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Biomedical subjects

B Gómez

Publications and source records attributed to B Gómez.

At least 19 recordsLinked to original sources
PubMed1992

Carotid blood flow in anesthetized rats: effects of carotid ligation and anastomosis.

An experimental model was developed for continuous measurement of the common carotid blood flow, in the anesthetized rat, with an electromagnetic flowmeter. The mean carotid blood flow for 41 rats averaged 3.2 +/- 0.2 ml/min at an average mean arterial pressure of 101 +/- 2.5 mm Hg and arterial pO2 of 106 +/- 3.4 mm Hg, pCO2 of 38 +/- 1.2 mm Hg, and pH of 7.36 +/- 0.02. This model allowed short- and long-term carotid hemodynamic changes to be recorded after contralateral carotid ligation or end-to-side carotid anastomosis. After ligation of the contralateral carotid, blood flow through the intact carotid increased 25% (at about 1 week) and 45% (at about 5-6 months), whereas, after anastomosis, carotid blood flow increased 76% and 89% at periods comparable to those after ligation. Arterial pressure and gases did not change throughout the experimental periods. Probable mechanisms involved in these carotid hemodynamic changes are discussed.

Anastomosis, Surgical↗
PubMed1992

Effects of nitric oxide synthesis inhibition on the goat coronary circulation under basal conditions and after vasodilator stimulation.

1. The role of nitric oxide in the coronary circulation under basal conditions and when exposed to various vasodilator stimuli was studied in instrumented, anaesthetized goats, by examining the action of inhibiting endogenous nitric oxide production with NG-nitro-L-arginine methyl ester (L-NAME). 2. In 12 goats, left circumflex coronary blood flow (electromagnetically measured), systemic arterial blood pressure and heart rate were continuously recorded. L-NAME (3-4, or 8-10 mg kg-1 injected i.v.) decreased resting coronary blood flow by 20 and 28%, increased mean arterial pressure by 23 and 30% and increased coronary vascular resistance by 47 and 65%, respectively, without affecting heart rate, or blood gases or pH. These haemodynamic effects were reversed by L-arginine (200-300 mg kg-1 by i.v. injection, 5 goats). 3. Acetylcholine (0.001-0.1 micrograms), sodium nitroprusside (0.01-0.3 mg), and diazoxide (0.1-3 mg), injected intracoronarily in 6 goats, produced dose-dependent increases in coronary blood flow; sodium nitroprusside (0.1-0.3 mg) also caused hypotension and tachycardia. 4. During the effects of L-NAME, the coronary vasodilatation to acetylcholine was attenuated, to sodium nitroprusside was increased, and to diazoxide was unaffected, in comparison with control conditions. The hypotensive effects of sodium nitroprusside were also increased during treatment with L-NAME. 5. Graded coronary hyperaemic responses occurred after 5, 10 or 20 s of coronary occlusion. The magnitude of hyerpaemia for each occlusion duration was increased during treatment with L-NAME, in comparison to control.6. The results suggest: (a) endogenous nitric oxide is involved in regulation of coronary circulation by producing a basal vasodilator tone, (b) acetylcholine-induced coronary vasodilatation is mediated, in part, by nitric oxide, and (c) inhibition of basal endogenous nitric oxide production induces supersensitivity of coronary vessels to nitrovasodilators and enhances hyperaemic responses after short periods of ischaemia of the myocardium.

Acetylcholine↗
PubMed1992

Cooling and response to adrenoceptor agonists of rabbit ear and femoral artery: role of the endothelium.

