Hyperemia In Patients Research Articles

Images in cardiovascular medicine. Avoiding papillary muscle infarction with myocardial contrast echocardiographic guidance of nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy.

Intracoronary myocardial contrast echocardiography (MCE) can be used to guide the delivery of ethanol during nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. The echocardiographic contrast agent is injected immediately before the injection of ethanol, down the lumen of the inflated balloon that resides in the target septal coronary artery. This is the artery that supplies the area of the septum involved with the mitral leaflet(s) in causing dynamic outflow tract obstruction. MCE provides a direct visualization of the myocardial territory that should receive ethanol and consequently undergo infarction. In rare instances, the cannulated vessel does not supply the culprit septal segment(s) but supplies instead …

Effect of the Somatostatin Analogue Lanreotide on Meal-Stimulated Portal Blood Flow in Patients with Liver Cirrhosis

Background: Lanreotide, a new long-acting somatostatin analogue, has been shown to inhibit the meal-stimulated increase of splanchnic blood flow in healthy volunteers. To date, similar data in patients with liver cirrhosis have not been available. We have examined the effect of lanreotide compared with placebo on meal-stimulated portal blood flow in patients with liver cirrhosis using Doppler ultrasound. Methods: 20 cirrhotic patients (placebo n = 12, lanreotide n = 8) with proven portal hypertension were studied after an overnight fast. Lanreotide, at a dose of 100 µg/h, was infused intravenously over 7 h after a 1-hour basal period. In parallel to the intravenous infusion, a liquid test meal (Ensure plus^TM, 1.5 kcal/min) was perfused for 7 h through an intraduodenal tube at a rate of 3 ml/min. Blood pressure, heart rate and portal vein blood flow (PVF, ml/min, Doppler technique) were determined at regular intervals. Results: Baseline PVF amounted to 725 ± 182 ml/min in the placebo and to 917 ± 252 ml/min in the lanreotide group (n.s.). The meal-stimulated increase in PVF was blunted by lanreotide (AUC, %·min): 62,709.6 ± 6,817 (placebo) vs. 45,237 ± 2,507 (lanreotide), p < 0.05. Lanreotide also blunted the postprandial increase in heart rate for the first 2 h of meal perfusion. Conclusions: Because of potent inhibition of postprandial splanchnic hyperemia in patients with liver cirrhosis, lanreotide may be useful in the treatment of complications of portal hypertension.

Abnormal longitudinal, base-to-apex myocardial perfusion gradient by quantitative blood flow measurements in patients with coronary risk factors.

A longitudinal, base-to-apex myocardial perfusion gradient has been described in patients with coronary artery disease (CAD) and was attributed to diffuse coronary luminal narrowing. We asked whether an abnormal perfusion gradient also existed in patients without CAD but with coronary risk factors. We measured myocardial blood flow (MBF) with (13)N-ammonia and PET at rest and during hyperemia in patients with coronary risk factors but without CAD. Regional MBF was measured in absolute units with (13)N-ammonia and PET at rest and during dipyridamole hyperemia in 36 patients with coronary risk factors (age, 55+/-10 years) and in 36 age-matched (age, 53+/-10 years) and in 28 young (age, 25+/-5 years) normal subjects. MBF was determined globally, for each of the 3 coronary territories, and in the mid and mid-to-apical sections of the left ventricle (LV). Myocardial perfusion on qualitative analysis was normal at rest and during hyperemia, and no flow defects were present. MBF in absolute units was similar in the 3 coronary territories. However, hyperemic MBFs in the mid-to-apical LV section were lower than in the mid LV section in the "at-risk" group (2.04+/-0.61 versus 1.71+/-0.40 mL. min(-1). g(-1); P<0.004) but not in the age-matched or in the young normal subjects. The abnormal longitudinal, base-to-apex perfusion gradient observed during dipyridamole MBF suggests the presence of a functional and/or structural alteration of the coronary circulation associated with coronary risk factors, possibly reflecting developing coronary atherosclerosis or preclinical CAD.

