Effects of Oral Alcohol on Superior Mesenteric Artery Blood Flow in Normal Man, Horizontal and Tilted

1993 ◽  
Vol 84 (4) ◽  
pp. 419-425 ◽  
Author(s):  
S. Maule ◽  
K. Ray Chaudhuri ◽  
T. Thomaides ◽  
D. Pavitt ◽  
J. McCleery ◽  
...  

1. The cardiovascular effects of oral alcohol (0.5 g/kg body weight diluted to 300 ml in sugar-free orange juice) were compared with those of placebo in 10 normal subjects. Measurements were made while the subjects were supine and horizontal for 45 min and after 10 min of 45° head-up tilt. 2. After alcohol, plasma alcohol levels rose from 1.9 ± 1.3 to 61.6 ± 6.5 mg/100 ml. After placebo, plasma alcohol levels did not increase. After alcohol and placebo, supine blood pressure was unchanged; heart rate, both supine and during tilt, rose after alcohol only. 3. After alcohol, superior mesenteric artery and digital skin blood flow increased and calculated vascular resistances fell. There was no change after placebo. 4. Forearm blood flow, forearm vascular resistance and cardiac index did not change in either phase, except for a fall in cardiac index during tilt but only after alcohol. 5. In conclusion, the acute ingestion of 0.5 g of alcohol/kg body weight in normal subjects raised heart rate and actively dilated the superior mesenteric artery and digital skin vessels. There was no effect on blood pressure, cardiac output and skeletal muscle vascular tone. During head-up tilt after alcohol, there was a tendency for blood pressure to fall with a compensatory rise in heart rate.

2011 ◽  
Vol 122 (6) ◽  
pp. 271-279 ◽  
Author(s):  
Laurence G. Trahair ◽  
Lora Vanis ◽  
Diana Gentilcore ◽  
Kylie Lange ◽  
Christopher K. Rayner ◽  
...  

PPH (postprandial hypotension), leading to increased morbidity and mortality, is an important clinical problem, particularly in the elderly and individuals with autonomic dysfunction. The magnitude of the postprandial fall in BP (blood pressure) appears to be dependent on the rate of nutrient entry into the small intestine and may be related to changes in splanchnic blood flow and sympathetic nerve activity. We aimed at determining the comparative effects of different ID (intraduodenal) glucose loads on BP, HR (heart rate), SMA (superior mesenteric artery) flow and vascular conductance and plasma NA (noradrenaline) in ‘young’ and ‘older’ subjects. A total of 12 ‘young’ (six male and six female; age, 22.2±2.3 years) and 12 ‘older’ (six male and six female; age, 68.7±1.0 years) subjects, the latter who have been studied previously [Vanis, Gentilcore, Rayner, Wishart, Horowitz, Feinle-Bisset and Jones (2011) Am. J. Physiol. Regul. Integr. Comp. Physiol., 300, R1524–R1531], had measurements of BP, HR, SMA flow and plasma NA before, and during, ID infusions of glucose at 1, 2 or 3 kcal/min (‘G1’, ‘G2’ and ‘G3’) (where 1 kcal≈4.184 J), or ‘S’ (saline) for 60 min. In ‘young’ subjects, there was no change in BP during any of the four infusions. In contrast, in ‘older’ subjects, SBP (systolic BP) fell during ‘G2’, and ‘G3’ (P<0.005 for both), but not during ‘S’ or ‘G1’. In ‘young’ and ‘older’ subjects HR increased during ‘G2’ (P<0.05) and ‘G3’ (P<0.001), a response that was greater (P<0.05) in the young, but not during ‘S’ or ‘G1’. The rise in SMA flow and vascular conductance in response to ID glucose were load-dependent in both ‘young’ and ‘older’ subjects (P<0.001 for all), with no difference between them. Plasma NA rose in response to ‘G2’ and ‘G3’ (P<0.05) in the young, but in ‘G3’ (P<0.05) only in the ‘older’ subjects, with no difference between them. Hence, in response to small intestinal glucose infusions at 1, 2 and 3 kcal/min, ‘older’, but not ‘young’, subjects exhibit a comparable fall in BP in response to the two higher glucose loads, which may reflect an inadequate, compensatory, rise in HR, in the ‘older’ subjects, but not a greater increase in SMA conductance.


1989 ◽  
Vol 77 (6) ◽  
pp. 589-597 ◽  
Author(s):  
W. Reid ◽  
D. J. Ewing ◽  
S. L. Lightman ◽  
D. Eadington ◽  
T. D. M. Williams ◽  
...  