1. The effects of cooling on the response of the rabbit central ear (cutaneous) and femoral (non-cutaneous) arteries to stimulation of adrenoceptors and the role of the endothelium in these effects, were studied in 2 mm long cylindrical segments. 2. Concentration-response curves for noradrenaline (10(-9)-3 x 10(-4) M), phenylephrine (alpha 1-adrenoceptor agonist, 10(-9)-3 x 10(-4) M) and B-HT 920 (alpha 2-adrenoceptor agonist, 10(-7)-10(-3) M) were recorded isometrically in arteries with and without endothelium at 37 degrees C and at 24 degrees C (cooling). To analyze further the endothelial mechanisms in the responses to adrenoceptor stimulation during cooling, the effects of the adrenoceptor agonists on ear arteries in the presence of NG-nitro-L-arginine methyl esther (L-NAME) (10(-5) M) were also determined. 3. In every condition tested, the three adrenoceptor agonists produced a concentration-dependent arterial contraction and the order of potency in ear and femoral arteries was noradrenaline greater than or equal to phenylephrine greater than B-HT 920. The response of ear and femoral arteries to phenylephrine or B-HT 920 was blocked by prazosin (10(-6) M). Yohimbine (10(-6) M) decreased slightly the response of ear arteries and increased that of femoral arteries to B-HT 920. 4. The sensitivity of both ear and femoral arteries to the three adrenoceptor agonists was significantly lower at 24 degrees C than at 37 degrees C. 5. In ear arteries, endothelium removal or treatment with L-NAME did not influence the response at 37 degrees C, but did increase it during cooling to adrenoceptor stimulation.In femoral arteries, endothelium removal increased the sensitivity to noradrenaline and, especially, to B-HT 920 at 37 degrees C, but did not affect the response at 24 degrees C.6. The results suggest that: (a) rabbit ear and femoral arteries are equipped mainly with alpha 1-adrenoceptors;(b) at 37 degrees C, the contraction of the ear artery to adrenoceptor agonists is mostly endothelium-independent, and in the femoral artery the contraction to alpha 2-adrenoceptor activation is endothelium-dependent; (c) cooling inhibits the contraction to adrenoceptor agonists in both ear and femoral arteries: in the ear artery probably by increasing the availability of endothelial nitric oxide, but in the femoral artery by depressing the sensitivity of alpha-adrenoceptors in the smooth musculature.7. The results suggest that the endothelium may modulate the adrenoceptor response of cutaneous arteries during changes in temperature.

Adrenergic alpha-Agonists↗
PubMed1992

Cerebrovascular and coronary effects of endothelin-1 in the goat.

In vivo and in vitro effects of endothelin-1 (ET-1) on cerebral and coronary vasculature of goats were examined and compared. In six anesthetized goats intravenous injections of ET-1 (0.1-0.8 nmol) increased arterial pressure, did not change the middle cerebral (MCA) and left anterior descending or left circumflex coronary (LCC) arterial blood flows (electromagnetically measured), and increased cerebral and coronary vascular resistances. In four other anesthetized goats intra-arterial injections of ET-1 (0.01-0.3 nmol) decreased the MCA flow less than the LCC flow (maximal reduction was 20 and 80%, respectively) and only the highest dose increased arterial pressure. In isolated segments from large arteries ET-1 (10(-11) to 10(-7) M) caused concentration-dependent isometric contractions, the concentration causing 50% of the maximal effect and the maximal contraction being lower in cerebral arteries than in coronary arteries. The in vitro reactivity of both arteries was unaffected by endothelium removal or by indomethacin (10(-5) M). Therefore ET-1 produces cerebral and coronary vasoconstriction in vivo and in vitro, probably by acting directly on vascular musculature. Although the sensitivity is higher in isolated cerebral arteries than in coronary arteries, the reactivity in vivo could be lower in the cerebral circulation than in the coronary circulation to this endothelium-derived peptide.

Animals↗
PubMed1992

Effects of hypoglycemia on the cerebral circulation in awake goats.

We electromagnetically measured blood flow to one cerebral hemisphere and determined cerebrovascular reactivity to vasoconstrictor and vasodilator stimuli during normoglycemia and insulin-induced hypoglycemia in unanesthetized goats. Control blood glucose concentration was 84 +/- 4 mg, and insulin, injected intravenously, decreased glycemia with a concomitant increment in cerebral blood flow and reduction in cerebrovascular resistance in all the animals. When glycemia decreased to 60 to 65 mg/dl, the animals began to show signs of increased adrenergic activity, and when it decreased to less than 30 mg/dl, they showed signs of CNS depression. Cerebral blood flow began to rise significantly at a glycemia of 50 to 55 mg/dl, and progressively increased to reach an increment of 36% +/- 4% when glycemia was less than 30 mg/dl. Norepinephrine (0.3 to 9 micrograms), tyramine (50 to 500 micrograms), and 5-hydroxytryptamine (0.1 to 9 micrograms) reduced cerebral blood flow, and this effect was lower during severe hypoglycemia. Acetylcholine (0.01 to 1 microgram), isoproterenol (0.03 to 3 micrograms), diazoxide (0.3 to 9 mg), and inhalation of 10% CO2 in air increased cerebral blood flow, and this effect was also lower during severe hypoglycemia. The results show that insulin-induced hypoglycemia causes cerebral vasodilation and reduction of the capacity of cerebral blood vessels to constrict and dilate. They also show that the glycemic thresholds for increasing cerebral blood flow are near to, or slightly lower than, the thresholds for hypoglycemic symptoms. This experimental model of hypoglycemia closely resembles the conditions in hypoglycemic patients and permits serial evaluation of the cerebrovascular effects of hypoglycemia without using anesthesia.

