while HR(peak) remained unchanged, significantly higher W(peak), VO(2peak), VE(peak) and O2P(peak) were obtained in both training groups, on both ergometers. The amplitude of the increase in W(peak), VO(2peak) and O2P(peak) was significantly higher for specific than for cross tests ( approximately 19% vs. approximately 8 % in CYC; approximately 22% vs. approximately 9% in ARM, P < 0.01) while the increase in same test condition was similar. No change was observed in the C group. The results indicate that aerobic training brought about with different muscle masses, produce similar improvements in maximal and submaximal exercise capacity. Roughly half of such improvements are specific to exercise mode, which suggests peripheral adaptations to training. The other half is non-specific since it influences also the alternative exercise modality, and is probably due to central adaptations.

Evidence of parasympathetic impairment in some patients with cardiac syndrome X.

OBJECTIVES: Cardiac syndrome X (SX) is a clinical condition characterised by angina, positive exercise stress test and negative coronary angiography; it has often been attributed to sympathetic hyperactivity. Here we tested the hypothesis that a parasympathetic, rather than a sympathetic, dysfunction could be the cause of the autonomic imbalance observed in SX. METHODS: In 20 subjects with diagnosed SX and in 12 age-matched controls, we studied autonomic function by performing spectral analysis of RR interval and finger arterial pressure (SAP), in supine position and during head-up tilting. We also carried out a set of tests of parasympathetic function. RESULTS: The group of SX patients did not differ significantly from control subjects in any of the variables tested. In a subgroup of 13 SX, however, tilting increased the low-frequency power of SAP, but did not induce the expected increase in low-frequency and decrease in high-frequency power of RR. These patients, in supine position, had significantly lower sinus arrhythmia and a higher ratio of low to high frequency of RR, in comparison with control subjects. We interpreted these differences as signs of reduced parasympathetic, but essentially normal sympathetic, activity. The parasympathetic tests confirmed vagal impairment in the same SX subjects. On the other hand, all the tests indicated normal parasympathetic functions in the control subjects and in those SX patients who displayed the expected spectral changes in tilting. CONCLUSIONS: In about two thirds of the patients with SX, the pathophysiological mechanism causing the symptoms could be related to the reduced parasympathetic tone, rather than to an augmented sympathetic activity.

Spectral and cross-spectral autoregressive analysis of cardiovascular variables in subjects with different degrees of orthostatic tolerance.

The mechanisms leading to vasovagal syncope are still unclear. A simple discriminating test for the identification of syncope-prone subjects is not presently available. Fifty-two subjects had a stepwise orthostatic test with 60 degrees tilt and -20 and -40 mm Hg lower-body negative pressure before the appearance of impending syncope symptoms. Spectral and cross-spectral analyses of heart period and systolic pressure time series were performed to estimate the power of the high-frequency (approximately equals 0.25 Hz) and low-frequency (approximately equals 0.1 Hz) oscillations, the coherence between heart period and systolic pressure, and the mean low-frequency and high-frequency central frequency, phase shift, and transfer function at maximal coherence. According to time to presyncope, the 52 subjects were divided into two groups: 25 with normal orthostatic tolerance, and 27 with poor orthostatic tolerance. In the supine positions, the mean central low-frequency was significantly lower in poor-tolerance group than in normal-tolerance group, discriminating poor from normal orthostatic tolerance with 80% specificity and 83% sensitivity, and was significantly correlated to time to presyncope. In the 2 to 3 minutes preceding syncope, subjects with poor orthostatic tolerance had less tachycardia, lower low-frequency power of systolic pressure, higher respiratory frequency, and a less negative phase shift in high-frequency range. In presyncope, sympathetic activation is reduced in subjects with poor orthostatic tolerance. In addition, the higher breathing frequency and the smaller negativity of phase shift in high-frequency range, which may indicate an inadequate engagement of the baroreflex, suggest a causal role of respiration in the development of syncope. Supine central values of low frequency may be proposed as a valuable clinical index of orthostatic intolerance.

Post-exercise recovery of autonomic cardiovascular control: a study by spectrum and cross-spectrum analysis in humans.