1. The release of arginine vasopressin (AVP) after an osmotic stimulus and head-up tilt was assessed in diabetic subjects with and without autonomic neuropathy 2. Six diabetic subjects with (DAN +ve) and five without (DAN − ve) evidence of autonomic neuropathy and five normal subjects were infused with 5% (w/v) NaCl at a rate of 0.05 ml min−1 kg−1 body weight for 120 min. Blood pressure, heart rate and plasma AVP were measured over this period 3. Seven DAN +ve, six DAN −ve and six normal subjects were tilted head-up to 45° for 120 min. Blood pressure, heart rate and plasma AVP were measured during the study 4. Infusion of 5% (w/v) NaCl produced appropriate rises in plasma osmolality and plasma AVP levels which did not differ between the three groups, confirming the normal osmotic release of AVP in the diabetic subjects 5. During head-up tilt, there were no differences in AVP responses between the three groups, despite a major hypotensive stimulus in the DAN + ve group 6. We conclude that osmotic release of AVP is normal in diabetes, but that cardiovascular release of AVP is impaired in diabetic subjects with cardiovascular reflex evidence of autonomic neuropathy, reflecting an afferent defect.


Medicina ◽  
2021 ◽  
Vol 58 (1) ◽  
pp. 28
Author(s):  
C. (Linda) M. C. van Campen ◽  
Peter C. Rowe ◽  
Frans C. Visser

Background and Objectives: Symptoms and hemodynamic findings during orthostatic stress have been reported in both long-haul COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), but little work has directly compared patients from these two groups. To investigate the overlap in these clinical phenotypes, we compared orthostatic symptoms in daily life and during head-up tilt, heart rate and blood pressure responses to tilt, and reductions in cerebral blood flow in response to orthostatic stress in long-haul COVID-19 patients, ME/CFS controls, and healthy controls. Materials and Methods: We compared 10 consecutive long-haul COVID-19 cases with 20 age- and gender-matched ME/CFS controls with postural tachycardia syndrome (POTS) during head-up tilt, 20 age- and gender-matched ME/CFS controls with a normal heart rate and blood pressure response to head-up tilt, and 10 age- and gender-matched healthy controls. Identical symptom questionnaires and tilt test procedures were used for all groups, including measurement of cerebral blood flow and cardiac index during the orthostatic stress. Results: There were no significant differences in ME/CFS symptom prevalence between the long-haul COVID-19 patients and the ME/CFS patients. All long-haul COVID-19 patients developed POTS during tilt. Cerebral blood flow and cardiac index were more significantly reduced in the three patient groups compared with the healthy controls. Cardiac index reduction was not different between the three patient groups. The cerebral blood flow reduction was larger in the long-haul COVID-19 patients compared with the ME/CFS patients with a normal heart rate and blood pressure response. Conclusions: The symptoms of long-haul COVID-19 are similar to those of ME/CFS patients, as is the response to tilt testing. Cerebral blood flow and cardiac index reductions during tilt were more severely impaired than in many patients with ME/CFS. The finding of early-onset orthostatic intolerance symptoms, and the high pre-illness physical activity level of the long-haul COVID-19 patients, makes it unlikely that POTS in this group is due to deconditioning. These data suggest that similar to SARS-CoV-1, SARS-CoV-2 infection acts as a trigger for the development of ME/CFS.


1998 ◽  
Vol 94 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Sharmini Puvi-Rajasingham ◽  
Gareth D. P. Smith ◽  
Adeola Akinola ◽  
Christopher J. Mathias

1. In human sympathetic denervation due to primary autonomic failure, food and exercise in combination may produce a cumulative blood pressure lowering effect due to simultaneous splanchnic and skeletal muscle dilatation unopposed by corrective cardiovascular reflexes. We studied 12 patients with autonomic failure during and after 9 min of supine exercise, when fasted and after a liquid meal. Standing blood pressure was also measured before and after exercise. 2. When fasted, blood pressure fell during exercise from 162 ± 7/92 ± 4 to 129 ± 9/70 ± 5 mmHg (mean arterial pressure by 22 ± 5%), P < 0.0005. After the meal, blood pressure fell from 159 ± 8/88 ± 6 to 129 ± 6/70 ± 4 mmHg (mean arterial pressure by 22 ± 3%), P < 0.0001, and further during exercise to 123 ± 6/61 ± 3 mmHg (mean arterial pressure by 9 ± 3%), P < 0.01. The stroke distance—heart rate product, an index of cardiac output, did not change after the meal. During exercise, changes in the stroke distance—heart rate product were greater when fasted. 3. Resting forearm and calf vascular resistance were higher when fasted. Calf vascular resistance fell further after exercise when fasted. Resting superior mesenteric artery vascular resistance was lower when fed; 0.19 ± 0.02 compared with 032 ± 0.06, P < 0.05. After exercise, superior mesenteric artery vascular resistance had risen by 82%, to 0.53 ± 0.12, P < 0.05 (fasted) and by 47%, to 0.29 ± 0.05, P < 0.05 (fed). 4. On standing, absolute levels of blood pressure were higher when fasted [83 ± 7/52 ± 7 compared with 71 ± 2/41 ± 3 (fed), each P < 0.05]. Subjects were more symptomatic on standing post-exercise when fed. 5. In human sympathetic denervation, exercise in the fed state lowered blood pressure further than when fasted and worsened symptoms of postural hypotension.