Animals↗
PubMed1992

Serosurveillance of susceptibility to rubella in a Mexican female group.

The susceptibility to rubella of a group of Mexican females of childbearing age was determined. Members of the group were selected based on the highest probability of having been exposed to the virus they were older than 15, and from a low socio-economic urban stratum. Anti-viral antibodies were determined by hemagglutination inhibition. Concentration was expressed as International Units of IgG anti-rubella hemagglutinin (IU). Antibody concentrations lower than 15.6 IU/ml were regarded as non-protective. A 16% susceptibility was found.

Adolescent↗
PubMed1991

Alpha 1- and alpha 2-adrenergic response in human isolated skin arteries during cooling.

1. Dose-response curves for noradrenaline, phenylephrine and clonidine were determined isometrically in 2-mm cylindrical segments from human skin arteries at 24 degrees C and compared to those previously reported at 37 degrees C. 2. Noradrenaline (3 x 10(-10)-3 x 10(-4) M) induced dose-dependent contraction and the sensitivity was increased during cooling. Phentolamine (10(-6) M), prazosin (10(-6) M) or yohimbine (10(-6) M) produced a higher rightward shift of the control curve for noradrenaline during cooling. 3. Phenylephrine (10(-11)-3 x 10(-4) M) and clonidine (10(-11)-10(-6) M) caused dose-dependent contraction and the sensitivity of the arteries was augmented at 24 degrees C. 4. The arteries also showed a lower maximal contraction to the adrenergic agonists used and KCl (50 mM) during cooling. 5. The results suggest that cooling: (a) increases sensitivity of postjunctional alpha 1- and alpha 2-adrenoceptors in human skin arteries and (b) depresses contractility of these arteries to alpha-adrenergic stimulation and direct activation of vascular smooth muscle.

Adult↗
PubMed1991

Response of rabbit ear artery to endothelin-1 during cooling.

1. The effects of cooling on the response of rabbit central ear artery to endothelin-1 and the role of the endothelium in these effects were studied in 2 mm long cylindrical arterial segments. 2. Concentration-response curves for endothelin-1 (10(-10)-3 x 10(-7) M) were recorded isometrically in arteries with and without endothelium at 37 degrees C and during cooling (24 degrees C). To analyze further the endothelial mechanisms of the response to endothelin-1 during cooling, the effects of this peptide in the presence of NG-nitro-L-arginine methyl ester (L-NAME) (10(-4) M) or meclofenamate (10(-5) M) were also determined. 3. In every condition tested, endothelin-1 produced a marked, concentration-dependent arterial contraction. Sensitivity of intact arteries to this peptide was consistently lower at 24 degrees C than at 37 degrees C. At 37 degrees C there were comparable responses of arteries with and without endothelium, but at 24 degrees C arteries without endothelium showed a higher sensitivity than intact arteries to endothelin-1. 4. L-NAME (10(-4) M) increased the maximal contraction at 37 degrees C, and both the sensitivity and maximal contraction at 24 degrees C of intact arteries to endothelin-1. Meclofenamate (10(-5) M) did not affect the arterial response to endothelin-1. 5. Sensitivity of arteries with and without endothelium to nitroprusside (10(-9)-10(-3) M) was significantly decreased during cooling, and endothelium removal did not affect the relaxation to this nitrovasodilator. 6. These results suggest that cooling decreases sensitivity of cutaneous arteries (ear artery) to endothelin-1 probably by increasing the availability of endothelial nitric oxide.

Animals↗
PubMed1991

Response of canine cerebral arteries to endothelin-1.

The effects of endothelin-1 (10(-10)-10(-7) M) were isometrically recorded in 4 mm cylindrical segments from the middle cerebral artery of dogs. Cumulative application of endothelin-1 produced marked, sustained contraction of arteries in a concentration-dependent-manner, the maximal response being about 2.6 times higher than that achieved with KCl (50 mM). The contraction by endothelin-1 was unaffected either by endothelium removal or by the cyclo-oxygenase inhibitors indomethacin (10(-6) M) and meclofenamate (10(-6) M). In a Ca(2+)-low (25 microM) solution the endothelin-1-induced arterial contraction was decreased. Therefore, the cerebral vasoconstriction induced by endothelin-1 could be caused by activation of specific receptors located on smooth muscle cells which would lead to the influx of extracellular calcium and vascular musculature contraction.