Effect of the angiotensin-converting enzyme inhibitor imidapril on reactive hyperemia in patients with essential hypertension: relationship between treatment periods and resistance artery endothelial function

OBJECTIVESThe purpose of this study was to evaluate the effects of the angiotensin-converting enzyme (ACE) inhibitor imidapril and the calcium antagonist amlodipine on endothelial function before and after 2, 4, 8, 12, 24 and 48 weeks of treatment.BACKGROUNDThere are limited data on whether and how long endothelial function is improved after initiation of ACE inhibitor treatment and how the grade of endothelial function further progresses after improvement of endothelial dysfunction in patients with essential hypertension.METHODSThe forearm blood flow (FBF) was measured in 25 patients with essential hypertension and in 25 normotensive subjects by using strain-gauge plethysmography during reactive hyperemia (RH) (280 mm Hg for 5 min) and after sublingual administration of nitroglycerin (NTG, 0.3 mg).RESULTSThe FBF of patients with essential hypertension during RH was significantly less than that of normotensive subjects. The increase in FBF after sublingual NTG was similar in both groups. Both imidapril (n = 13) and amlodipine (n = 12) significantly reduced systolic blood pressure and diastolic after eight weeks of treatment from the pretreatment values. Forearm vascular resistance was significantly decreased after two weeks of treatment. Imidapril significantly augmented RH after 12 weeks of treatment from the pretreatment values (31.6 ± 5.7 to 38.2 ± 6.0 ml/min per 100 ml tissue, p < 0.05), whereas amlodipine did not alter RH for each treatment period. The ability of imidapril to improve RH was maintained throughout the 48-week treatment period. There was no significant difference in RH at 12, 24 and 48 weeks. The increase in FBF after sublingual administration of NTG was similar in all treatment periods for the two groups. The infusion of NG-monomethyl-L-arginine, a nitric oxide (NO) synthase inhibitor, abolished the enhancement of RH in hypertensive patients treated with imidapril.CONCLUSIONSThese findings suggest that the ACE inhibitor imidapril augments RH after 12 weeks of treatment in patients with essential hypertension and that this ACE inhibitor-induced augmentation of RH may be due to an increase in NO.

Pathophysiology of brain edema in fulminant hepatic failure, revisited.

We have proposed a combined osmolar-hemodynamic disturbance to explain the presence of brain edema in fulminant hepatic failure, a major cause of death in this disorder. The concept of an osmotic disturbance in the brain, emphasizing the presence of astrocyte swelling and low-grade cerebral edema, has been expanded to the entire spectrum of liver disease. The mechanism of cerebral hyperemia in patients with FHF and brain swelling has been studied in experimental models linking hyperammonemia and glutamine generation in astrocytes to the development of this hemodynamic alteration. Measures to control cerebral hyperemia, such as mild hypothermia, are effective in preventing the development of brain edema in experimental models as well as intracranial hypertension in human disease.

Prostate vascular flow: the effect of ejaculation as revealed on transrectal power Doppler sonography.

The objective of our study was to determine the effect of ejaculation on prostate vascular flow. Using power Doppler technology, we performed four transrectal sonographic examinations before and immediately, 6 hr, and 24 hr after ejaculation in 10 healthy volunteers. Images were assessed by three independent observers. Ninety-seven percent of the images ranked as having the least flow were from the baseline examination. There was a significant difference between the rankings when categorized into the four time sets (mean score for the baseline group was 1.1, whereas for the immediate, 6-, and 24-hr postejaculation groups it was 2.5, 2.9, and 2.4, respectively (p<0.0001). The only statistically significant difference was between the baseline and the three remaining groups. Interobserver agreement was high, with the chance-corrected measure of agreement of 0.78. Transrectal sonography revealed that prostate vascular flow increases dramatically after ejaculation and remains elevated for at least 24 hr. This observation should be considered when power Doppler sonography is used to assess for potential hyperemia in patients suspected of having prostate abnormalities.