The recovery of the baseline autonomic control of cardiovascular activity after exercise has not been extensively studied. In 12 healthy subjects, we assessed the time-course of recovery by autoregressive spectrum and cross-spectrum analysis of heart period and systolic blood pressure during the 3 h after the end of 20 min of steady-state exercise at 50% (light workload, LW) and 80% (moderate workload, MW) of the individual's anaerobic threshold. The electrocardiogram and non-invasive blood pressure were simultaneously recorded during 10 min periods in the sitting position, at rest before exercise, and at 15, 60 and 180 min of recovery after exercise. At 15 min we observed a persistent tachycardia and relative hypotension; after MW, at 60 min heart rate was still slightly higher. Spectrum and cross-spectrum analysis showed, at 15 min, an increase in the low frequency component of systolic blood pressure, a reduction in the high frequency component of heart rate (larger in MW), and a decrease in baroreceptor sensitivity. After 60 and 180 min none of these parameters was significantly different from those at rest, although, in MW, some subjects still displayed signs of sympathetic activation after 1 h. We concluded that, after 15 min of recovery, the cardiovascular reflexes were blunted, that sympathetic nerve activity was still enhanced, and that the tone in the vagus had not fully recovered. Only the persistent vagal restraint seemed to be exercise intensity-dependent. For complete restoration of autonomic control after LW 1 h of rest was sufficient, and just enough after MW.

Baroreflex and oscillation of heart period at 0.1 Hz studied by alpha-blockade and cross-spectral analysis in healthy humans.

1. Parameters derived from frequency-domain analysis of heart period and blood pressure variability are gaining increasing importance in clinical practice. However, the underlying physiological mechanisms in human subjects are not fully understood. Here we address the question as to whether the low frequency variability (approximately 0.1 Hz) of the heart period may depend on a baroreflex-mediated response to blood pressure oscillations, induced by the alpha-sympathetic drive on the peripheral resistance. 2. Heart period (ECG), finger arterial pressure (Finapres) and respiratory airflow were recorded in eight healthy volunteers in the supine position with metronome respiration at 0.25 Hz. We inhibited the vascular response to the sympathetic vasomotor activity with a peripheral alpha-blocker (urapidil) and maintained mean blood pressure at control levels with angiotensin II. 3. We performed spectral and cross-spectral analysis of heart period (RR) and systolic pressure to quantify the power of low- and high-frequency oscillations, phase shift, coherence and transfer function gain. 4. In control conditions, spectral analysis yielded typical results. In the low-frequency range, cross-spectral analysis showed high coherence (> 0.5) and a negative phase shift (-65.1 +/- 18 deg) between RR and systolic pressure, which indicates a 1-2 s lag in heart period changes in relation to pressure. In the high-frequency region, the phase shift was close to zero, indicating simultaneous fluctuations of RR and systolic pressure. During urapidil + angiotensin II infusion the low-frequency oscillations of both blood pressure and heart period were abolished in five cases. In the remaining three cases they were substantially reduced and lost their typical cross-spectral characteristics. 5. We conclude that in supine rest conditions, the oscillation of RR at low frequency is almost entirely accounted for by a baroreflex mechanism, since it is not produced in the absence of a 0.1 Hz pressure oscillation. 6. The results provide physiological support for the use of non-invasive estimates of the closed-loop baroreflex gain from cross-spectral analysis of blood pressure and heart period variability in the 0.1 Hz range.

Does low-frequency variability of heart period reflect a specific parasympathetic mechanism?

Low frequency (LF, approximately 0.1 Hz) spontaneous oscillations of heart period in humans have been attributed to and correlated with the sympathetic efferent control of the heart. However, this interpretation is controversial, because sympathetic blockade does not suppress these oscillations, while parasympathetic blockade strongly affects them. The sympathetic origin of LF of arterial pressure, on the contrary, has been convincingly demonstrated. Four 10 min cycle-by-cycle time series of R-R interval (RR), and systolic (SAP) and diastolic (DAP) arterial pressure were produced by automatic analysis of data obtained with non-invasive methods in 10 healthy humans during supine rest and while standing, both before and after beta 1-selective blockade (atenolol). Time series were analysed by autoregressive transfer function analysis. beta-blockade failed to induce systematic changes on the power of the LF peak of RR, in any condition. The coherence between RR and SAP in the same region remained high (0.77 +/- 0.03) and a constantly negative phase (approximately 50-60 degrees, corresponding to a delay of 1-2 heart beats of RR on SAP) was always seen. beta-blockade decreased the power of the LF peak of SAP, increased the transfer function gain between SAP and RR at LF, and the HF power of RR. We conclude that LF oscillations of RR are not directly generated by the sympathetic drive to the heart but reflect mainly the parasympathetic activity. The results suggest that the LF oscillations of the vagal outflow, and of RR, are generated by the baroreceptor reflex, driven by sympathetically-induced blood pressure LF waves.