Animals↗
PubMed1991

Response of canine internal carotid system to acetylcholine.

The reactivity of the canine internal carotid system to acetylcholine (10(-8)-10(-4) M) was studied isometrically with 4-mm cylindrical segments from cervical and cavernous portions of the internal carotid artery and from the middle cerebral artery. Under control conditions, the cervical portion relaxed to every dose, the cavernous portion relaxed at low concentrations (10(-8)-10(-6) M) and contracted at higher concentrations (10(-5)-10(-4) M), whereas the middle cerebral artery contracted to every dose of acetylcholine. These responses were blocked by atropine (10(-6) M). Without endothelium, the cervical portion exhibited a lower relaxation, the cavernous portion contracted, and the middle cerebral artery was practically unresponsive to acetylcholine. These responses were also blocked by atropine. It suggests that the reactivity of the internal carotid system to acetylcholine 1) is endothelium dependent and 2) changes as it courses toward the brain, and this could be related to different embryological origin of the components of this arterial system.

Acetylcholine↗
PubMed1991

Endothelin action on cerebral circulation in unanesthetized goats.

The effects of endothelin 1 on the internal maxillary artery blood flow, measured as an index of cerebral blood flow, were examined in six unanesthetized goats under control conditions, hypercapnia induced by inhalation of 10% CO2 in air, hypertension by intravenous infusion of norepinephrine, and hypotension by intravenous injection of diazoxide. Under control, administration of endothelin (0.01-0.3 nmol) into the internal maxillary artery produced dose-dependent sustained decreases in cerebral blood flow and increases in cerebrovascular resistance; higher doses (0.1 and 0.3 nmol) also caused hypertension and bradycardia. During hypercapnia or hypertension, endothelin did not significantly affect cerebral blood flow, and only higher doses (0.1 and/or 0.3 nmol) increased cerebrovascular resistance, but this was lower than under control. However, under hypotension endothelin evoked a higher reduction in cerebral blood flow and increment in cerebrovascular resistance, and systemic effects were also more marked than under control. Therefore endothelin is a potent cerebral vasoconstrictor, and this effect is very attenuated during hypercapnia and hypertension but is increased under hypotension.

Animals↗
PubMed1990

Serologically proven acute rubella infection in patients with clinical diagnosis of dengue.

Patients with a clinical diagnosis of dengue but negative by serological testing were studied for rubella infection. Paired sera were obtained from 69 patients during an outbreak in Yucatán, México. The presence of specific anti-viral IgM in the acute sera was considered as diagnostic for rubella infection. The immunoglobulin was determined by measuring the difference in the inhibition of hemagglutination between the non-reduced and the reduced fractionated sera. Immunoglobulins were separated by sucrose density centrifugation. Acute rubella infection was found in 7 (10.1%) of the patients. These results demonstrate active rubella infection in patients clinically diagnosed as dengue.

Acute Disease↗
PubMed1990

Endothelial cells inhibit the vascular response to adrenergic nerve stimulation by a receptor-mediated mechanism.

Rabbit central ear arteries, with and without endothelium, were perfused at a constant flow rate and the perfusion pressure was measured as an index of the vessel resistance. Transmural nerve stimulation (TNS) induced a frequency-dependent increase in perfusion pressure in all vessels that was blocked by tetrodotoxin, phentolamine, and prazosin. Removal of endothelium significantly enhanced contractions induced by TNS. The inhibitory effect of endothelium was not modified by indomethacin but was abolished by hemoglobin, indicating that endothelium-derived relaxant factor (EDRF) was the vasodilator involved. The endothelium-dependent inhibitory effect (rubbed vessel minus control vessel contractions) increased with time during the first 10-20 s after the beginning of TNS, and was frequency dependent and inhibited by low doses of phentolamine, which suggest a receptor-mediated mechanism. To analyze whether amine neurotransmitters are able to permeate the artery wall and contact the endothelial cell membrane, the passage of [3H]acetylcholine from the abluminal side to the lumen was studied in intact vessels. [3H]acetylcholine readily permeated the vessel wall, as assessed by radioautography, and appeared in the perfusion fluid at a concentration that explains the relaxation induced by perivascular acetylcholine. These data suggest that endothelial cells modulate the effect of perivascular neurotransmitters by a receptor-mediated mechanism. In the case of the sympathetic innervation, such modulation would be more relevant at low levels of transmitter release and would be minimized during intense sympathetic stimulation.