A comparison of angiotensin-converting enzyme inhibitors, calcium antagonists, beta-blockers and diuretic agents on reactive hyperemia in patients with essential hypertension: a multicenter study

OBJECTIVESThe purpose of this study was to compare the effect of different antihypertensive agents, calcium antagonists, angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and diuretic agents on endothelial function.BACKGROUNDEndothelial dysfunction is a component of essential hypertension, and various antihypertensive drugs may be able to restore normal function.METHODSForearm blood flow (FBF) was measured in 296 patients with essential hypertension, including 46 untreated subjects using strain-gauge plethysmography during reactive hyperemia and after sublingual administration of nitroglycerin (NTG). Forty-seven normotensive subjects were similarly evaluated as control subjects.RESULTSThe FBF during reactive hyperemia in the 296 hypertensive patients was significantly less than that in age-matched normotensive subjects. The increase in FBF after administration of sublingual NTG was similar in both groups. Systolic and diastolic blood pressures and forearm vascular resistance were greater in the untreated group than in the four treated groups and did not differ with respect to the antihypertensive agent used. The maximal FBF response from reactive hyperemia was significantly greater in the ACE inhibitor–treated group than in the group treated with calcium antagonists, beta-blockers, diuretic agents, or nothing (40.5 ± 5.2 vs. 32.9 ± 5.8, 34.0 ± 5.6, 32.1 ± 5.9, and 31.9 ± 5.8 ml/min per 100 ml tissue, p < 0.05, respectively). Reactive hyperemia was similar in the calcium antagonist, beta-blocker, diuretic and untreated groups, and changes in FBF after sublingual NTG administration were similar in all groups. The infusion of NG-monomethyl-l-arginine, a nitric oxide (NO) synthase inhibitor, abolished the enhancement of reactive hyperemia in hypertensive patients treated with ACE inhibitors.CONCLUSIONSThese findings suggest that ACE inhibitors augment reactive hyperemia, an index of endothelium-dependent vasorelaxation, in patients with essential hypertension. This augmentation may be due to increases in NO.

Determinants of post-ischaemic reactive hyperaemia in patients with diabetes mellitus type II.

Dysfunction of resistance arteries is thought to be an early reversible stage in the development of atherosclerosis. Dynamics of post-ischaemic reactive hyperaemia are believed to constitute a useful tool for monitoring resistance vessel function. Patient characteristics influencing reactive hyperaemia, however, need to be defined more precisely. Since reactive hyperaemia is a dynamic process, yielding submaximal peak values after 5 min of ischaemia, this period was chosen to investigate the determinants of reactive hyperaemia in 100 type II diabetic patients as well as in 61 control subjects. Reactive hyperaemia was measured by venous-occlusion plethysmography; clinical and laboratory data were acquired by routine methods. Statistical comparison was performed with SYSTAT 5.0 for Apple Macintosh. Overall, no significant differences between diabetic patients and controls were observed by group comparison. In control subjects, only gender showed an influence on peak reactive hyperaemia (females 40.5 +/- 15.3; males 51.8 +/- 17.7 ml min-1 100 ml-1, P < 0.01). In diabetic patients, in addition to gender, actual blood glucose (r = 0.377, P < 0.05) and meal intake (non-fasting 42.8 +/- 19.2; fasting 51.2 +/- 19.5 ml min-1 100 ml-1, P < 0.05) were found to influence reactive hyperaemia. Further investigation revealed a loss of the correlation between peak reactive hyperaemia and actual blood glucose observed in the fasting state (P < 0.001) in non-fasting diabetic patients, indicating an influence of meal intake on resistance vessel reactivity. Our results suggest that, in diabetic subjects, in addition to gender actual blood glucose and the postprandial situation impacts on peak reactive hyperaemia.

Impaired maximum microvascular hyperaemia in patients with MODY 3 (hepatocyte nuclear factor-1alpha gene mutations).