Adipocyte morphology during hormone-induced lipid deposition and mobilization. An ultrastructural investigation in the perfused cardiac fat.

The rat pericoronary adipose tissue was perfused in the presence of either the liposynthetic hormone insulin or the lipolytic hormone noradrenaline. Insulin perfusion associated with a) larger adipocyte mean sectional diameter in comparison with noradrenaline perfusion; b) glycogen deposition; c) appearance of small fat globules at discrete sites at the periphery of the main lipid drop. The two latter phenomena were apparently dose-dependent. Massive lipid deposition was induced by addition of triglycerides to the perfusion medium and this associated with appearance of prominent endoplasmic reticulum in the cytoplasm. In noradrenaline-perfused adipose tissue many small lipid droplets surrounded the central lipid deposit and the endoplasmic reticulum was in the form of both thin long, dashed cisternae sometime surrounding lipid droplets and grouped, anastomosing tubular cisternae. The present work shows that the perfused white adipose tissue of the heart is a suitable model to study, in situ, the morphological effects of hormones in adipocytes.

Short term effects of intra-arterial propionyl-L-carnitine on isolated canine hind-limbs.

Treatment with propionyl-L-carnitine has been shown to increase the walking capacity of patients with peripheral vascular disease, but the mechanisms responsible for the effect are unknown. To study the effects of propionyl-L-carnitine on musculocutaneous vascular beds and the related mechanisms, a preparation of constant-pressure blood-perfused dog hind-limb was used. Since the propionyl-L-carnitine solution had a pH less than 4 the contralateral limb simultaneously received acidified saline. The substances were injected into the perfused arteries in 2 minutes or in 20 minutes, and the cumulative dose of propionyl-L-carnitine was 20 mg/kg for each administration. The preparation was well suited for this study, because there were no major systemic effects of propionyl-L-carnitine, nor signs of cross-circulation between the isolated limbs. Propionyl-L-carnitine increased flow by 130% in 2 minute infusions and by 49% in 20 minute infusions. Acidified saline increased flow by 47% in 2 minute infusions and by 34% in 20 minute infusions. The difference between propionyl-L-carnitine and acidified saline was significant in 2 minute infusions. The 2 minute infusions of propionyl-L-carnitine increased venous PO2 by 34% and PCO2 by 22% while pH decreased by 0.07. The 20 minute infusions of propionyl-L-carnitine increased PO2 by 22% and PCO2 by 24% while pH decreased 0.10 units. Acidified saline increased only venous PO2 in 2 minute infusions (16%). Calculated oxygen consumption of the perfused limbs increased in 2 minute infusions of propionyl-L-carnitine, but not significantly. It was concluded that propionyl-L-carnitine has a direct vasodilator effect in musculocutaneous vascular beds at high doses and probably enhances tissue metabolism.

Arterial baroreceptors are not essential for low frequency oscillation of arterial pressure.