1992 ◽  
Vol 83 (5) ◽  
pp. 535-540 ◽  
Author(s):  
P. J. Lacolley ◽  
B. M. Pannier ◽  
M. A. Slama ◽  
J. L. Cuche ◽  
A. P. G. Hoeks ◽  
...  

1. Pulsatile changes in the diameter of the common carotid artery were studied transcutaneously using an echo-tracking technique in 15 normal subjects: eight subjects before and during application of graded lower-body negative pressure from −5 to −15 mmHg, and seven subjects before and during weight-bearing head-up tilt at 30 and 60 degrees. 2. In concomitant studies of changes in forearm vascular resistance, it was seen that mild lower-body negative pressure produced deactivation of cardiopulmonary receptors without changes in systemic blood pressure or heart rate. 3. After lower-body negative pressure, a significant decrease in carotid arterial diastolic diameter [from 0.662 ± 0.028 to 0.624 ± 0.033 cm (lower-body negative pressure −10 mmHg) and 0.640 ± 0.030 cm lower-body negative pressure −15 mmHg), P<0.001 and <0.05] was observed. 4. After head-up tilt, carotid arterial diameter was also significantly decreased at 30 and 60 degrees, whereas a significant increase in heart rate occurred only at 60 degrees and mean blood pressure did not change. 5. The study provides evidence that the geometry of the arterial wall is substantially modified by noninvasive manoeuvres such as head-up tilting and lower-body negative pressure. The latter is assumed to selectively deactivate human cardiopulmonary receptors, but the present data suggest that local changes may also influence carotid baroreceptors.


2000 ◽  
Vol 89 (3) ◽  
pp. 947-955 ◽  
Author(s):  
Giuseppe Insalaco ◽  
Salvatore Romano ◽  
Adriana Salvaggio ◽  
Alberto Braghiroli ◽  
Paola Lanfranchi ◽  
...  

The ventilatory and arterial blood pressure (ABP) responses to isocapnic hypoxia during wakefulness progressively increased in normal subjects staying 4 wk at 5,050 m (Insalaco G, Romano S, Salvaggio A, Braghiroli A, Lanfranchi P, Patruno V, Donner CF, and Bonsignore G; J Appl Physiol 80: 1724–1730, 1996). In the same subjects ( n = 5, age 28–34 yr) and expedition, nocturnal polysomnography with ABP and heart rate (HR) recordings were obtained during the 1st and 4th week to study the cardiovascular effects of phasic (i.e., periodic breathing-dependent) vs. tonic (i.e., acclimatization-dependent) hypoxia during sleep. Both ABP and HR fluctuated during non-rapid eye movement sleep periodic breathing. None of the subjects exhibited an ABP increase during the ventilatory phases that correlated with the lowest arterial oxygen saturation of the preceding pauses. Despite attenuation of hypoxemia, ABP and HR behaviors during sleep in the 4th wk were similar to those in the 1st wk. Because ABP during periodic breathing in the ventilatory phase increased similarly to the ABP response to progressive hypoxia during wakefulness, ABP variations during ventilatory phases may reflect ABP responsiveness to peripheral chemoreflex sensitivity rather than the absolute value of hypoxemia, suggesting a major tonic effect of hypoxia on cardiorespiratory control at high altitude.


1991 ◽  
Vol 1 (1) ◽  
pp. 37-42 ◽  
Author(s):  
K. Ray Chaudhuri ◽  
T. Thomaides ◽  
P. Hernandez ◽  
M. Alam ◽  
C. J. Mathias ◽  
...  

1982 ◽  
Vol 63 (s8) ◽  
pp. 331s-333s ◽  
Author(s):  
P. C. Rubin ◽  
Kathleen McLean ◽  
J. L. Reid