Functional abnormalities of blood flow and capillary pressure may be involved in the pathogenesis of diabetic microangiopathy. Important differences in microvascular behaviour are observed between Type 1 and Type 2 diabetes mellitus, raising the possibility that the pathogenesis of microangiopathy may differ between these. MODY3 patients have hyperglycaemia as a result of genetic defect of beta-cell function rather than increased insulin resistance and are susceptible to microvascular complications and offer an opportunity to examine microvascular behaviour in this setting. The maximum microvascular hyperaemic response to local heating of the skin was studied in 12 MODY3 patients and age and sex-matched control subjects using laser Doppler fluximetry. Maximum hyperaemia was reduced in MODY3 patients (median 1.17 (range 0.88-1.92)V vs. 1.70 (1.07-2.19)V normal control subjects; P=0.03) and thus was negatively associated with duration of diabetes (r(s)=-0.79; P = 0.002). The results suggest that the duration of diabetes is a determinant of impaired microvascular hyperaemia in MODY3 patients. The pattern of vasodilatory impairment is similar to that observed in Type 1 diabetes mellitus and differs from that seen in Type 2 diabetes. This provides support for the concept that beta cell dysfunction and insulin resistance may have differing effects on microvascular behaviour.

Latanoprost treatment for glaucoma: effects of treating for 1 year and of switching from timolol

PURPOSETo determine the efficacy and safety of latanoprost treatment for 1 year in glaucoma patients, and to evaluate the effects of switching from timolol to latanoprost therapy.METHODSLatanoprost 0.005% was topically applied once daily without masking for 6 months in 223 patients with elevated intraocular pressure after previous treatment with latanoprost once daily or 0.5% timolol twice daily for 6 months in a multicenter, randomized, double-masked, parallel group study.RESULTSCompared with baseline values before treatment, a significant (P < .0001) diurnal reduction in intraocular pressure of 6 to 8 mm Hg was maintained with minimal fluctuation for the duration of treatment. When treatment was switched from timolol to latanoprost, intraocular pressure was reduced by 1.5 ± 0.3 mm Hg (mean ± SEM; 8% change in intraocular pressure; 31% of the intraocular pressure reduction produced by timolol; P < .001) compared with the change in intraocular pressure in patients remaining on latanoprost therapy. Of the patients initially enrolled, 95% successfully completed treatment. There was a slight overall increase in conjunctival hyperemia in patients who switched from timolol to latanoprost, but no change in those who continued latanoprost. The timolol-induced reduction of resting heart rate returned to baseline levels after switching to latanoprost. Of the 247 patients treated with latanoprost during the masked and/or open-label studies, 12 (5%) demonstrated a definite (n = 4) or possible (n = 8) increase in iris pigmentation.CONCLUSIONSLatanoprost is a well-tolerated ocular hypotensive agent that appears to be more effective than timolol in reducing intraocular pressure. The increase in iris pigmentation appears to be harmless but requires further investigation.

Role of endothelium in control of forearm bloodflow in patients with heart failure

We studied the role of endothelium in control of forearm blood flow during reactive and exercise hyperemia in patients with heart failure as well as in normal subjects. First, endothelium-dependent forearm vasodilation in response to acetylcholine (ACh), substance P, and endothelium-independent forearm vasodilation in response to sodium nitroprusside (SNP) were examined in patients with heart failure and in normal subjects. Endothelium-dependent forearm vasodilation in response to ACh but not to substance P was impaired in patients with heart failure. Endothelium-independent forearm vasodilation to SNP was also preserved in patients with heart failure. Second, the role of nitric oxide (NO) in reactive hyperemia and exercise hyperemia was examined in normal subjects using NG-monomethyl-L-arginine (L-NMMA), a blocker of NO synthesis. Results suggest that NO plays a minimal role in peak reactive hyperemia and exercise hyperemia in normal human forearm vessels. Finally, we determined if L-arginine, a precursor of NO, improves impaired endothelium-dependent vasodilation due to ACh and reactive and exercise hyperemia in patients with heart failure. L-Arginine augmented impaired ACh-induced vasodilation as well as reactive and exercise hyperemia in patients with heart failure. Our results suggest that defective endothelial function may contribute to abnormal control of forearm blood flow in patients with heart failure.

Postprandial splanchnic hemodynamic response in patients with cirrhosis of the liver: evaluation with "triple-vessel" duplex US.