Cardiovascular parameters exhibit spontaneous oscillations at the respiratory frequency, and in the low frequency range (LF < 0.20 Hz). Although LF is attributed to the sympathetic control, the mechanism responsible for the oscillation, whether instability of the baroreflex loop, or activity of a central nervous system pattern generator, is controversial. To answer this question, time series of arterial blood pressure, heart period and left external iliac blood flow from chloralose-anaesthetised dogs were examined by standard statistics as well as by autoregressive spectral and cross-spectral analysis. The circulation to the left hind-limb was isolated and connected to a constant-pressure perfusing system, to obtain mechanical uncoupling from the central circulation. Three steady-state conditions were studied. A device inserted into the common carotid arteries allowed the carotid sinus region to be in continuity with the animal's arterial system (CONTROL) or perfused at constant pressure by an external source (CAROTID BUFFER); bilateral cervical vagotomy was also performed (VAGI CUT). Intra-individual (beat-to-beat) variability of each parameter was evaluated by standard deviation (SD) of time series in the three conditions. The average SD of heart period was reduced in CAROTID BUFFER and in VAGI CUT; the SDs of arterial pressure and iliac flow were not changed by these interventions. Autospectra of iliac flow time series in CONTROL showed a prominent peak at 0.05 +/- 0.04 Hz (mean +/- SD of all experiments), accounting for 90 +/- 11% of the total variance.(ABSTRACT TRUNCATED AT 250 WORDS)

Vascular resistance and arterial pressure low-frequency oscillations in the anesthetized dog.

The spontaneous variability of heart rate and arterial blood pressure was investigated in chloralose-anesthetized dogs with the left iliac vascular bed mechanically uncoupled from the central circulation. Electrocardiogram, mean arterial pressure (ABP), iliac perfusion and venous pressures, and flow (FLOW) were recorded for 5 min in steady state. Autoregressive spectral and cross-spectral analyses and digital filtering were performed. The variation coefficient (VC%), calculated from the overall variance of each signal, was 5-7%, with the exception of perfusion pressure (VC% = 1%). The frequency-related percentage of total variance was distributed among three frequency bands: two were < 0.20 Hz [lower (F1) and higher (F2; low-frequency range = F1 + F2)], and one was > 0.20 Hz (respiratory, F3). F3 was not always present in RR, which, however, oscillated also in F1 and F2, although with limited amplitude; ABP showed large respiratory and low-frequency oscillations; the FLOW oscillations were in the low-frequency range. Cross-spectral analysis showed high squared coherence in the relevant frequency bands between variables in the three couples: RR-ABP, RR-FLOW, and ABP-FLOW. Changes in RR preceded changes in ABP and in FLOW by > or = 3 s, whereas FLOW was approximately in phase opposition to ABP. It was concluded that, in the chloralose-anesthetized dog, 1) arterial pressure and heart rate oscillate with frequencies corresponding to those described in conscious humans, 2) low-frequency arterial pressure oscillations are due to changes in peripheral vascular resistance, and 3) peripheral vascular resistance does not display respiratory oscillations. Furthermore it was suggested that oscillations of vasomotor tone are generated by a rhythm of central origin and that F1 and F2 oscillations may recognize a common mechanism.

Biochemical and morphological changes in isolated rabbit hearts after prolonged hypothermic ischaemia: comparison of two cardioplegic solutions.

This work evaluates the myocardial protective potential of potassium cardioplegia on ischaemically arrested and reperfused hearts by two cardioplegic solutions: the University of Wisconsin solution (UW) and the standard crystalloid solution of St. Thomas' Hospital (ST). Evaluation of myocardial preservation was based on creatine kinase and lactate releases and on high-energy phosphate preservation of isolated rabbit hearts after 4 hours' hypothermic ischaemia. A morphometric ultrastructural evaluation of mitochondria in cardiomyocytes was also performed. The hearts of 24 rabbits were normothermally perfused with oxygenated Krebs-Henseleit solution for 30 min (Langendroff preparation), and the baseline contractile performance and biochemical parameters were evaluated. The hearts were then arrested and stored in the cardioplegic solutions (12 UW and 12 ST) at 4 degrees C for 4 hours. The hearts were then rewarmed and reperfused with oxygenated Krebs-Henseleit solution for further 30 min. At the end of reperfusion, creatine phosphate and high energy phosphates were higher with UW (p < 0.05); creatine kinase release during reperfusion was significantly lower with UW both at 15 min (p < 0.01) and at 30 min (p < 0.05). Lactate release during the first 15 min of reperfusion was about doubled (p < 0.05) with respect to controls in both groups; at 30 min this increase had almost vanished (+8%) with UW but not with ST (+30%). Ultrastructural morphometry did not show any significant difference at the level of mitochondria between the two treatments. The results indicate, for UW, an improved myocardial preservation associated with relative retention of high-energy phosphates and higher recovery of mechanical function, accelerated metabolic recovery and reduced stress of cell membranes.