Acetylcholine↗
PubMed1989

Mechanics of arteries forming the carotid rete of goat and cattle.

To determine the mechanics of arteries forming the carotid rete mirabile of goat and cattle, the wall tension-circumference length relationship was recorded isometrically in isolated retial arteries of 350-600 microns in external diameter under relaxed and potassium-activated conditions. The results are compared to those of pial arteries of similar size. In relaxed retial and cerebral vessels, tension-length relationship had nonlinear characteristics and the incremental elastic modulus rose as the circumference length increased, the modulus being lower in retial than in pial arteries. However, the stiffness of the artery considered as a whole (stiffness parameter beta) was similar in the two types of vessels. In activated arteries, force development was a function of length and the magnitude of the response increased until an optimal length was reached after which the response decreased with further stretch. In all stretches studied the developed force was much lower in retial arteries. The calculated active stress at the various lengths was also smaller in retial than in cerebral arteries and the maximum active stress for retial arteries was about 30-50% of that for cerebral arteries. Therefore, the passive mechanical properties of retial arteries closely resemble those of cerebral arteries but retial arteries have a small contractility. This suggests that the carotid rete mirabile of Artiodactyla has a minor role in actively controlling blood supply to the brain. Comments on the hemodynamic significance of the carotid rete are included.

Animals↗
PubMed1989

In vitro reactivity of dog cavernous carotid artery to stretch and adrenergic stimulation.

The reactivity of the dog cavernous carotid artery to stretch, field electrical stimulation, and norepinephrine was studied using arterial segments under isometric conditions. Light microscopy revealed that this artery is of muscular type and its external surface is covered by venous endothelium, and fluorescence microscopy showed a dense adrenergic innervation. On stretch, arteries exhibited an immediate, transient contraction (phasic response) and a late, maintained contraction (tonic response) that were unaffected by tetrodotoxin (10(-6) M) or endothelium removal but were reduced by the inhibitors of cyclooxygenase indomethacin (10(-6) M), acetylsalicylic acid (3 x 10(-5) M), or meclofenamate (10(-5) M). Electrical stimulation (0.5-4 Hz) contracted the arteries in a frequency-dependent manner, and the response was reduced by tetrodotoxin, phentolamine, (10(-6) M), or the inhibitors of cyclooxygenase used but was unaffected by endothelium removal. Norepinephrine (10(-9)-3 x 10(-4) M) caused dose-dependent contraction that was blocked by phentolamine and by the inhibitors of cyclooxygenase but was not modified by endothelium removal. The results indicate that the dog cavernous carotid artery develops myogenic tone on stretch and contracts on adrenergic stimulation. They also suggest that in these responses prostaglandins but not the endothelium are involved. Therefore, the cavernous carotid artery, because of its location and reactivity, could be of relevance in regulating blood flow or pressure within the cerebral circulation when arterial pressure or adrenergic activity increases.

Acetylcholine↗
PubMed1989

Postjunctional alpha-1 and alpha-2 adrenoceptors in human skin arteries. An in vitro study.

Experiments were performed to characterize the postjunctional alpha adrenoceptors that mediate adrenergic constriction in human skin arteries. Abdominal s.c. arteries were obtained from patients who died 3 to 12 hr before, and vascular segments 2 mm in length and 600 to 1050 microns in external diameter were prepared for isometric tension recording. On application of norepinephrine, phenylephrine (alpha-1 adrenergic agonist) or clonidine (alpha-2 adrenergic agonist) the arteries contracted in a dose-dependent manner and, in terms of the mean EC50 values, the order of potencies was clonidine greater than norepinephrine greater than phenylephrine. With regard to their ability to induce maximal contraction, the order was norepinephrine = phenylephrine greater than clonidine. In the presence of phentolamine (nonspecific alpha adrenergic antagonist) or yohimbine (selective alpha-2 adrenergic antagonist) the control curve for norepinephrine was displaced to the right in a parallel way. Prazosin (selective alpha-1 adrenergic antagonist) depressed both the slope and maximal response of the control curve for norepinephrine but the shift was not significant. Prazosin and yohimbine produced a parallel rightward shift in the control curve for phenylephrine and clonidine, respectively. These results suggest that skin arteries of humans have a mixed population of postjunctional alpha-1 and alpha-2 adrenoceptors and that alpha-2 adrenoceptors are more prominent. They also suggest that the alpha-2 adrenergic component of the response to norepinephrine is a low-maximum effect compared to the alpha-1 adrenergic component. This could be of significance in regulating skin blood flow and thermoregulatory function.

Adult↗