To investigate the effect of a meal on splanchnic circulation in patients with cirrhosis of the liver. Ten adult patients with cirrhosis and 10 adult control subjects (mean age, 54 years) underwent duplex ultrasonography. Flow volumes of the portal vein, superior mesenteric artery, splenic artery, and collateral vessels (difference between the splanchnic inflow [the sum of the superior mesenteric arterial and the splenic arterial blood flows] and the portal venous blood flow) were measured before and after a meal every 15 minutes for 60 minutes. Integrated post-prandial changes (the sum of the changes at each time point) were also calculated. Portal venous blood flow increased after the meal in control subjects (P < .01) and patients (P < .01). The integrated postprandial change in the portal venous blood flow was lower in patients than in control subjects (P < .05). Superior mesenteric arterial blood flow increased after the meal in control subjects (P < .01) and patients (P < .01); the integrated postprandial change in the superior mesenteric arterial blood flow was similar. In the two groups, splenic arterial blood flow remained unchanged after the meal. Collateral blood flow increased after the meal in patients (P < .01). Postprandial portal hyperemia is mainly due to mesenteric arterial vasodilation; reduced postprandial portal hyperemia in patients with cirrhosis is attributable to portocollateral runoff.

Dynamic planar myocardial perfusion imaging in patients with one-vessel disease with intracoronary injection of technetium 99m teboroxime during papaverine-induced coronary hyperemia

This study examined the imaging results and kinetics of technetium 99m teboroxime after its intracoronary injection during papaverine-induced coronary hyperemia in patients with one-vessel disease before and after coronary angioplasty. Thirteen patients with ≥90% diameter stenosis of either the left anterior descending or the left circumflex coronary artery were included. Two patients were excluded because of ventricular tachycardia during papaverine injection in one patient and unsuccessful angioplasty in the second patient. One mCi of technetium 99m teboroxime was injected into the left main coronary artery during coronary hyperemia induced by intracoronary injection of papaverine. Dynamic acquisition in a frame mode (20 sec/frame) was performed for 5 minutes in the left anterior oblique projection with a multicrystal gamma camera before and after successful angioplasty. Ischemic:normal count ratio increased from 0.75 ± 0.4 before to 1.00 ± 0.50 after angioplasty ( p < 0.1). The T 1 2 of teboroxime was 6.5 ± 1.5 min in the normal zone and 7.2 ± 1.9 min in the ischemic zone ( p, NS). Perfusion defects were visible in the territory of the stenosed coronary artery in 9 of 11 patients before angioplasty and in 7 of 11 patients after angioplasty. The image quality was excellent in all studies. Thus this study shows that performing dynamic imaging with intracoronary injection of technetium 99m teboroxime is feasible. This technique may be useful to study the impact of angioplasty on coronary flow and tracer kinetics.

Enhancement of coronary reactive hyperemia in patients with ischemic myocardial tolerance during angioplasty

The purpose of this study was to elucidate the effect of repeated brief coronary occlusions on reactive hyperemia during percutaneous transluminal coronary angioplasty (PTCA) in patients with or without ischemic tolerance. Seventeen patients undergoing PTCA for chronic stable angina were studied. Patients with well developed collateral vessels were excluded. After successful predilatation, coronary flow velocity was recorded with the use of a Doppler flow guide wire, and reactive hyperemia was assessed immediately after each of two 2-min coronary occlusions followed by 2 mins of reperfusion. The intracoronary electrocardiogram (icECG) was recorded via the flow guide wire placed in the center of the ischemic zone. Patients were divided into two groups: those who showed a reduction of ST elevation in the icECG recorded at the time of the second coronary occlusion (group I), and those who showed no difference in ST elevation between the two occlusions (group II). There were no significant differences in blood pressure, heart rate, or baseline coronary flow velocity between the two groups before the first occlusion, but the ST elevation at the time of the first coronary occlusion was greater in group I than in group II (8.9 +/- 6.2 versus 1.1 +/- 2.0 mm, P < 0.01). Reactive hyperemia was significantly greater after the second coronary occlusion than after the first in group I (22.1 +/- 15.8 versus 30.4 +/- 21.0 cm/s, P < 0.05), but it did not change in group II (25.6 +/- 13.0 versus 23.5 +/- 11.2 cm/s NS). Reactive hyperemia was enhanced in patients with ischemic tolerance who showed a reduction in St elevation in the icECG. These results suggest that observed reactive hyperemia does not necessarily reflect the severity of ischemia.