Preservation of rabbit hearts with different cardioplegic solutions at low temperature.

An organ-preserving solution, including in its composition also organic molecules, prepared at the University of Wisconsin (UW), has been successfully used for preservation of liver, pancreas and kidney, and has recently been tested for long-term storage of isolated hearts. We have compared the effectiveness of the UW solution with that of a standard crystalloid cardioplegic solution (St. Thomas, ST) in the functional and structural preservation of isolated hearts. The hearts taken from 24 rabbits were mounted on a Langendorff preparation. After assessment of the left ventricular function by an intraventricular balloon, 40 ml of either cardioplegic solution were injected to arrest the hearts (12 UW and 12 ST), which were then immersed in the same solution for 4 h at 4 degrees C without perfusion. After this period, the hearts were normothermally reperfused with oxygenated Krebs-Henseleit solution for 30 min, and finally left ventricular function was assessed again. An electron microscopic evaluation was performed as well. Significantly higher recovery of left ventricular developed pressure (p < 0.01) and of negative dP/dt (p < 0.05), was observed after preservation with UW, while no difference on positive dP/dt was found. After reperfusion, left ventricular end-diastolic pressure significantly rose with ST (p < 0.01), but did not change with UW; the difference between ST and UW was significant (p < 0.01). Tissue water content was significantly lower in the hearts preserved with UW (p < 0.05). Electron microscopic examination revealed generally good preservation with no substantial difference between the two solutions.(ABSTRACT TRUNCATED AT 250 WORDS)

Peripheral blood flows during colorectal distension in anaesthetised dogs.

Distension of the descending colon elicits reflex cardiovascular responses, including increases in heart rate and arterial blood pressure. To study the relative contribution of vasoconstriction in individual vascular beds to this reflex response, experiments were performed on seven dogs anaesthetised with chloralose and instrumented with electromagnetic flowmeters around the superior mesenteric, the left renal and the left external iliac arteries. The colorectal portion of the intestine was distended at constant pressure (36.6 mm Hg, 4.9 kPa mean; range 25-50 mm Hg, 3.3-6.7 kPa) with warm Ringer solution for periods of 2 min. After a set of control distensions, the experiments were performed whilst the reflex rise in arterial pressure was prevented by removal of blood from the arterial tree. In control distensions arterial pressure increased by 11.3 +/- 1.5 mm Hg, 1.51 +/- 0.12 kPa (mean +/- SEM). In distensions at constant arterial pressure, peripheral blood flows were altered to different extents in the three territories studied: vascular resistance increased by 30.8 +/- 5.6% (P < 0.01) in the mesenteric, by 4.1 +/- 1.5% (P < 0.03) in the renal, and by 15.2 +/- 6.8% (NS) in the external iliac bed. We conclude that colorectal distension may reflect activation of a function-specific pathway of the sympathetic nervous system, which leads to much greater vasoconstriction in the splanchnic circulation than in renal or musculocutaneous circulations.

Protective effect of selenium in cardiac ischemia and reperfusion.

The purpose of the present investigation was to establish whether pretreatment with selenium enhances the stores of selenium-dependent glutathione peroxidase in the tissues and to verify if and to what extent alterations of mechanical and biochemical cardiac properties induced by ischemia in the myocardium may be thus prevented. Ten rats had sodium selenite (6 micrograms/day) added to their drinking water for 4 weeks, while 10 control rats received no treatment. At the end of 4 weeks, the hearts were perfused by the Langendorff technique with oxygenated Krebs-Henseleit solution at a rate of 10 ml/min for 30 minutes at 37 degrees C. Ischemia was then induced by reducing the perfusion to 1 ml/min for 60 minutes; reperfusion followed at the control rate for a further 30 minutes. Isometrically developed pressure and its maximum first derivative at different ventricular volumes was measured before and after the ischemic period. Lactate and creatine kinase activity were measured in the effluent throughout. Tissue concentrations of adenine nucleotides and creatine phosphate and lutathione peroxidase activity were estimated after reperfusion. The rats treated with selenium showed a wide-spread increase in the activity of Se-dependent glutathione peroxidase in all tissues. There was an improved recovery of ventricular contraction during reperfusion and an increased myocardial content of adenine nucleotides and creatine phosphate. During reperfusion, the loss of creatine kinase into the perfusate was less in the treated animals, and there was a similar trend for the production of lactate.(ABSTRACT TRUNCATED AT 250 WORDS)

Efferent limb of the coronary vasoconstrictor reflex elicited by distension of the descending colon in anesthetized dogs.