1. Two studies were performed to elucidate the role of opioids in blood pressure control in man. 2. Study 1: nine normal subjects, 18–32 years, received in a randomized single blind manner, volume matched infusions of a Met-enkephalin analogue (DAMME) 0.5 mg, naloxone 0.2 mg/kg or saline. Blood pressure, heart rate and plasma noradrenaline were determined supine and after a 5 min, 70° head-up tilt at 0, 3/4, 2, 3, 4, 5 and 6 h. 3. Study 2: seven subjects, after baseline recordings of blood pressure and heart rate received six incremental infusions of sodium nitroprusside, 1.5–7.5 μg min−1 kg−1. They then received DAMME or naloxone and the nitroprusside infusions were repeated between 3 and 4 h. There was a significant linear relationship between fall in mean arterial pressure and rise in heart rate in each case and the slope was used as an index of baroreflex sensitivity. 4. Neither naloxone nor DAMME influenced supine blood pressure or heart rate. Blood pressure after head-up tilt was significantly (analysis of variance) decreased by DAMME for up to 5 h but not by naloxone, the effect being most marked at 3 h: systolic (mean ± sd), placebo 110 ± 6, naloxone 106 ± 10, DAMME 96 ± 16 (P< 0.02); diastolic (mean ± sd), placebo 78 ± 7, naloxone 79 ± 5, DAMME 67 ± 8 (P < 0.01). The increases in heart rate and plasma noradrenaline on tilting after DAMME were not significantly different from values with placebo or naloxone. The 3 h values for heart rate were: placebo 87 ± 16, naloxone 88 ± 19, DAMME 89 ± 23 (P > 0.1); for plasma noradrenaline (nmol/l): placebo 6.0 ± 2.2, naloxone 5.8 ± 1.9, DAMME 6.0 ± 1.9 (P > 0.1). 5. Naloxone significantly increased the slope (beats per min/mmHg) of the regression relationship from a mean of 1.8 ± 0.07 to 3.0 ± 1.3 (P < 0.05), and DAMME reduced the slope from 2.7 ± 1.7 to 1.2 ± 0.5 (P < 0.05). 6. We conclude that endogenous opioids modulate baroreflex function in man.


1993 ◽  
Vol 84 (2) ◽  
pp. 193-199 ◽  
Author(s):  
G. D. Braatvedt ◽  
A. Stanners ◽  
P. G. Newrick ◽  
M. Halliwell ◽  
R. J. M. Corrall

1. Previous studies have suggested that glucagon in supraphysiological doses may mediate postprandial and hypoglycaemia-induced splanchnic vasodilatation in man and experimental animals. There are no reported studies investigating the role of glucagon in doses producing circulating concentrations within the physiological range. 2. Two separate studies were performed. In study 1, superior mesenteric artery blood flow was measured by Doppler ultrasound in six normal subjects during either saline or glucagon infusion at 1, 3 and 6 ng min−1 kg−1, which resulted in circulating glucagon levels within the physiological range. Mean superior mesenteric artery blood flow fell during the 3 and 6 ng min−1kg−1 glucagon infusions (3 ng min−1kg−1: −31.8%, range −20 to −56% of baseline; 6 ng min−1 kg−1: −20.7%, range −8 to −53% of baseline; P < 0.05). 3. In study 2, superior mesenteric artery blood flow was measured during hypoglycaemia induced by an insulin infusion in 12 normal subjects. In six of these subjects the effect of suppression of glucagon release during hypoglycaemia was assessed by preteatment with the somatostatin analogue octreotide (0.8 μg/kg subcutaneously) given 30 min before the insulin infusion. 4. The nadir in blood glucose concentration at the hypoglycaemic reaction was similar in both groups and glucose recovery was complete by 60 min after the hypoglycaemic reaction. Plasma catecholamine concentrations rose in both groups after the hypoglycaemic reaction. 5. Superior mesenteric artery blood flow rose at the hypoglycaemic reaction in both groups despite suppression of glucagon release with octreotide. 6. These data suggest that at physiological concentrations glucagon does not mediate splanchnic vasodilatation in man.


1973 ◽  
Vol 45 (6) ◽  
pp. 733-742 ◽  
Author(s):  
N. K. Hollenberg ◽  
D. F. Adams ◽  
P. Mendell ◽  
H. L. Abrams ◽  
J. P. Merrill

1. The renal vascular response to intravenously administered dopamine was assessed in normal man by selective renal arteriography and xenon washout. Infusion of 3 μg min−1 kg−1 induced renal vasodilatation with an increase in the cortical component of blood flow. Arterial blood pressure was not influenced and a systemic effect was not demonstrable. Lower doses did not induce a renal response. Increasing dosage raised arterial blood pressure and induced subjective symptoms, but did not result in a further increase in renal blood flow. 2. Renal vascular resistance increased with increasing age in the normal subjects. A significant inverse relationship was found between the initial vascular resistance and the renal vasodilator response to dopamine. It thus appears that the vascular effects of increasing age (nephrosclerosis) may limit the dilator response to dopamine. 3. It is concluded that dopamine is an effective renal cortical vasodilator when administered intravenously at doses which are free from other systemic cardiovascular effects. The dose-response relationship must be considered in attempts at reversal of conditions characterized by renal vasoconstriction.


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