Octreotide prevents postprandial splanchnic hyperemia in patients with portal hypertension

An increase in splanchnic blood flow is a physiological response to food intake. In patients with cirrhosis whose hepatic vascular resistance is already high, this increase in flow leads to marked increases in portal pressure. This study investigates whether octreotide prevents the increases in hepatic flow and portal pressure that follow the ingestion of a meal in patients with cirrhosis. Twenty-two patients with cirrhosis and portal hypertension were randomized to receive a mixed liquid meal (520 kcal) plus a single subcutaneous injection of either placebo or octreotide (200 micrograms). In the placebo group the ingestion of a meal was followed by an increase in the hepatic venous pressure gradient (+ 19.4 +/- 4.3%, p < 0.01) and hepatic blood flow (+ 38.2 +/- 14.6%, p < 0.05) at 30 min. In contrast, in the octreotide group eating caused no significant change in the hepatic venous pressure gradient (-2.8 +/- 3.6%, NS), while hepatic flow was decreased (-6.08 +/- 5.4%, p < 0.05). Octreotide blunted the postprandial increase in serum insulin and glucagon levels observed in the placebo group. In conclusion, in patients with cirrhosis and portal hypertension, octreotide prevents the postprandial increase in hepatic blood flow, and consequently also in portal pressure. These findings suggest that this drug could play a role in the long-term management of portal hypertension.

Regional specificity of peak hyperemic responses in patients with congestive heart failure: Correlation with peak aerobic capacity

Objectives. The aim of this study was to compare peak reactive peremic blood flows in the forearm and calf of patients with congestive heart failure and in age- and gender-matched normal subjects. In addition, we attempted to correlate peak oxygen consumption with forearm and calf peak reactive hyperemic flows in the patients with heart failure.Background. Disparate results have been reported regarding forearm peak reactive hyperemia in patients with congestive heart failure. Because training significantly increases peak reactive hyperemic flow in normal subjects, we hypothesized that in patients with congestive heart failure who curtail walking because of exertional symptoms, calf peak reactive hyperemic flow would be preferentially attenuated and that impairment of calf vasculature may correlate with peak oxygen consumption.Methods. Forearm and calf blood flows were measured by venous occlusive plethysmography at rest and after 5 min of arterial occlusion in 46 patients with congestive heart failure and 7 age- and gender-matched normal subjects. Peak oxygen consumption was measured during graded exercise on a bicycle ergometer.Results. Calf peak reactive hyperemic flow was lower in patients with congestive heart failure than in normal subjects (22 ± 1 vs. 32.5 ± 3.5 ml/min per 100 ml, p < 0.001), whereas forearm reactive hyperemic flows were similar in the two groups. Calf peak reactive hyperemic flow was linearly related to peak oxygen consumption (r = 0.58, p < 0.0001), but forearm peak reactive hyperemic flow was not. Forearm and calf peak reactive hyperemic flows were not related at rest or after 5 min of arterial occlusion in the patients with heart failure.Conclusions. Calf peak reactive hyperemic flow is reduced in patients with congestive heart failure, whereas forearm peak reactive hyperemic flow is identical to that of age- and gender-matched normal subjects. Calf peak reactive hyperemic flow is linearly related to peak oxygen consumption in patients with congestive heart failure, but forearm peak reactive hyperemic flow is not.

The effects of ionic and nonionic radiographic contrast media on coronary hyperemia in patients during coronary angiography