Distension of the descending colon elicits reflex coronary vasoconstriction. To study the efferent branch of this reflex, experiments were performed on 5 dogs anesthetized with pentobarbitone. A pouch was formed from the distal 15 cm of the descending colon and distended at constant pressure (54 +/- 8.9 mmHg) with warm Ringer solution from a pressurized bottle. During distensions of the colon, arterial blood pressure and heart rate were kept constant by the withdrawal of blood and pacing of the heart, respectively. Experiments were performed before and after intravenous bretylium tosylate (10 mg/kg), a compound which prevents the outflow of catecholamines from the sympathetic postganglionic neurons. Before chemical sympathectomy, colon distension at constant heart rate and blood pressure caused a decrease in mean coronary blood flow by 7 +/- 3.3% (mean +/- SD, p less than 0.0005). This response was abolished after the administration of bretylium (-0.07 +/- 0.95%, p greater than 0.40). We conclude that the efferent branch of the reflex coronary vasoconstriction elicited by colon distension is through sympathetic nerves.

Haemodynamic effects of distension of the descending colon in anaesthetized dogs.

1. This study was undertaken to determine whether distension of the descending colon in anaesthetized dogs reflexly affects the heart rate, arterial blood pressure or the left ventricular inotropic state. 2. Experiments were performed on twenty-six dogs, which were anaesthetized with sodium pentobarbitone and artificially ventilated. A segment of the distal descending colon was isolated and was distended with warm Ringer solution at a steady intraluminal pressure. 3. In each animal, distension of the colon caused an increase in heart rate and aortic blood pressure. The response of an increase in heart rate was augmented by preventing changes in aortic blood pressure, and was graded in seven dogs by step increments in the distending pressure. In the same animals, distension of the colon always caused a small increase in left ventricular (dP/dt)max at constant heart rate and aortic blood pressure. 4. In four of the twenty-six dogs, cutting the pelvic nerves did not abolish the observed responses to the distension. In seven of the twenty-six dogs, which included the four animals with sectioned pelvic nerves, cutting the hypogastric nerves completely abolished all the observed responses. 5. In thirteen of the twenty-six dogs, propranolol or bretylium tosylate completely abolished the reflex increases in heart rate and left ventricular (dP/dt)max, and phentolamine or bretylium tosylate abolished the reflex increase in aortic blood pressure. 6. These results showed that distension of the colon reflexly increased the heart rate, arterial blood pressure and left ventricular inotropic state. These reflex responses were mediated by sympathetic effects and their afferent limb involved the hypogastric nerves.

The efferent mechanisms of reflex hemodynamic responses to distension of the descending colon in anesthetized dogs.

We have recently shown that distension of the descending colon in anesthetized dogs causes reflex increases in heart rate, aortic blood pressure and the maximal rate of rise of left ventricular pressure, involving afferent pathways in the hypogastric nerves. In this study we have examined the efferent mechanisms involved in those responses. The descending colon was distended using Ringer solution at constant pressure in 13 anesthetized dogs. As previously shown, distension of the colon caused an increase in aortic blood pressure, heart rate and the maximal rate of rise of left ventricular pressure. The increase in the aortic blood pressure was abolished by either bretylium tosylate or phentolamine. Propranolol or bretylium tosylate abolished the increases in heart rate when changes in the aortic blood pressure were prevented, and abolished the increases in the maximal rate of rise of left ventricular pressure when the increases in heart rate were also prevented. These results indicate that the reflex increases in heart rate, arterial blood pressure and the maximal rate of rise of left ventricular pressure involved efferent sympathetic pathways.