The purpose of this study was to compare the differential effects of ionic, high-osmolar meglumine diatrizoate; ionic, low-osmolar ioxaglate meglumine; and nonionic, low-osmolar iohexol (all radiographic contrast agents) on coronary blood flow velocity and hyperemic responses during diagnostic coronary angiography. Coronary flow velocity and arterial pressure were measured at baseline and during maximal hyperemia after contrast media were randomly injected (4 to 6 ml into left coronary artery) in 22 patients with the use of a Judkins-style 20 MHz Doppler-tipped angiographic catheter. Contrast media-induced hyperemic responses were compared to those induced with intracoronary nitroglycerin (200 μg) and papaverine (10 mg). There were no significant differences in systolic, diastolic, or mean arterial pressure measurements among the three contrast agents. The increase in mean coronary flow velocity during hyperemia was 118 ± 93%, 133 ± 73%, and 136 ± 86% for iohexol, ioxaglate meglumine, and diatrizoate, respectively ( p = NS among agents vs 264 ± 109% for papaverine; p < 0.05 for all). Coronary vasodilatory reserve (calculated as the ratio of hyperemic to basal mean flow velocity) was also similar among agents. It was comparable to the coronary vasodilatory reserve with nitroglycerin (2.1 ± 1.0 to 2.2 ± 1.1) and significantly less than that with papaverine (3.3 ± 2.2, p < 0.05). These data indicate that the clinical advantages of nonionic or low-osmolar contrast media are not mechanistically related to significant attenuation of the coronary hyperemic response.

Skin perfusion patterns (fluorescein perfusography) during reactive hyperaemia in peripheral arterial occlusive disease

From the pathophysiological point of view the regional distribution of blood flow is of special importance in ischaemic tissues. Within this study foot sole skin perfusion was investigated by means of fluorescein perfusography at rest and during reactive hyperaemia in patients with peripheral arterial occlusive disease confined to one limb (Fontaine stage II). Ambient temperatures were maintained around 21 degrees C. Mean fluorescein appearance times on the one side and their standard deviations (SD) and coefficients of variation (CV) on the other side were taken as measures of overall blood supply and homogeneity of flow, respectively. At rest no differences in these parameters could be detected between diseased legs and controls. After a 3-min supra-systolic circulatory arrest at the thigh, a significant reduction of fluorescein appearance times was observed for both groups but was statistically more pronounced in the controls. Furthermore, during reactive hyperaemia standard deviations as well as coefficients of variation decreased significantly only in normal limbs whereas they either remained constant (SD) or even increased (CV) in those with arterial obstructions. All effects associated with reactive hyperaemia showed statistically significant correlations with systolic ankle pressure indices. From these results it is concluded that haemodynamically effective arterial obstructions are followed by not only a restriction of overall hyperaemic blood supply but also a failure to homogenize microcirculatory perfusion in the case of increased flow requirements.

Hypertonic glucose infusion causes splanchnic hyperemia in patients with cirrhosis

Hypertonic glucose infusion causes splanchnic hyperemia in patients with cirrhosis

Effect of diltiazem on coronary reactive hyperemia in patients with flow-limiting coronary artery stenosis

The acute effects of diltiazem on coronary reactive hyperemia were studied in 12 patients with flow-limiting coronary stenosis. Reactive hyperemia was elicited by injection of 8 ml contrast medium into the left coronary artery, while coronary sinus blood flow and left ventricular and aortic pressures were continuously recorded. Relative magnitude of hyperemia was estimated by the ratio of coronary flow at peak hyperemia to baseline flow (hyperemic ratio). Coronary resistance was calculated as the ratio between mean aortic pressure minus left ventricular mean diastolic pressure and coronary sinus blood flow. The 12 patients studied had flow-limiting coronary stenosis since their hyperemic ratio was significantly restrained when compared to that of seven control subjects (1.45 ± 0.17 vs 2.02 ± 0.24, respectively; < 0.001). The intravenous infusion of ditiazem (0.30 mg · kg −1) reduced heart rate, mean aortic pressure, and myocardial oxygen consumption (all p < 0.001). After diltiazem the hyperemic ratio was blunted when compared to the basal state (1.36 ± 0.15 vs 1.45 ± 0.17, respectively; p < 0.05), and hyperemia volume was reduced (−33%; p < 0.001). The decrease in coronary resistance at peak hyperemia was also reduced from −30 ± 8% to −25 ± 8% ( p < 0.05). We conclude that diltiazem blunts coronary reactive hyperemia in patients with demonstrated flow-limiting coronary stenosis. This reduction of coronary flow response to a hyperemic stimulus could favorably influence blood flow distribution in patients with significant coronary stenosis.